The  human microbiota  consists of 10–100 trillion microorganisms. [ 31 ]  Several studies have confirmed that the microbiota composition is different in patients with IBD compared to healthy individuals. [ 32 ]  This difference is more pronounced in patients with Crohn's disease than in those with ulcerative colitis. [ 33 ]  In IBD patients, there is a decrease or absence of beneficial bacteria such as  Bifidobacterium longum ,  Eubacterium rectale ,  Faecalibacterium prausnitzii , and  Roseburia intestinalis , while harmful species like  Bacteroides fragilis ,  Ruminococcus torques , and  Ruminococcus  are more abundant. [ 34 ]
The activation of  reactive oxygen species  and  reactive nitrogen species  leads to  oxidative stress  for both host cells and the  gut microbiome . Consequently, in IBD, there is a microbial imbalance, known as  dysbiosis , characterized by an increase in functional pathways involved in the microbial response to oxidative stress. This oxidative stress can promote the growth of certain species such as  R. gnavus . [ 35 ]  Another opportunistic bacterium called  A. muciniphila  contributes to IBD development and is more prevalent in individuals lacking  NOD-like receptor 6  (NLRP6). [ 36 ]  Both  R. gnavus  and  A. muciniphila  are bacterial species that are more abundant in IBD.
Patients with IBD often exhibit stronger  antibody  and  T-cell  responses to microbial  antigens . [ 37 ]  The gut microbiome employs various approaches to interact with the host immune system. For instance,  B. fragilis , which is  symbiotic  in humans, can transfer immune regulatory molecules to immune cells through the secretion of  outer membrane vesicles . This mechanism plays a protective role in IBD by activating the non-classical  autophagy  pathway, dependent on  Atg16L1  and  NOD2  genes. [ 38 ]   B. thetaiotaomicron  induces the differentiation of  T regulatory cells  (Tregs) to modulate gut immunity, thus increasing the expression of  Gata3  and  FoxP3  genes. [ 39 ]
The colonization of  Clostridium  spp. can enhance the aggregation of RORγT+ FOXP3 Treg cells, which inhibit the development of  Th2  and Th17 cells. Ultimately, this colonization could decrease the response of colonic Th2 and Th17 cells. [ 40 ]
Also  F. prausnitzii  attracts  CD4  and  CD8a  (DP8α) regulatory T cells. [ 41 ]
 E. coli  Nissle 1917 has the capability to inhibit the growth of  Salmonella  and other harmful bacteria. It prevents these pathogens from adhering to and invading  intestinal epithelial  cells, which significantly reduces the likelihood of inflammation in the gut and may also prevent the onset of IBD. [ 42 ]


Loss of integrity of the  intestinal epithelium  plays a key  pathogenic  role in IBD. [ 43 ]  Dysfunction of the  innate immune system  as a result of abnormal signaling through immune receptors called  toll-like receptors  (TLRs)—which activates an immune response to molecules that are broadly shared by multiple pathogens—contributes to acute and chronic inflammatory processes in IBD colitis and associated cancer. [ 44 ]  Changes in the composition of the  intestinal microbiota  are an important environmental factor in the development of IBD. Detrimental changes in the intestinal microbiota induce an inappropriate (uncontrolled)  immune response  that results in damage to the intestinal epithelium. Breaches in this critical barrier (the intestinal epithelium) allow further infiltration of microbiota that, in turn, elicit further immune responses. IBD is a multifactorial disease that is nonetheless driven in part by an exaggerated immune response to gut microbiota that causes defects in epithelial barrier function. [ 45 ]


Oxidative stress  and  DNA damage  likely have a role in the pathophysiology of IBD. [ 46 ]  Oxidative DNA damage as measured by  8-OHdG  levels was found to be significantly increased in people with IBD compared to healthy controls, and in inflamed mucosa compared with noninflamed mucosa. [ 46 ]  Antioxidant capacity as measured by the total action of all antioxidants detected in blood plasma or body fluids was found to be significantly decreased in people with IBD compared to healthy controls, and in inflamed mucosa compared with noninflamed mucosa. [ 46 ]


A genetic component to IBD has been recognized for over a century. [ 47 ]  Research that has contributed to understanding of the genetics include studies of ethnic groups (e.g.,  Ashkenazi Jews ,  Irish ), familial clustering, epidemiological studies, and twin studies. With the advent of molecular genetics, understanding of the genetic basis has expanded considerably, particularly in the past decade. [ 48 ]  The first gene linked to IBD was  NOD2  in 2001.


Genome-wide association studies have since added to understanding of the genomics and pathogenesis of the disease. More than 200  single nucleotide polymorphisms  (SNPs or "snips") are now known to be associated with susceptibility to IBD. [ 49 ]  One of the largest genetic studies of IBD was published in 2012. [ 50 ]  The analysis explained more of the variance in Crohn's disease and ulcerative colitis than previously reported. [ 48 ]  The results suggested that commensal microbiota are altered in such a way that they act as pathogens in inflammatory bowel diseases. Other studies show that mutations in IBD-associated genes might interfere with the cellular activity and interactions with the  microbiome  that promote normal immune responses. [ 51 ]  Many studies identified that  microRNAs  dysregulation involved in IBD and to promote  colorectal cancer . [ 52 ]  By 2020,  single-cell RNA sequencing  analysis was launched by a small consortium using IBD patient biopsy material in a search for therapeutic targets. [ 53 ]


According to an article published on Nature, ETS2 gene plays a vital role in the development of the disease. [ 54 ]


The diagnosis is usually confirmed by  biopsies  on  colonoscopy .  Fecal calprotectin  is useful as an initial investigation, which may suggest the possibility of IBD, as this test is sensitive but not specific for IBD. [ 55 ] [ 56 ]


Inflammatory bowel diseases are  autoimmune diseases , in which the body's own immune system attacks elements of the digestive system. [ 57 ]  The chief types of IBD are  Crohn's disease  (CD) and  ulcerative colitis  (UC). [ 58 ]  Several other conditions are variously referred to either as being inflammatory bowel diseases or as being similar to but distinct from inflammatory bowel diseases. These conditions include:


Crohn's disease and ulcerative colitis are both common differential diagnoses for the other, and confidently diagnosing a patient with one of the two diseases may sometimes not be possible. No disease specific markers are currently known in the blood that would enable the reliable separation of patients with Crohn's disease and ulcerative colitis. [ 63 ]  Physicians tell the difference between Crohn's disease and UC by the  location  and  nature  of the inflammatory changes. Crohn's can affect any part of the  gastrointestinal tract , from  mouth  to  anus  ( skip lesions ), although a majority of the cases start in the  terminal ileum . Ulcerative colitis, in contrast, is restricted to the  colon  and the rectum. [ 64 ]   Microscopically , ulcerative colitis is restricted to the  mucosa  ( epithelial lining  of the gut), while Crohn's disease affects the full thickness of the bowel wall ("transmural lesions"). Lastly, Crohn's disease and ulcerative colitis present with extra-intestinal manifestations (such as liver problems, arthritis, skin manifestations and eye problems) in different proportions. [ 65 ]  In 10–15% of cases, a definitive diagnosis neither of Crohn's disease nor of ulcerative colitis can be made because of idiosyncrasies in the presentation. In these cases, a diagnosis of  indeterminate colitis  may be made. [ 66 ]


Irritable bowel syndrome  can present with similar symptoms as either disease, as can  nonsteroidal anti-inflammatory drug  (NSAID)  enteritis  and  intestinal tuberculosis . Conditions that can be mistaken particularly for Crohn's disease include  Behçet's disease  and  coeliac disease , while conditions that can be symptomatically similar to ulcerative colitis in particular include acute self-limiting  colitis ,  amebic colitis ,  schistosomiasis  and  colon cancer . [ 67 ]  Other diseases may cause an increased excretion of fecal calprotectin, such as  infectious diarrhea , untreated  celiac disease ,  necrotizing enterocolitis , intestinal  cystic fibrosis  and  neoplastic pediatric tumor cells . [ 68 ]


Liver function tests  are often elevated in IBD, and are often mild and generally return spontaneously to normal levels. [ 69 ]  The most relevant mechanisms of elevated liver functions tests in IBD are drug-induced hepatotoxicity and fatty liver. [ 69 ]


CD and UC are chronic inflammatory diseases, and are not medically curable. [ 73 ]  However, Ulcerative Colitis can in most cases be cured by  proctocolectomy , although this may not eliminate extra-intestinal symptoms. An  ileostomy  will collect feces in a bag. Alternatively, a pouch can be created from the small intestine; this serves as the rectum and prevents the need for a permanent ileostomy. Between one-quarter and one-half of patients with  ileo-anal pouches  do have to manage occasional or chronic  pouchitis . [ 74 ]


Surgery cannot cure Crohn's disease but may be needed to treat complications such as abscesses, strictures or fistulae. [ 75 ]  Severe cases may require  surgery , such as  bowel resection ,  strictureplasty  or a temporary or permanent  colostomy  or  ileostomy . In Crohn's disease, surgery involves removing the worst inflamed segments of the intestine and connecting the healthy regions, but unfortunately, it does not cure Crohn's or eliminate the disease. At some point after the first surgery, Crohn's disease can recur in the healthy parts of the intestine, usually at the resection site. [ 76 ]  (For example, if a patient with Crohn's disease has an ileocecal anastomosis, in which the caecum and terminal ileum are removed and the ileum is joined to the ascending colon, their Crohn's will nearly always flare-up near the anastomosis or in the rest of the ascending colon). [ 77 ]


Medical treatment of IBD is individualised to each patient. [ 73 ]  The choice of which drugs to use and by which route to administer them (oral, rectal, injection, infusion) depends on factors including the type, distribution, and severity of the patient's disease, as well as other historical and biochemical prognostic factors, and patient preferences. For example,  mesalazine  is more useful in  ulcerative colitis  than in  Crohn's disease . [ 70 ]  Generally, depending on the level of severity, IBD may require  immunosuppression  to control the symptoms, with drugs such as  prednisone ,  tumor necrosis factor inhibitors  (TNF inhibitors), [ 78 ]   azathioprine ,  methotrexate , or  6-mercaptopurine . [ 79 ]


Steroids , such as the glucocorticoid  prednisone , are frequently used to control disease flares and were once acceptable as a maintenance drug.  Biological therapy for inflammatory bowel disease , especially the TNF inhibitors, are used in people with more severe or resistant Crohn's disease and sometimes in ulcerative colitis. [ 80 ]


Treatment is usually started by administering drugs with high anti-inflammatory effects, such as prednisone. Once the inflammation is successfully controlled, another drug to keep the disease in remission, such as  mesalazine  in UC, is the main treatment. If further treatment is required, a combination of an immunosuppressive drug (such as azathioprine) with mesalazine (which may also have an anti-inflammatory effect) may be needed, depending on the patient. Controlled release  budesonide  is used for mild ileal Crohn's disease. [ 73 ]


Exclusive enteral nutrition is a first-line therapy in pediatric Crohn's disease with weaker data in adults. [ 81 ] : 331  [ 82 ]  Evidence supporting exclusive enteral nutrition in ulcerative colitis is lacking. [ 81 ] : 333


Nutritional deficiencies play a prominent role in IBD. Malabsorption, diarrhea, and GI blood loss are common features of IBD. Deficiencies of B vitamins, fat-soluble vitamins, essential fatty acids, and key minerals such as magnesium, zinc, and  selenium  are extremely common and benefit from replacement therapy. Dietary interventions, including certain exclusion diets like the  specific carbohydrate diet  (SCD) can be beneficial for symptom management. [ 83 ]  Dietary fiber interventions, such as psyillium supplementation (a mixture of soluble and insoluble fibers), may relieve symptoms as well as induce/maintain remission by altering the microbiome composition of the GI tract, thereby improving regulation of immune function, reducing inflammation, and helping to restore the intestinal mucosal lining. [ 84 ]  Low serum levels of  alanine transaminase  can be a marker of  sarcopenia  which is underdiagnosed in patients with IBD and associated with a higher disease activity. [ 85 ]


Anemia  is commonly present in both ulcerative colitis and Crohn's disease. Due to raised levels of inflammatory  cytokines  which lead to the increased expression of  hepcidin ,  parenteral iron  is the preferred treatment option as it bypasses the gastrointestinal system, has lower incidence of adverse events and enables quicker treatment. Hepcidin itself is also an anti-inflammatory agent. In the murine model very low levels of iron restrict hepcidin synthesis, worsening the inflammation that is present. [ 86 ]  Enteral nutrition has been found to be efficient to improve hemoglobin level in patients with IBD, especially combined with erythropoietin. [ 87 ]


Gastrointestinal bleeding , occurring especially during ulcerative colitis relapse, can contribute to anemia when chronic, and may be life-threatening when acute. To limit the possible risk of dietary intake disturbing  hemostasis  in acute gastrointestinal bleeding, temporary  fasting  is often considered necessary in hospital settings. [ 88 ]  The effectiveness of this approach is unknown; a  Cochrane  review in 2016 found no published clinical trials including children. [ 89 ]


Low levels of vitamin D are associated with  crohn's disease  and  ulcerative colitis  and people with more severe cases of inflammatory bowel disease often have lower vitamin D levels. It is not clear if vitamin D deficiency causes inflammatory bowel disease or is a symptom of the disease. [ 90 ]   There is some evidence that vitamin D supplementation therapy may be associated with improvements in scores for clinical inflammatory bowel disease activity and biochemical markers. [ 90 ]  Vitamin D treatment may be associated with less inflammatory bowel disease reoccurrence of symptoms (relapse). It is not clear if this treatment improves the person's quality of life or what the clinical response to vitamin D treatment. The ideal treatment regime and dose of vitamin D therapy has not been well enough studied. [ 90 ]


There is preliminary evidence of an infectious contribution to IBD in some patients that may benefit from antibiotic therapy, such as with  rifaximin . [ 91 ]  The evidence for a benefit of rifaximin is mostly limited to Crohn's disease with less convincing evidence supporting use in ulcerative colitis. [ 92 ] [ 93 ]


The use of oral  probiotic  supplements to modify the composition and behaviour of the microbiome has been considered as a possible therapy for both induction and maintenance of remission in people with Crohn's disease and ulcerative colitis. A Cochrane review in 2020 did not find clear evidence of improved remission likelihood, nor lower adverse events, in people with Crohn's disease, following probiotic treatment. [ 94 ]


For ulcerative colitis, there is low-certainty evidence that probiotic supplements may increase the probability of clinical remission. [ 95 ]  People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects. [ 95 ]  Although there was no clear evidence of greater remission when probiotic supplements were compared with  5‐aminosalicylic acid  treatment as a  monotherapy , the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy. [ 95 ]  Whereas in people who are already in remission, it is unclear whether probiotics help to prevent future relapse, either as a monotherapy or  combination therapy . [ 96 ]


Fecal microbiota transplant  is a relatively new treatment option for IBD which has attracted attention since 2010. [ 97 ] [ 98 ]  Some preliminary studies have suggested benefits similar to those in  Clostridioides difficile  infection  but a review of use in IBD shows that FMT is safe, but of variable efficacy. Systematic reviews showed that 33% of ulcerative colitis, and 50% of Crohn's disease patients reach clinical remission after  fecal microbiota transplant . [ 99 ]


Complementary and alternative medicine approaches have been used in inflammatory bowel disorders. [ 100 ]  Evidence from controlled studies of these therapies has been reviewed; risk of bias was quite heterogeneous. The best supportive evidence was found for herbal therapy, with  Plantago ovata  and  curcumin  in UC maintenance therapy,  wormwood  in CD, mind/body therapy and self-intervention in UC, and  acupuncture  in UC and CD. [ 101 ]


Stem cell therapy  is undergoing research as a possible treatment for IBD. A review of studies suggests a promising role, although there are substantial challenges, including cost and characterization of effects, which limit the current use in clinical practice. [ 102 ]


Patients with IBD have a higher prevalence of depressive and anxiety disorders compared to the general population, women with IBD are more likely than men to develop affective disorders since up to 65% of them may have depression and anxiety disorder. [ 103 ] [ 104 ]
Currently, there is no evidence to recommend psychological treatment, such as  psychotherapy ,  stress management  and patient's education, to all adults with IBD in general. [ 105 ]  These treatments had no effect on  quality of life ,  emotional well-being  and disease activity. [ 105 ]  The need for these approaches should be individually assessed and further researched to identify subgroups and determine type of therapy that may benefit individuals with IBD. [ 105 ]  In adolescents population such treatments may be beneficial on  quality of life  and  depression , although only short-term effects have been found, which also imposes the need for further research. [ 105 ]


A meta analysis of interventions to improve mood (including talking therapy, antidepressants, and exercise) in people with IBD found that they reduced inflammatory markers such as C-reactive protein and faecal calprotectin. Psychological therapies reduced inflammation more than antidepressants or exercise. [ 106 ] [ 107 ]


Crohn's and Colitis Australia, the peak body for IBD in Australia, where prevalence is one of the highest in the world, reviewed the quality of care for patients admitted to Australian hospitals. They found that only one hospital met accepted standards for multidisciplinary care, but that care was improved with the availability of even minimal specialised services. [ 108 ]


While IBD can limit quality of life because of pain, vomiting, and diarrhea, it is rarely fatal on its own. Fatalities due to complications such as  toxic megacolon ,  bowel perforation  and surgical complications are also rare. [ 112 ]  Fatigue is a common symptom of IBD and can be a burden. [ 113 ]


Around one-third of individuals with IBD experience persistent gastrointestinal symptoms similar to  irritable bowel syndrome  (IBS) in the absence of objective evidence of disease activity. [ 114 ]  Despite enduring the side-effects of long-term therapies, this cohort has a quality of life that is not significantly different to that of individuals with uncontrolled, objectively active disease, and escalation of therapy to biological agents is typically ineffective in resolving their symptoms. [ 115 ]  The cause of these IBS-like symptoms is unclear, but it has been suggested that changes in the  gut-brain axis , epithelial barrier dysfunction, and the  gut flora  may be partially responsible. [ 116 ] [ needs update ]


While patients of IBD do have an increased risk of  colorectal cancer , this is usually caught much earlier than the general population in routine surveillance of the colon by colonoscopy, and therefore patients are much more likely to survive. [ 117 ]


New evidence suggests that patients with IBD may have an elevated risk of  endothelial dysfunction  and  coronary artery disease . [ 118 ] [ 119 ]


The goal of treatment is toward achieving remission, after which the patient is usually switched to a lighter drug with fewer potential side effects. Every so often, an acute resurgence of the original symptoms may appear; this is known as a "flare-up". Depending on the circumstances, it may go away on its own or require medication. The time between flare-ups may be anywhere from weeks to years, and varies wildly between patients – a few have never experienced a flare-up. [ 120 ]


Life with IBD can be challenging; however, many with the condition lead relatively normal lives. IBD carries a psychological burden due to stigmatization of being diagnosed, leading to high levels of anxiety, depression, and a general reduction in the quality of life. [ 121 ] [ 122 ]  Although living with IBD can be difficult, there are numerous resources available to help families navigate the ins and out of IBD, such as the  Crohn's and Colitis Foundation of America  (CCFA).


IBD resulted in a global total of 51,000 deaths in 2013 and 55,000 deaths in 1990. [ 123 ]  The increased incidence of IBD since  World War II  has been correlated to the increase in meat consumption worldwide, supporting the claim that animal protein intake is associated with IBD. [ 124 ]  However, there are many environmental risk factors that have been linked to the increased and decreased risk of IBD, such as smoking, air pollution and greenspace, urbanization and Westernization. [ 125 ]  Inflammatory bowel diseases are increasing in Europe. [ 126 ]  Incidence and prevalence of IBD has risen steadily for the last decades in Asia, which could be related changes in diet and other environmental factors. [ 127 ]


Around 0.8% of people in the UK have IBD. [ 128 ]  Similarly, around 270,000 (0.7%) of people in Canada have IBD, [ 129 ]  with that number expected to rise to 400,000 (1%) by 2030. [ 130 ]


The following treatment strategies are not used routinely, but appear promising in some forms of IBD.


Initial reports [ 131 ]  suggest that  helminthic therapy  may not only prevent but even control IBD: a drink with roughly 2,500 ova of the  Trichuris suis  helminth taken twice monthly decreased symptoms markedly in many patients. It is even speculated that an effective "immunization" procedure could be developed—by ingesting the cocktail at an early age. [ 132 ]


Prebiotics  and  probiotics  are focusing increasing interest as treatments for IBD. Currently, there is evidence to support the use of certain probiotics in addition to standard treatments in people with ulcerative colitis but there is no sufficient data to recommend probiotics in people with Crohn's disease. Both single strain and multi-strain probiotics have been researched for mild to moderate cases of ulcerative colitis.  The most clinically researched multi-strain probiotic with over 70 human trials is the  De Simone Formulation . [ 133 ]   Further research is required to identify specific probiotic strains or their combinations and prebiotic substances for therapies of intestinal inflammation. [ 134 ]


Currently, the probiotic strain, frequency, dose and duration of the probiotic therapy are not established. [ 135 ]  In severely ill people with IBD there is a risk of the passage of viable bacteria from the gastrointestinal tract to the internal organs (bacterial translocation) and subsequent  bacteremia , which can cause serious adverse health consequences. [ 135 ]  Live bacteria might not be essential because of beneficial effects of probiotics seems to be mediated by their DNA and by secreted soluble factors, and their therapeutic effects may be obtained by systemic administration rather than oral administration. [ 135 ] [ 136 ]


In 2005  New Scientist  published a joint study by  Bristol University  and the  University of Bath  on the apparent healing power of  cannabis  on IBD. Reports that cannabis eased IBD symptoms indicated the possible existence of  cannabinoid receptors  in the intestinal lining, which respond to molecules in the plant-derived chemicals.  CB1 cannabinoid receptors  – which are known to be present in the  brain  – exist in the  endothelial cells  which line the gut, it is thought that they are involved in repairing the lining of the gut when damaged. [ 137 ]


The team deliberately damaged the cells to cause inflammation of the gut lining and then added synthetically produced  cannabinoids ; the result was that gut started to heal: the broken cells were repaired and brought back closer together to mend the tears. It is believed that in a healthy gut, natural endogenous cannabinoids are released from endothelial cells when they are injured, which then bind to the CB1 receptors. The process appears to set off a wound-healing reaction, and when people use cannabis, the cannabinoids bind to these receptors in the same way. [ 137 ]


Previous studies have shown that CB1 receptors located on the nerve cells in the gut respond to cannabinoids by slowing gut  motility , therefore reducing the painful muscle contractions associated with diarrhea.  CB2 , another cannabinoid receptor predominantly expressed by  immune cells , was detected in the gut of people with IBD at a higher concentration. These receptors, which also respond to chemicals in cannabis, appear to be associated with  apoptosis  – programmed cell death – and may have a role in suppressing the overactive  immune system  and reducing  inflammation  by mopping up excess  cells . [ 137 ]


Activation of the  endocannabinoid system  was found efficient in ameliorating  colitis  and increasing the survival rate of mice, and reducing remote  organ  changes induced by colitis, further suggest that modulation of this system is a potential  therapeutic  approach for IBDs and the associated remote organ lesions. [ 138 ]


Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human  ICAM-1  messenger  RNA  through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. [ 139 ]  ICAM-1 propagates an inflammatory response promoting the extravasation and activation of  leukocytes  (white blood cells) into inflamed tissue. [ 139 ]  Increased expression of ICAM-1 has been observed within the inflamed intestinal  mucosa  of people with ulcerative colitis, pouchitis and Crohn's, where ICAM-1 over production correlated with disease activity. [ 140 ]  This suggests that ICAM-1 is a potential therapeutic target in the treatment of these diseases. [ 141 ] [ 142 ]


Cannabinoid CB2 receptor  agonists  are found to decrease the induction of ICAM-1 and  VCAM-1  surface expression in human  brain tissues  and primary human brain endothelial cells (BMVEC) exposed to various pro-inflammatory mediators. [ 143 ]


In 2014, an alliance among the  Broad Institute ,  Amgen  and  Massachusetts General Hospital  formed with the intention to "collect and analyze patient DNA samples to identify and further validate genetic targets." [ 144 ]


In 2015, a meta-analysis on 938 IBD patients and 953 controls, IBD was significantly associated with having higher odds of  vitamin D  deficiency. [ 145 ]


Gram-positive bacteria present in the lumen could be associated with extending the time of relapse for ulcerative colitis. [ 134 ]


Bidirectional pathways between  depression  and IBD have been suggested  [ 146 ]  and psychological processes have been demonstrated to influence self-perceived physical and psychological health over time. [ 147 ]  IBD-disease activity may impact  quality of life  and over time may significantly affect individual's  mental well-being , which may be related to the increased risk to develop  anxiety  and/or depression. [ 146 ] [ 148 ] [ 149 ]  On the other hand, psychological distress may also influence IBD activity. [ 150 ]


Higher rates of  anxiety  and depression are observed among those with IBD compared to healthy individuals, which correlated with disease severity. [ 148 ] [ 150 ]  Part of this phenotypic correlation is due to a shared genetic overlap between IBD and psychiatric comorbidities. [ 151 ]  Moreover, anxiety and depression rates increase during active disease compared with inactive phases. [ 150 ]


Flu vaccines are recommended for people with IBD in the UK; however, research suggests that vaccine uptake is low. Researchers analysed data on 13,631 adults with IBD on immune-suppressing drugs during the 2018 – 2019 flu season. Only half of this population received a vaccine during this period and few (32%) were vaccinated before the flu circulated in the community. This could be due to the belief that flu vaccines cause IBD flares; however, the same study did not find a link between vaccination and IBD flares. [ 152 ] [ 153 ]


IBD also occurs in dogs and is thought to arise from a combination of host genetics, intestinal microenvironment, environmental components and the immune system. There is an ongoing discussion, however, that the term "chronic enteropathy" might be better to use than "inflammatory bowel disease" in dogs because it differs from IBD in humans in how the dogs respond to treatment. For example, many dogs respond to only dietary changes compared to humans with IBD, who often need  immunosuppressive  treatment. Some dogs may also need immunosuppressant or antibiotic treatment when dietary changes are not enough. After having excluded other diseases that can lead to vomiting, diarrhea, and abdominal pain in dogs, intestinal biopsies are often performed to investigate what kind of inflammation is occurring (lymphoplasmacytic,  eosinophilic , or  granulomatous ). In dogs, low levels of  cobalamin  in the blood have been shown to be a risk factor for negative outcome. [ 154 ] [ 155 ] [ 156 ]


An  inflammatory fibroid polyp   (IFP)  is an uncommon  digestive system   tumor . [ 1 ]  J. Vanek initially identified it as a separate pathological entity in 1949 when he reported six case reports of eosinophilic infiltration in gastric submucosal  granulomas . [ 2 ]  It is a single, non-encapsulated polypoid lesion that is typically submucosal. It is characterized by a large number of small blood vessels, oedematous  connective tissue , and an inflammatory eosinophilic infiltrate. [ 3 ]


Inflammatory fibroid polyp has also been referred to as polypoid myo-endothelioma, [ 4 ]  fibroma with eosinophilic infiltration, [ 5 ]  inflammatory pseudotumour, [ 5 ]  myxoma, [ 6 ]  haemangiopericytoma, [ 7 ]  eosinophilic granuloma, [ 5 ]  Vanek's tumour, [ 8 ]  and gastric eosinophilic submucosal granuloma. [ 2 ]


When the lesions are symptomatic, they typically measure less than 3 cm in size and are linked to symptoms such as  iron deficiency anemia , bleeding,  weight loss , and dyspeptic symptoms. Significant complications like  obstruction ,  intussusception , and even  hypovolemic shock  can result from larger lesions. [ 9 ]


The tumor's size, location, and complications will affect how it presents itself. [ 1 ]  Common symptoms include  epigastric pain  and bleeding in the stomach and intestinal symptoms. [ 10 ]  When it is in the  esophagus , symptoms such as bleeding, [ 11 ]   gastroesophageal reflux , [ 12 ]  and  dysphagia  may occur. [ 13 ]


Although the inflammatory fibroid polyp's natural history is unknown, it has been known to grow quickly, within a few months, [ 1 ]  and to reach sizes of up to 20 cm. [ 14 ]


Inflammatory fibroid polyps emerge from the  submucosa  and pierce the  lamina propria , causing the mucosal layer to bulge. On rare occasions, they may develop ulcers through the  mucosa , resulting in bleeding and symptoms similar to  hypovolemic shock . [ 15 ]


The inflammatory fibroid polyp is a benign lesion whose cause is unknown; [ 13 ]  some reports attribute its genesis to  myofibroblasts , [ 16 ]  while others propose vascular or perivascular tissue. [ 17 ]  It is widely acknowledged that this is a reactive process to chemical, physical, or microbiological stimuli rather than a  neoplasm . [ 18 ]  In the past, it was believed that the etiology was caused by an inflammatory reaction to an underlying  granuloma . [ 15 ]  An irritating stimulus is frequently linked to the development of a submucosal granuloma (such as trauma,  tuberculosis ,  helicobacter pylori ,  Crohn's disease , or  sarcoidosis ). [ 19 ]


Parasites have also been implicated as a potential cause of inflammatory fibroid polyps. [ 20 ]


There have been suggestions that a factor that has not yet been identified [ 21 ]  may cause  hyperplasia  of vessels and  stromal cells , leading to localized vascular inflammation. [ 22 ]


The inflammatory fibroid polyp may be connected to neoplastic and neoplastic GI lesions occurring simultaneously or synchronously, but the literature does not support a causal relationship. [ 23 ] [ 24 ]  Isolated reports have been made of inflammatory fibroid polyps at different locations coexisting with  granular cell tumors [ 25 ]  and certain  immune system  conditions, such as  neurofibromatosis , [ 26 ]   Crohn's disease , [ 10 ] [ 27 ]   ankylosing spondylitis , [ 22 ]  and  human immunodeficiency virus infection , [ 28 ]  however, these results are inconsistent and most likely coincidental. [ 10 ]


Inflammatory fibroid polyps have demonstrated a higher incidence in individuals with a family history of gastrointestinal polyps. [ 29 ]  Activating mutations in the  platelet-derived growth factor receptor alpha  ( PDGFRA ) gene were found in 70% of cases in a genetic study involving inflammatory fibroid polyps. [ 30 ]


Over 90% of gastrointestinal polyps found during routine endoscopic examination are present in patients who are asymptomatic and do not appear to be cancerous. [ 31 ]  By using a gross examination alone, these polyps cannot be identified from those that need additional treatment. [ 15 ]  Consequently, to identify the type of polyp and whether underlying  dysplasia  is present, histological analysis is always recommended. [ 32 ]  To accurately determine the type of polyp, additional diagnostic techniques such as tandem  biopsies ,  immunohistochemistry  staining, and  endoscopic ultrasound  (EUS) may also be required. [ 31 ]


An inflammatory fibroid polyp presents histologically as an exuberant, [ 10 ]  non-encapsulated, localized proliferation of spindle-shaped  mononuclear cells , [ 4 ]  with an inflammatory infiltrate that is frequently dominated by  eosinophils . [ 33 ]  The fuzzy borders visible on  endoscopic ultrasound  correspond with the non-encapsulated proliferating spindle cells. [ 34 ]  Most inflammatory fibroid polyps are vascular, consisting of a network of varying diameter blood vessels. [ 35 ]  Occasionally, the spindle-shaped cells are arranged in a concentric pattern that resembles "onion skin". [ 36 ] [ 4 ]  Surface ulceration in focal areas can occasionally be observed. [ 6 ]  Though usually polypoidal, [ 7 ]  the lesion is thought to originate in the lower layer of the  lamina propria [ 23 ]  and may be sessile. [ 24 ] [ 7 ]  The layers of the muscle wall atrophy, fraying, and splitting are brought on by inflammatory fibroid polyps. [ 6 ]


When inflammatory fibroid polyps from different GI sites are stained with  immunohistochemistry , the spindle cell component exhibits nearly 100% positivity for  vimentin [ 5 ]  and  CD34 , [ 17 ]  but varying staining for smooth muscle actin,  HHF-35 , KP1, and Mac 387. [ 23 ]


The literature describes four histopathological groups into which inflammatory fibroid polyps can be divided: classical fibrovascular, nodular, sclerotic, and edematous. [ 3 ]


The only available treatment option is surgical excision of the lesion using either an open or endoscopic approach, depending on the location and size of the tumor. [ 1 ]  In certain instances, a formal  oesophagectomy  or lateral oesophagotomy was required for resection. [ 37 ]  Moreover, reports of using  Nd YAG laser  and thermocautery to treat tiny polyps exist. [ 1 ]


Individuals who have inflammatory fibroid polyps usually show up in their fifth or seventh decade of life. [ 38 ]  In children, it is uncommon. [ 39 ]  Even though the female-to-male ratio has varied from 2.8:1 [ 24 ]  to 0.7:1, [ 7 ]  both sexes seem to be equally affected. [ 38 ]


Intestinal metaplasia  is the transformation ( metaplasia ) of  epithelium  (usually of the  stomach  or the  esophagus ) into a type of epithelium resembling that found in the  intestine .  In the esophagus, this is called  Barrett's esophagus . Chronic inflammation caused by  H. pylori  infection in the stomach and  GERD  in the esophagus are seen as the primary instigators of metaplasia and subsequent  adenocarcinoma  formation. Initially, the transformed epithelium resembles the  small intestine  lining; in the later stages it resembles the lining of the  colon . It is characterized by the appearance of  goblet cells  and expression of intestinal cell markers such as the  transcription factor ,  CDX2 .


Although  H. pylori  infection can cause gastrointestinal metaplasia, its eradication does not reverse the process. [ 1 ]   Bile reflux  is an additional pathogenic factor in gastrointestinal metaplasia that can continuously irritate the  gastric mucosa .  Bile acids in refluxed fluid are widely reported to be associated with gastrointesinal metaplasia. [ 1 ] [ 2 ]


Although it was originally reported that people of East Asian ethnicity with gastric intestinal metaplasia are at increased risk of  stomach cancer , [ 3 ]  it is now clear that gastric intestinal metaplasia is also a risk factor in low-incidence regions like Europe. [ 4 ]  Risk factors for progression of gastric intestinal metaplasia to full blown cancer are smoking and family history. [ 5 ]


Intestinal metaplasia lesions that have an active  DNA damage  response are likely to experience extended latency in the premalignant state until the incidence of damages overrides the DNA damage response leading to clonal expansion and progression to cancer. [ 6 ]  During the DNA damage response, proteins are expressed that detect DNA damages and activate downstream responses like  DNA repair ,  cell cycle checkpoints  or  apoptosis . [ 6 ]


Intestinal neuronal dysplasia  ( IND ) is an inherited disease of the intestine that affects one in 3000 children and adults. The intestine uses  peristalsis  to push its contents toward the  anus ; people with IND have a problem with the  motor neurons  that lead to the intestine, inhibiting this process and thus preventing digestion.


It can often be confused for  Hirschsprung's disease , as both have similar symptoms. [ 1 ]


IND can be grouped into NID A and NID B, with the "A" form affecting the  sympathetic  innervation, and the "B" version affecting the  parasympathetic  innervation. [ 2 ] [ 3 ]
In 2002 Martucciello and colleagues published the first analysis of associated anomalies in IND population is an important clinical approach to investigate possible pathogenetic correlations. Two recessive syndromes were identified (3 families). The first was characterized by NID B, intestinal malrotation, and congenital short bowel, the second by NID B, short stature, mental retardation, and facial dysmorphism. In this study, gastrointestinal anomalies accounted for 67.4% of all associated disorders. These data suggest a strong correlation between IND and intestinal development. [ 4 ]


Conservative treatment involves the long term use of  laxatives  and  enemas , and has limited success. Dietary changes in order to control the disease are ineffective and high fiber diets often worsen the symptoms in children. As a last resort, surgical treatment (internal sphincter myectomy or  colon resection ) is used. [ 5 ]   In extreme cases, the only effective cure is a complete transplant of the affected parts. [ citation needed ]


A famous case of IND is that of Adele Chapman, who had a triple transplant of the small intestine, pancreas and liver, the first of its kind in the UK; therefore the official charity of IND is the Adele Chapman Foundation. [ citation needed ]


An  intestinal parasite infection  is a condition in which a  parasite  infects the  gastro-intestinal tract  of humans and other animals. Such parasites can live anywhere in the body, but most prefer the intestinal wall.


Routes of exposure and infection include ingestion of undercooked meat, drinking infected water,  fecal–oral transmission  and skin absorption.


Some types of  helminths  and  protozoa  are classified as intestinal parasites that cause infection—those that reside in the  intestines . These infections can damage or sicken the host (humans or other animals). If the intestinal parasite infection is caused by helminths, the infection is called  helminthiasis .


Signs and symptoms depend on the type of infection. Intestinal parasites produce a variety of symptoms in those affected, most of which manifest themselves in gastrointestinal complications and general weakness. [ 1 ]  Gastrointestinal conditions include  inflammation  of the  small  and/or  large intestine ,  diarrhea / dysentery ,  abdominal pains , and  nausea / vomiting . These symptoms negatively impact nutritional status, including decreased absorption of  micronutrients , loss of appetite, weight loss, and intestinal blood loss that can often result in  anemia . It may also cause physical and mental disabilities,  delayed growth  in children, and skin irritation around the anus and vulva. [ 2 ]


The prevalence of intestinal parasites is the  highest among children that are  living in the poorest communities in developing nations. [ 1 ]  The most common causes of intestinal parasites are through consumption of contaminated water, infected soil, inadequate sanitation and hygiene, and improper hygiene. [ 3 ]  Specifically, lack of access to facilities for safe disposal of human waste can result in intestinal parasites and disease. Poor hygiene habits or lacking available hygiene resources, such as  hand washing  facilities, also negatively impact rates of disease. [ 4 ]  Parasitic contamination can also occur from eating raw produce, [ 5 ]   soil-eating behaviour , [ 6 ]  and low availability of safe drinking water. [ 6 ]


Parasites can get into the intestines by going through the mouth from uncooked or unwashed food, contaminated  water  or hands, or by  skin  contact with  larva  infected  soil ; they can also be transferred by the sexual act of  anilingus  in some cases. When the organisms are swallowed, they move into the intestines, where they can reproduce and cause symptoms. Children are particularly susceptible if they are not thoroughly cleaned after coming into contact with infected soil that is present in environments that they may frequently visit such as sandboxes and school playgrounds. People in developing countries are also at particular risk due to drinking water from sources that may be contaminated with parasites that colonize the gastrointestinal tract. [ citation needed ]


Due to the wide variety of intestinal parasites, a description of the symptoms rarely is sufficient for diagnosis. Instead, medical personnel use one of two common tests: they search stool samples for the parasites, or apply an adhesive to the  anus  to search for eggs.


Major groups of parasites include  protozoans  (organisms having only one cell) and  parasitic worms  (helminths). Of these, protozoans, including  cryptosporidium ,  microsporidia , and  isospora , are most common in  HIV -infected persons. Each of these parasites can infect the digestive tract, and sometimes two or more can cause infection at the same time.


Good hygiene is necessary to avoid reinfection.  The Rockefeller Foundation 's hookworm campaign in Mexico in the 1920s was extremely effective at eliminating hookworm from humans with the use of  anthelmintics . However, preventative measures were not adequately introduced to the people that were treated. Therefore, the rate of reinfection was extremely high and the project evaluated through any sort of scientific method was a marked failure. More education was needed to inform the people of the importance of wearing shoes, using  latrines  (better access to  sanitation ), and good hygiene. [ 7 ]


Intestinal parasite prevention methods are not isolated to specific geographical areas; however, many of the research-based interventions have primarily taken place in underdeveloped countries and regions, where sanitation is a large concern for spreading disease. [ citation needed ] Current best practice behaviors that prevent intestinal parasites include: using proper hand washing practices, using correctly-built latrines with ample ventilation, having a piped water source, and wearing shoes. [ 8 ] [ 9 ]  Currently, in some parts of Ethiopia where disease prevalence is high, up to 80% of people in a population lack access to washing facilities. While this is high, 93% did have access to a latrine, but only 29.2% of those latrines had proper construction to decrease parasitic infections. [ 9 ]  Behavioral interventions have focused on promoting washing, sometimes with soap, in context of education at schools and child care facilities. [ 10 ]  In recent studies, the best interventions follow a multidisciplinary approach by:


Specific evidence-based interventions that may lower disease prevalence include:


Drugs are frequently used to kill parasites in the host. In earlier times,  turpentine  was often used for this, but modern drugs do not poison intestinal worms directly. Rather, anthelmintic drugs now inhibit an enzyme that is necessary for the worm to make the substance that prevents the worm from being digested. [ citation needed ]


For example,  tapeworms  are usually treated with a medicine taken by mouth. The most commonly used medicine for tapeworms is  praziquantel . [ 14 ]


Human intestinal spirochetosis , often called just  intestinal spirochetosis  when the human context is implicit, is an infection of the  colonic -type  mucosa  with certain species of  spirochetal  bacteria. Similar infections sometimes occur in pigs, dogs, and birds;  porcine intestinal spirochaetosis  is an economically important disease of livestock.


No clear association exists with complaints. However, potential associations include  abdominal pain  and watery  diarrhea , which may be seen with  blood ; however, these findings are not specific and may be due to a number of other causes. [ 2 ]


Human intestinal spirochetosis is caused by  Brachyspira pilosicoli  and  Brachyspira aalborgi . [ 3 ]  Porcine and avian intestinal spirochetosis are caused by  Brachyspira hyodysenteriae  and  Brachyspira pilosicoli . [ citation needed ]


It is diagnosed by examination of  tissue , i.e.,  biopsy . [ citation needed ]


Symptomatic individuals can be treated with oral metronidazole.


Intestinal varices  are dilated submucosal  veins  in the  intestine . [ citation needed ] One treatment includes a  transjugular intrahepatic portosystemic shunt . [ 1 ]


This article about a medical condition affecting the circulatory system is a  stub . You can help Wikipedia by  expanding it .


An  intracolonic explosion  or  colonic gas explosion  is an explosion inside the  colon  of a person due to ignition of explosive gases such as  methane . This can happen during colonic exploration, as a result of the electrical nature of a  colonoscope .


A colonic gas explosion is rare; [ 1 ]  however, the result can be acute colonic  perforation , which can be fatal. [ 1 ]


An explosion is triggered by a combination of combustible gases such as hydrogen or methane, combustive gas such as oxygen, and heat. An explosion can also be caused by Crohn's disease. [ 1 ]


Careful bowel preparation, such as cleansing the colon before a procedure, is key to preventing an intracolonic explosion. [ 2 ]


This  surgery  article is a  stub . You can help Wikipedia by  expanding it .


Ischemic colitis  (also spelled  ischaemic colitis ) is a medical condition in which inflammation and injury of the  large intestine  result from inadequate blood supply ( ischemia ). Although uncommon in the general population, ischemic colitis occurs with greater frequency in the elderly, and is the most common form of  bowel ischemia . [ 1 ] [ 2 ] [ 3 ]  Causes of the reduced blood flow can include changes in the  systemic circulation  (e.g.  low blood pressure ) or local factors such as  constriction of blood vessels  or a  blood clot . In most cases, no specific cause can be identified. [ 4 ]


Ischemic colitis is usually suspected on the basis of the clinical setting,  physical examination , and laboratory test results; the diagnosis can be confirmed by  endoscopy  or by using sigmoid or endoscopic placement of a visible light spectroscopic catheter (see  Diagnosis ). Ischemic colitis can span a wide spectrum of severity; most patients are treated supportively and recover fully, while a minority with very severe ischemia may develop  sepsis  and become critically, [ 5 ]  sometimes fatally, ill. [ 6 ]


Patients with mild to moderate ischemic colitis are usually treated with IV fluids,  analgesia , and  bowel rest  (that is, no food or water by mouth) until the symptoms resolve. Those with severe ischemia who develop complications such as sepsis, intestinal  gangrene , or  bowel perforation  may require more aggressive interventions such as  surgery  and  intensive care . Most patients make a full recovery; occasionally, after severe ischemia, patients may develop long-term complications such as a  stricture [ 7 ]  or chronic  colitis . [ 8 ]


Three progressive phases of ischemic colitis have been described: [ 9 ] [ 10 ]


Symptoms of ischemic colitis vary depending on the severity of the ischemia. The most common early signs of ischemic colitis include  abdominal pain  (often left-sided), with mild to moderate amounts of  rectal bleeding . [ 11 ]  The sensitivity of findings among 73 patients were: [ 12 ]


Physical examination [ 12 ]


Ischemic colitis is often classified according to the underlying cause.  Non-occlusive  ischemia develops because of low blood pressure or constriction of the vessels feeding the colon;  occlusive  ischemia indicates that a  blood clot  or other blockage has cut off blood flow to the colon. [ citation needed ]


In hemodynamically unstable patients (i.e. shock) the mesenteric perfusion may be compromised. This condition is commonly asymptomatic, and usually only apparent through a systemic inflammatory response. [ citation needed ]


Mostly the result of a thromboembolism. Commonly the embolism is caused by  atrial fibrillation , valvular disease,  myocardial infarction , or  cardiomyopathy . [ citation needed ]


In addition, ischemic colitis is a well-recognized complication of abdominal aortic aneurysm repair, when the origin of the inferior mesenteric artery is covered by the aortic graft. [ 13 ] [ 14 ]   In a 1991 review concerning 2137 patients the accidental inferior mesenteric artery ligation was the most common cause (74%) of ischemic colitis. [ 15 ]  Thus, patients without adequate collateralization are at risk for ischemia of the descending and sigmoid colon.  Bloody diarrhea and leukocytosis in the postoperative period are essentially diagnostic of ischemic colitis. The complication can be prevented through careful selection of subjects that may require replanting inferior mesenteric artery (IMA) and completing the pre surgical procedure information with an instrumental evaluation during surgical treatment. [ 16 ]


The colon receives blood from both the  superior  and  inferior mesenteric arteries . The blood supply from these two major arteries overlaps, with abundant collateral circulation via the  marginal artery of the colon . However, there are weak points, or "watershed" areas, at the borders of the territory supplied by each of these arteries, such as the splenic flexure and the rectosigmoid junction. These watershed areas are most vulnerable to ischemia when blood flow decreases, as they have the fewest vascular collaterals. [ citation needed ]


The  rectum  receives blood from both the inferior mesenteric artery and the  internal iliac artery ; the rectum is rarely involved by colonic ischemia due to this dual blood supply. [ citation needed ]


Under ordinary conditions, the colon receives between 10% and 35% of the total cardiac output. [ 17 ] [ 18 ]  If blood flow to the colon drops by more than about 50%, ischemia will develop. The arteries feeding the colon are very sensitive to vasoconstrictors; presumably this is an evolutionary adaptation to shunt blood away from the bowel and to the  heart  and  brain  in times of stress. [ 19 ]  As a result, during periods of  low blood pressure , the arteries feeding the colon clamp down vigorously; a similar process can result from vasoconstricting drugs such as  ergotamine ,  cocaine , or  vasopressors . This vasoconstriction can result in non-occlusive ischemic colitis. [ citation needed ]


A range of pathologic findings are seen in ischemic colitis, corresponding to the spectrum of clinical severity. In its mildest form, mucosal and submucosal  hemorrhage  and  edema  are seen, possibly with mild  necrosis  or  ulceration . [ 4 ]  With more severe ischemia, a pathologic picture resembling  inflammatory bowel disease  (i.e. chronic ulcerations, crypt  abscesses  and pseudopolyps) may be seen. [ 20 ]  In the most severe cases, transmural infarction with resulting perforation may be seen; after recovery, the muscularis propria may be replaced by fibrous tissue, resulting in a stricture. [ 4 ]  Following restoration of normal blood flow,  reperfusion injury  may also contribute to the damage to the colon. [ 21 ]


Ischemic colitis must be differentiated from the many other causes of  abdominal pain  and  rectal bleeding  (for example,  infection ,  inflammatory bowel disease ,  diverticulosis , or  colon cancer ). It is also important to differentiate ischemic colitis, which often resolves on its own, from the more immediately life-threatening condition of acute  mesenteric ischemia  of the  small bowel . [ citation needed ]


There are devices which test the sufficiency of oxygen delivery to the colon. The first device approved by the U.S. FDA in 2004 uses visible light spectroscopy to analyze capillary oxygen levels. Use during aortic aneurysm repair detected when colon oxygen levels fell below sustainable levels, allowing real-time repair. In several studies, Specificity has been 90% or higher for acute colonic ischemia, and 83% for chronic mesenteric ischemia, with a sensitivity of 71%-92%. This device must be placed using endoscopy, however. [ 22 ] [ 23 ] [ 24 ]


There is a recent optical test, but it requires endoscopy (see Diagnosis). There are no specific blood tests for ischemic colitis. The sensitivity of tests among 73 patients were: [ 12 ]


Plain  X-rays  are often normal or show non-specific findings. [ 25 ]  In a series of 73 patients, plain abdominal radiography (56%) showing colic distension in 53% or a pneumoperitoneum in 3%. [ 12 ]


CT scans  are often used in the evaluation of abdominal pain and rectal bleeding, and may suggest the diagnosis of ischemic colitis, pick up complications, or suggest an alternate diagnosis. [ 26 ] [ 27 ] [ 28 ]


Endoscopic  evaluation, via  colonoscopy  or flexible  sigmoidoscopy , is the procedure of choice if the diagnosis remains unclear. Ischemic colitis has a distinctive endoscopic appearance; endoscopy can also facilitate alternate diagnoses such as  infection  or  inflammatory bowel disease .  Biopsies  can be taken via endoscopy to provide more information. Visible light spectroscopy, performed using catheters placed through the 5 mm channel of the endoscope, is diagnostic (see Diagnosis). [ citation needed ]


Except in the most severe cases, ischemic colitis is treated with supportive care.  IV fluids  are given to treat  dehydration , and the patient is placed on bowel rest (meaning nothing to eat or drink) until the symptoms resolve. If possible, cardiac function and oxygenation should be optimized to improve oxygen delivery to the ischemic bowel. A  nasogastric tube  may be inserted if an  ileus  is present. [ citation needed ]


Antibiotics  are sometimes given in moderate to severe cases; the data supporting this practice date to the 1950s, [ 29 ]  although there is more recent animal data suggesting that antibiotics may increase survival and prevent  bacteria  from crossing the damaged lining of the colon into the bloodstream. [ 30 ] [ 31 ] [ 32 ]  The use of  prophylactic  antibiotics in ischemic colitis has not been prospectively evaluated in  humans , but many authorities recommend their use based on the animal data. [ 33 ]


Patients being treated supportively are carefully monitored. If they develop worsening symptoms and signs such as  high white blood cell count ,  fever , worsened abdominal pain, or increased bleeding, then they may require  surgical intervention ; this usually consists of  laparotomy  and  bowel resection . [ citation needed ]


Most patients with ischemic colitis recover fully, although the prognosis depends on the severity of the ischemia. Patients with pre-existing  peripheral vascular disease  or ischemia of the ascending (right) colon may be at increased risk for complications or death. [ citation needed ]


Non-gangrenous ischemic colitis, which comprises the vast majority of cases, is associated with a mortality rate of approximately 6%. [ 34 ]  However, the minority of patients who develop  gangrene  as a result of colonic ischemia have a mortality rate of 50–75% with surgical treatment; the mortality rate is almost 100% without surgical intervention. [ 35 ]


About 20% of patients with acute ischemic colitis may develop a long-term complication known as  chronic ischemic colitis . [ 8 ]  Symptoms can include recurrent infections, bloody diarrhea, weight loss, and chronic abdominal pain. Chronic ischemic colitis is often treated with surgical removal of the chronically diseased portion of the bowel. [ citation needed ]


A  colonic stricture  is a band of scar tissue which forms as a result of the ischemic injury and narrows the  lumen  of the colon. Strictures are often treated observantly; they may heal spontaneously over 12–24 months. If a  bowel obstruction  develops as a result of the stricture, surgical resection is the usual treatment, [ 36 ]  although  endoscopic dilatation  and  stenting  have also been employed. [ 37 ] [ 38 ]


The exact incidence of ischemic colitis is difficult to estimate, as many patients with mild ischemia may not seek medical attention. Ischemic colitis is responsible for about 1 in 2000 hospital admissions and is seen on about 1 in 100 endoscopies. [ 4 ]  Men and women are affected equally; ischemic colitis is a disease of the elderly, with more than 90% of cases occurring in people over the age of 60. [ 4 ]


Isolated superior mesenteric artery dissection (ISMAD)  is a rare but potentially life-threatening condition that causes acute abdominal pain. It refers to a dissection that occurs solely in the  superior mesenteric artery  (SMA), typically spontaneously, and does not involve the  aorta . [ 1 ]
Although  aortic dissection  can frequently extend into its peripheral territories, it is rare for these branches to have dissection without main aortic trunk involvement. The SMA is the most common site of dissection among visceral arteries compared to other gastrointestinal arteries. [ 2 ]


ISMAD primarily manifests through a sudden onset of pain, which can vary in location and intensity. [ 2 ]   The nature of the pain and its location can provide clues to the diagnosis of ISMAD. [ 2 ]  The types of pain reported in ISMAD cases include:


ISMAD is more common in males, accounting for 80.6% of cases, and typically occurs in individuals in their fifth decade of life, with a mean age of 55.7 years. [ 2 ]  Other risk factors include smoking and hypertension. [ 4 ]


ISMAD can be associated with isolated arterial dissections and aneurysms, such as those in the celiac and renal arteries, suggesting a systemic component. [ 5 ]  It has been linked to certain vascular diseases like  fibromuscular dysplasia , medial degeneration, and  atherosclerosis . [ 5 ]


The structure of the SMA itself can contribute to ISMAD. Certain anatomical variants are more susceptible to shear stress, leading to dissection. This stress occurs when the SMA, lacking mechanical support from the pancreas, bends within the mesenteric root. The anterior wall, the most common site of ISMAD, faces increased stress due to the SMA's convexity after bending. [ 5 ]


Genetics also plays a role in ISMAD. It has been hypothesized that a genetic component exists, as most reported cases are from East Asia. This hypothesis is supported by a familial case of ISMAD from China linked to a chromosomal locus of 5q13–14. [ 5 ]


In terms of the diagnosis of ISMAD, the following is done: [ 5 ]


The management of isolated superior mesenteric artery dissection (ISMAD) often involves conservative treatment, which includes blood pressure lowering therapy,  analgesics , and initial bowel rest. [ 4 ]  Periodic follow-ups with  CT angiography  are a part of the conservative treatment approach. Over time, many patients show improvement or no change in their condition as observed through these follow-ups. A small percentage of patients reported mild abdominal discomfort during the follow-up period, but no patient developed recurrent abdominal pain following conservative treatment. Importantly, there was no mortality related to SISMAD. These observations suggest that conservative treatment can be an effective approach for managing patients with SISMAD. [ 6 ]


In cases where conservative treatment is not sufficient, endovascular procedures may be considered. These include stenting/stent-grafting of the true lumen, (coil) embolization of the false lumen/aneurysm, catheter-directed local thrombolysis, percutaneous transluminal angioplasty, and catheter-directed local papaverine infusion at 30 mg/h. [ 4 ]


In related surgical procedures such as Minimally Invasive Pancreaticoduodenectomy (MIPD), various approaches for dissection around the SMA have been reported, including anterior, posterior, right, and left approaches. [ 7 ] While these methods are not specifically used for ISMAD, understanding these surgical techniques could potentially inform future treatment strategies for ISMAD. [ 7 ]


The prognosis for patients with ISMAD who undergo conservative treatment is generally positive. Follow-up studies show that the majority of patients either improve or do not show progression of the condition. This is evidenced by CT angiograms, which often show a decrease in the size of the false lumen, a decrease in the length of the dissection, or complete remodeling of the dissection. [ 6 ]


During the follow-up period, some patients reported mild, nonspecific abdominal discomfort. However, no patient developed recurrent abdominal pain following conservative treatment, and there was no mortality related to ISMAD. These findings further support the effectiveness of conservative treatment for managing patients with ISMAD. [ 6 ]


In cases where conservative treatment is not sufficient, endovascular procedures may be considered. These include stenting/ stent -grafting of the true lumen, (coil) embolization of the false lumen/aneurysm, catheter-directed local thrombolysis, percutaneous transluminal angioplasty, and catheter-directed local papaverine infusion at 30 mg/h. [ 6 ]


Keriorrhea  is the production of greasy, orange-colored stools which results from the consumption of indigestible  wax esters  found in  oilfish  and  escolar . [ 1 ] [ 2 ]


This medical  symptom  article is a  stub . You can help Wikipedia by  expanding it .


Lower gastrointestinal bleeding  ( LGIB ) is any form of  gastrointestinal bleeding  in the  lower gastrointestinal tract . LGIB is a common reason for seeking medical attention at a hospital's emergency department. [ 1 ]  LGIB accounts for 30–40% of all gastrointestinal bleeding and is less common than  upper gastrointestinal bleeding  (UGIB). [ 2 ]  It is estimated that UGIB accounts for 100–200 per 100,000 cases versus 20–27 per 100,000 cases for LGIB. [ 3 ]  Approximately 85% of lower gastrointestinal bleeding involves the  large intestine , 10% are from bleeds that are actually upper gastrointestinal bleeds, and 3–5% involve the  small intestine . [ 4 ]


A lower gastrointestinal bleed is defined as bleeding originating distal to the  ileocecal valve , which includes the  colon ,  rectum , and  anus . [ 2 ]  LGIB was previously defined as any bleed that occurs distal to the  ligament of Treitz , which included the aforementioned parts of the intestine and also included the last 1/4 of the  duodenum  and the entire area of the  jejunum  and  ileum . [ 1 ]  This has been divided into middle gastrointestinal bleeding (from the ligament of Treitz to the ileocecal valve) and lower gastrointestinal bleeding which involves a bleed anywhere from the ileocecal valve to the anus. [ 2 ]


The  stool  of a person with a lower gastrointestinal bleed is a good (but not infallible) indication of where the bleeding is occurring. Black tarry appearing stools medically referred to as  melena  usually indicates blood that has been in the GI tract for at least 8 hours. [ 1 ]  Melena is four-times more likely to come from an upper gastrointestinal bleed than from the lower GI tract; however, it can also occur in either the duodenum and jejunum, and occasionally the portions of the  small intestine  and  proximal colon . [ 5 ]  Bright red stool, called  hematochezia , is the sign of a fast moving active GI bleed. [ 1 ]  The bright red or maroon color is due to the short time taken from the site of the bleed and the exiting at the anus. The presence of hematochezia is six-times greater in a LGIB than with a UGIB. [ 5 ]


Occasionally, a person with a LGIB will not present with any signs of internal bleeding, especially if there is a chronic bleed with ongoing low levels of blood loss. In these cases, a diagnostic assessment or pre-assessment should watch for other signs and symptoms that the patient may present with. These include, but are not limited to,  hypotension ,  tachycardia ,  angina ,  syncope ,  weakness ,  confusion ,  stroke ,  myocardial infarction / heart attack , and  shock .


The following are possible causes of a LGIB:


Diagnostic evaluation must be performed after patients have been adequately resuscitated. If an upper GI source is suspected, an  upper endoscopy  should be performed first.  Lower gastrointestinal series  evaluation can be performed with  anoscopy , flexible  sigmoidoscopy ,  colonoscopy , rarely  barium enema , and various  radiologic  studies. [ 6 ]


The history in these patients should focus on factors that could be associated with potential causes: blood coating the stool suggests hemorrhoidal bleeding while blood mixed in the stool implies a more proximal source; bloody diarrhea and tenesmus is associated with  inflammatory bowel disease  while bloody diarrhea with fever and  abdominal pain  especially with recent travel history suggests infectious colitis; pain with defecation occurs with hemorrhoids and anal fissure; change in stool caliber and weight loss is concerning for  colon cancer ; abdominal pain can be associated with inflammatory bowel disease, infectious colitis, or ischemic colitis; painless bleeding is characteristic of diverticular bleeding,  arteriovenous malformation  (AVM), and radiation proctitis;  nonsteroidal anti-inflammatory drug  (NSAID) use is a risk factor for diverticular bleeding and NSAID-induced colonic ulcer; and recent colonoscopy with polypectomy suggests postpolypectomy bleeding. Patients should be asked about symptoms of hemodynamic compromise, including dyspnea, chest pain, lightheadedness, and fatigue. [ 7 ]


Orthostatic hypotension  implies at least a 15% loss of blood volume and suggests a more severe bleeding episode. Evaluate for abdominal tenderness, masses, and  enlargement of the liver  and  spleen . Additional key elements include a careful and thorough inspection of the anus, palpation for rectal masses, characterization of the stool color, and a stool guaiac card test to evaluate for the presence of blood. [ citation needed ]


Among the blood tests that should be performed are a  complete blood count ,  prothrombin time ,  partial thromboplastin time ,  electrolytes , and typing and cross-matching for transfusion of blood products. [ 8 ]
A  clotting abnormality  and  low platelet concentration in the blood  should be immediately corrected if possible. Platelets should be maintained above 50,000/mL and clotting abnormalities should be corrected with  vitamin K  or  fresh frozen plasma . Vitamin K should be taken orally unless the patient has  cirrhosis  or biliary obstruction, in which case it should be administered subcutaneously. The full effect of vitamin K is not obtained for 12–24 hours, unlike fresh frozen plasma which immediately reverses clotting abnormalities. The intravenous formulation of  vitamin K  reverses coagulopathy more quickly and may be used in cases of severe bleeding, however, patients should be monitored for anaphylaxis. The effects of fresh frozen plasma last about 3–5 hours and large volumes (> 2–3 L) may be required to completely reverse clotting abnormalities, depending on the initial prothrombin time. Recombinant activated factor VII has been approved for use in patients with  hemophilia  A and B with factor VIII and IX inhibitors. Evidence of possible benefit in patients with  cirrhosis  and GI bleeding has been demonstrated, although the optimal dose is unclear and recombinant activated factor VII is very expensive. [ 6 ]


Anoscopy is useful only for diagnosing bleeding sources from the anorectal junction and anal canal, including internal  hemorrhoids  and anal fissures. It is superior to flexible sigmoidoscopy for detecting hemorrhoids in an outpatient setting and can be performed quickly in the office or at the bedside as an adjunct to flexible sigmoidoscopy and colonoscopy. [ citation needed ]


Flexible sigmoidoscopy  uses a 65-cm long sigmoidoscope that visualizes the left  colon . It can be performed without sedation and only minimal preparation with enemas. However, the diagnostic yield of flexible sigmoidoscopy in acute lower GI bleeding is only 9%. The role of anoscopy and flexible sigmoidoscopy in inpatients with acute lower GI bleeding is limited, as most patients should undergo colonoscopy. [ citation needed ]


Colonoscopy is the test of choice in the majority of patients with acute Lower GI bleeding as it can be both diagnostic and therapeutic. The diagnostic accuracy of colonoscopy in lower GI bleeding ranges from 48% to 90%, and urgent colonoscopy appears to increase diagnostic yield. This wide range in yield is partially explained by different criteria for diagnosis, as often if no active bleeding, nonbleeding visible vessel, or adherent clot is found, bleeding is attributed to a lesion if blood is present in the area. The presence of fresh blood in the  terminal ileum  is presumed to indicate a non colonic source of bleeding.
The overall complication rate of colonoscopy in acute lower GI bleeding is 1.3%. Bowel preparation is safe and well tolerated in most patients. The complication rate of colonoscopy in an unprepped colon may be higher. About 2–6% of colonoscopy preparations in acute lower GI bleeding are poor. Between 4 and 8 L of G olytely  should be administered orally or via nasogastric tube until the effluence is clear. [ 9 ]


In most cases requiring emergency hospital admission, the bleeding will resolve spontaneously. [ 2 ] [ 10 ]  If a patient is suspected of having  severe blood loss  they will most likely be placed on a vital sign monitor and administered oxygen either by  nasal cannula  or  simple face mask . An  intravenous catheter  will be placed into an easily accessible area and IV fluids will be administered to replace lost blood volume. [ 1 ]  Endoscopic evaluation with a  colonoscopy  (and possibly an  esophagogastroduodenoscopy  to exclude an UGIB) should typically occur within 24 hours of hospital presentation. [ 2 ]


If the person with LGIB is on low-dose  aspirin  for prevention of a first heart attack (i.e., the person has never had a heart attack before), stopping the aspirin is recommended. [ 2 ]  In contrast, if the person has previously had a heart attack, the aspirin should be continued despite the active LGIB due to the benefits of preventing another heart attack and consequent death outweighing the risk of bleeding. [ 2 ]   Dual antiplatelet therapy  (e.g., use of both aspirin and  clopidogrel ) should continue if the person with a LGIB underwent  stenting  of the heart's  coronary arteries  within the last 30 days or a recent  acute coronary syndrome  episode (e.g.,  unstable angina  or a  myocardial infarction ) within 90 days of the LGIB event. [ 2 ]  Individuals at high risk of another heart attack but not meeting the above criteria should continue their aspirin during the LGIB event but stop the other antiplatelet medication for 1–7 days following cessation of the bleed. [ 2 ]


Predicting which patients will develop adverse outcomes, complications or severe bleeding can be difficult. One recent study identified poor kidney function (creatinine > 150 μm), age over 60 years, abnormal haemodynamic parameters on presentation (low blood pressure) and persistent bleeding within the first 24 hours as risk factors for worse outcome. [ 10 ]


Surgical intervention  is warranted in cases of LGIB that persist despite attempts to stop the bleeding with endoscopic or interventional radiology interventions. [ 2 ]   It is most likely that a  surgical consult  will be ordered if the patient is unable to be stabilized by non-invasive techniques, or if a perforation is found that requires surgery (e.g., subtotal  removal of the colon ). [ 1 ]


Malabsorption  is a state arising from abnormality in  absorption  of  food nutrients  across the  gastrointestinal (GI) tract . Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to  malnutrition  and a variety of  anaemias . [ 1 ]


Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency. A typical Western diet ingested by an adult in one day includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the required  sodium ,  potassium ,  chloride ,  calcium ,  vitamins , and other elements.  [ citation needed ]   Salivary ,  gastric ,  intestinal ,  hepatic , and  pancreatic  secretions add an additional 7–8 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents. This massive load is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1–2 g of nitrogen, and less than 20 mmol each of  Na + ,  K + ,  Cl − ,  HCO − 3 ,  Ca 2+ , or  Mg 2+ .


If there is impairment of any of the many steps involved in the complex process of nutrient digestion and absorption, intestinal  malabsorption  may ensue. If the abnormality involves a single step in the absorptive process, as in primary  lactase deficiency , or if the disease process is limited to the very proximal small intestine, then selective malabsorption of only a single nutrient may occur. However, generalized  malabsorption  of multiple dietary nutrients develops when the disease process is extensive, thus disturbing several digestive and absorptive processes, as occurs in  coeliac disease  with extensive involvement of the  small intestine . [ 1 ]


Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent.  Diarrhea ,  weight loss ,  flatulence , abdominal  bloating , abdominal  cramps , and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with  steatorrhea  and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as  coeliac disease . In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed  bile acids  both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with a primary or secondary  disaccharidase  deficiency, such as  lactose intolerance  or  sucrose intolerance . Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and  Crohn's disease , but it is absent in many patients with coeliac disease or postgastrectomy malabsorption. [ 1 ]


Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with  anemia  and  osteopenia  in the absence of significant classic gastrointestinal symptoms. Microcytic,  macrocytic , or dimorphic anemia may reflect impaired  iron , folate, or  vitamin B12  absorption.  Purpura ,  subconjunctival hemorrhage , or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of  steatorrhea . Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by  lymphatic obstruction  or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids. [ 2 ]


Symptoms can manifest in a variety of ways and features might give a clue to the underlying condition. Symptoms can be  intestinal  or extra-intestinal - the former predominates in severe malabsorption. [ citation needed ]


The main purpose of the  gastrointestinal tract  is to  digest  and  absorb  nutrients ( fat ,  carbohydrate ,  protein , micronutrients ( vitamins  and  trace minerals ), water, and  electrolytes .  Digestion  involves both mechanical and  enzymatic  breakdown of food.  Mechanical processes  include chewing, gastric churning, and the to-and-fro mixing in the  small intestine .  Enzymatic hydrolysis  is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the  intestinal epithelial  cells. [ citation needed ]


Malabsorption constitutes the pathological interference with the normal physiological sequence of  digestion  (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients. [ 3 ]


Intestinal  malabsorption can be due to: [ 7 ]


There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided by  symptoms  and signs. A range of different conditions can produce malabsorption and it is necessary to look for each of these specifically. Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption). [ citation needed ]


Some [ who? ]  prefer to classify malabsorption clinically into three basic categories: [ 8 ]


Treatment is directed largely towards management of underlying cause: [ 1 ]


Megacolon  is an abnormal dilation of the  colon  (also called the large  intestine ). [ 1 ] [ 2 ]  This leads to  hypertrophy  of the colon. [ 2 ]  The dilation is often accompanied by a  paralysis  of the  peristaltic  movements of the bowel. In more extreme cases, the  feces  consolidate into hard masses inside the colon, called  fecalomas  (literally,  fecal tumor ), which can require  surgery  to be removed.


A human colon is considered abnormally enlarged if it has a  diameter  greater than 12  cm [ 3 ]  in the  cecum  (it is usually less than 9 cm [ 4 ] ), greater than 6.5 cm [ 3 ]  in the  rectosigmoid  region and greater than 8 cm [ 3 ]  for the  ascending colon . The transverse colon is usually less than 6 cm in diameter. [ 4 ]


A megacolon can be either  acute  or  chronic . It can also be classified according to cause. [ 5 ]


External signs and symptoms are  constipation  of very long duration, [ 2 ]  abdominal  bloating , abdominal tenderness and  tympany ,  abdominal pain ,  palpation  of hard fecal masses and, in  toxic megacolon ,  fever , low blood  potassium ,  tachycardia  and may lead to  shock .  Stercoral ulcers  are sometimes observed in chronic megacolon, which may lead to perforation of the intestinal wall in approximately 3% of the cases, leading to  sepsis  and risk of death. [ 6 ] [ 7 ]


Also called  Hirschsprung's disease , it is a  congenital  disorder of the colon in which  nerve cells  of the  myenteric plexus  in its walls, also known as ganglion cells, are absent.  It is a rare disorder (1:5000), with prevalence among males being four times that of females.  Hirschsprung's disease develops in the  fetus  during the early stages of  pregnancy .  A genetic predisposition to Hirschsprung's disease has been linked to  chromosome 13  where a  missense mutation  at an ultraconserved region impairs functionality of the W276C receptor.  Seven other genes seem to be implicated, however.  If untreated, the patient can develop  enterocolitis . [ citation needed ]


Toxic megacolon is mainly seen in  ulcerative colitis  and  pseudomembranous colitis , two chronic  inflammations  of the colon (and occasionally, in the other type of  inflammatory bowel disease ,  Crohn's disease ). Its mechanism is incompletely understood. It is probably due to excessive production of  nitric oxide , at least in ulcerative colitis. The prevalence is about the same for both sexes. [ citation needed ]


In patients with HIV/AIDS,  cytomegalovirus  (CMV) colitis is the leading cause of toxic megacolon and emergency laparotomy. CMV may also increase the risk of toxic megacolon in non-HIV/AIDS patients with IBD. [ 10 ]


Megacolon can be associated with  Chagas disease . [ 11 ]  Chagas disease is caused by  Trypanosoma cruzi , a flagellate  protozoan  transmitted by the  assassin bug . Chagas disease can also be acquired congenitally, through blood transfusion or organ transplant, and rarely through contaminated food (for example  garapa ). There are several theories on how megacolon (and also  megaesophagus ) develops in Chagas disease. The   Austrian - Brazilian   physician  and  pathologist   Fritz Köberle  was the first to propose the  neurogenic hypothesis  based on the documented destruction of the  myenteric plexus  in the walls of the intestinal tracts of Chagas patients. In this, the destruction of the  autonomic nervous system  innervation of the colon leads to a loss of the normal  smooth muscle  tone of the wall and subsequent gradual dilation. His research proved that, by extensively quantifying the number of neurons of the autonomic nervous system in the Auerbach's plexus, that: [ citation needed ]


Why  T. cruzi  causes the destruction, however, remains to be determined. There is evidence for the presence of specific  neurotoxins  as well as a disorderly  immune system  reaction. [ citation needed ]


Diagnosis  is achieved mainly by plain and contrasted  radiographical  and  ultrasound  imaging. Colonic marker transit studies are useful to distinguish colonic inertia from functional outlet obstruction causes. In this test, the patient swallows a water-soluble bolus of  radiocontrast agent  and films are obtained 1, 3, and 5 days later. Patients with colonic inertia show the marker spread throughout the large intestines, while patients with outlet obstruction exhibit slow accumulations of markers in some places. A  colonoscopy  can also be used to rule out mechanical obstructive causes.  Anorectal manometry  may help to differentiate acquired from congenital forms. Rectal biopsy is recommended to make a final diagnosis of Hirschsprung disease. [ 12 ]


Possible treatments include: [ 13 ]


There are several surgical approaches to treat megacolon, such as a  colectomy [ 2 ] [ 14 ]  (removal of the entire colon) with ileorectal  anastomosis  (ligation of the remaining ileum and rectum segments), or a total  proctocolectomy  (removal of colon, sigmoid and rectum) followed by  ileostomy  or followed by ileoanal anastomosis.


Megarectum  is a large  rectum  as a result of underlying  nerve  supply abnormalities or  muscle  dysfunction, which remains after disimpaction of the rectum.  [ citation needed ]


The Principles of Surgery textbook describes any rectum that can hold more than 1500cc of fluid as a megarectum. The term megarectum is also used for a large rectal mass on  rectal examination , a wide rectum on an  abdominal x-ray , the presence of impaired rectal sensation or the finding of large maximal rectal volumes on  anorectal manometry . In addition, can be the bloating of the colon due to infection, also called  megacolon .  [ citation needed ]


On  defecography , megarectum is suggested by a rectal width of >9 cm at the level of the distal  sacrum . [ 1 ]


Melanosis coli , also  pseudomelanosis coli , is a disorder of pigmentation of the wall of the  colon , often identified at the time of  colonoscopy . It is benign and may have no significant correlation with disease. The brown pigment is  lipofuscin  in  macrophages , not  melanin . [ citation needed ]  It is most commonly associated with the use of certain laxatives.


The most common cause of melanosis coli is the extended use of  laxatives , and commonly  anthraquinone  containing laxatives such as  senna ,  aloe vera , and other plant  glycosides . [ 1 ]  The anthranoid laxatives pass through the gastrointestinal tract unabsorbed until they reach the large intestine, where they are changed into their active forms. The resulting active compounds cause damage to the cells in the lining of the intestine and leads to apoptosis (a form of cell death). The damaged (apoptotic) cells appear as darkly pigmented bodies that may be taken up by scavenger cells known as macrophages. When enough cells have been damaged, the characteristic pigmentation of the bowel wall develops. The condition can develop after just a few months of laxative use. [ 2 ]


However, other causes are identified, including an increase in colonic epithelial  apoptosis . [ 3 ]   Endoscopically , the  mucosa  may show a brownish discoloration in a  moiré pattern . [ citation needed ]


On  biopsy , melanosis coli shows characteristic pigment-laden  macrophages  within the mucosa on  PAS  staining. [ 4 ]


The histologic  differential diagnosis  of mucosal pigmentation is:  lipofuscin  (melanosis coli),  hemosiderin-laden macrophages , and  melanin  (rare).


No adverse effects or consequences of melanosis coli have been identified. [ 4 ]


The condition is unrelated to true melanoses, such as  Peutz–Jeghers syndrome  and  smoker's melanosis . [ 5 ]


Peutz–Jeghers syndrome causes pigmentation of the skin and mucous surfaces with  melanin , and polyps in the  digestive tract .


Pseudomelanoses of other parts of the  gastrointestinal tract  have also been reported, and are of unclear relevance. [ 6 ]


Patients with  colostomies  can have melanosis involving the  stoma , which is also of no significance. [ 7 ]


Microsporidiosis  is an opportunistic intestinal infection that causes  diarrhea  and  wasting  in  immunocompromised  individuals ( HIV , for example). It results from different species of  microsporidia , a group of microbial (unicellular) fungi. [ 1 ]


In  HIV -infected individuals, microsporidiosis generally occurs when  CD4 +  T cell  counts fall below 150.


Microsporidia  have emerged with significant mortality risk in  immunocompromised  individuals. These are small, single-celled, obligately  intracellular parasites  linked to water sources as well as wild, and domestic animals. [ 2 ]  They were once considered  protozoans  or  protists , but are now known to be  fungi , [ 3 ]  or a sister group to fungi. [ 4 ]   The most common causes of microsporidiosis is  Enterocytozoon bieneusi  and  Encephalitozoon intestinalis.


At least 15 microsporidian species have been recognized [ 5 ]  as human  pathogens , spread across nine genera:


The primary causes are  Enterocytozoon bieneusi  and  Encephalitozoon intestinalis . [ 6 ]


(Coded to  image  at right).


The best option for diagnosis is using PCR. [ citation needed ]


Diagnosis with Microsporidia can be done through  gram - positive ,  acid-fast  spores in stool and biopsy material with morphologic demonstration of the organism. Initial detection through light microscopic examination of tissue sections, stools, duodenal aspirates, nasal discharges,  bronchoalveolar lavage  fluids, and conjunctival smears. [ 7 ]  Definitive diagnosis can also be achieved through fluorescein-tagged antibody  immunofluorescence  or electron microscopy, [ 7 ]  and species identification can be done through  PCR . [ 8 ]


Although it is classified as a  protozoal disease  in  ICD-10 , their phylogenetic placement has been resolved to be within the  Fungi , and some sources classify microsporidiosis as a  mycosis , [ 9 ]  however, they are highly divergent and rapidly evolving. [ 10 ] [ 11 ] [ 12 ]


Fumagillin  has been used in the treatment. [ 6 ] [ 13 ]  Another agent used is  albendazole . [ 2 ]


Because of its severe mortality risk in immunocompromised individuals, two main agents are used:  Albendazole , which inhibits  tubulin , and  Fumagillin , which inhibits methionine aminopeptidase type two. [ 14 ]


Microvillus inclusion disease , previously known as  Davidson's disease ,  congenital microvillus atrophy  and, less specifically,  microvillus atrophy  (note: microvillus is often misspelled as microvillous), is a rare  genetic disorder  of the  small intestine  that is inherited in an  autosomal recessive  pattern. [ 1 ] [ 2 ]


It is characterized by chronic, intractable  diarrhea  in new-born infants, starting in the first few days of life. [ 3 ]
This results in  metabolic acidosis  and severe  dehydration . Pregnancy and birth are usually normal. [ citation needed ]


It is caused by a congenital villus atrophy, atrophy of apical  microvilli  and intracellular accumulation of apical enzymes and transporters in the  epithelial cells  of the small intestine. [ 4 ]  MVID is in most cases caused by mutations in the MYO5B gene. Other genes are also responsible of the disease:  STXBP2  or Munc18-2 (also causing  Familial Hemophagocytic Lymphohistiocytosis (FHL) , STX3 and UNC45A. [ citation needed ] [ 5 ]


Prenatal screening  in utero  is currently offered by several medical centers since the  gene (s) involved in the disease were recently discovered to be  MYO5B ; [ 6 ] [ 7 ]  Diagnosis is typically made by  biopsy  of the small intestine. [ 1 ]


The appearance of microvillous inclusion disease on  light microscopy  is similar to  celiac sprue ; however, it usually lacks the intraepithelial  lymphocytic  infiltration characteristic of celiac sprue and stains positive for  carcinoembryonic antigen  (CEA). [ 2 ]  The definitive diagnosis is dependent on  electron microscopy . [ 8 ]


The differential diagnosis of chronic and intractable diarrhea is: [ 9 ]


It is nearly always fatal unless, like short bowel syndrome patients, treated with  parenteral nutrition  or an  intestinal transplant . [ 3 ]  The patient is often classified as being in "intestinal failure" and treated with the cohort of patients known as "short bowel syndrome" patients. [ citation needed ]


One patient from the UK was documented as achieving nutritional independence at age 3. [ 10 ]  On 26 June 2009, a six-year-old girl with microvillus inclusion disease became the third person in the UK to die of swine flu. This was attributed to her weakened immune system. [ 11 ]


Microvillus inclusion disease is extremely rare, however, no prevalence data have been published. An estimate of a few hundred children with the disease in Europe has been made but no time frame to which this count applies is given. Countries with a higher degrees of  consanguinity  experience higher prevalence rates due to its autosomal recessive transmission. [ 12 ]


Microvillus inclusion disease was first described in 1978 by Davidson et al. [ 13 ]  It was originally described as  familial enteropathy . [ citation needed ]


Monomorphic epitheliotropic intestinal T cell lymphoma  (MEITL) (formerly termed enteropathy-associated T cell lymphoma, type II) is an extremely rare  peripheral T-cell lymphoma  that involves the malignant proliferation of a type of  lymphocyte , the  T cell , in the  gastrointestinal tract  (i.e. GI tract). [ 1 ]  Over time, these T cells commonly spread throughout the  mucosal  lining of a portion of the GI tract [ 2 ]  (particularly the jejunum and ileum of the small intestine [ 3 ] ), lead to GI tract nodules and ulcerations, and cause symptoms such as abdominal pain, weight loss, diarrhea,  obstruction ,  bleeding , and/or  perforation . [ 2 ]


In 2008, the  World Health Organization  defined a specific type of lymphoma,  enteropathy-associated T cell lymphoma  (EATL), as having two different types: EATL type I, a lymphoma occurring in patients with the chronic,  autoimmune  GI tract disorder,  celiac disease , and EATL type II, a similar bowel lymphoma that was not associated with celiac disease. However, subsequent studies found significant clinical, pathologic, and pathophysiological differences between these two types of lymphoma. Consequently, the World Health Organization (2016) redefined these lymphomas as separate entities, terming the celiac disease-associated lymphoma as enteropathy-associated T cell lymphoma (EATL) and the lymphoma not associated with celiac disease as monomorphic epitheliotropic intestinal T cell lymphoma (MEITL). [ 4 ]  MEITL is only 1/5 to 1/10 as common as EATL. [ 5 ]  The Organization (2016) also termed a third type of intestinal T cell lymphoma that could not be classified as ATL or MEITL as  intestinal T cell lymphoma, not otherwise specified . [ 6 ]


MEITL is a highly aggressive GI tract lymphoma [ 7 ]  which typically has had very short survival times following its diagnosis. [ 2 ]  The disease often occurs in elderly patients who are afflicted with other ailments and consequently have little tolerance for the standard  chemotherapy  regimens that are used to treat other types of lymphomas. Moreover, these therapeutic regimens have shown little effectiveness in treating MEITL. To date, the best but still only marginally effective therapeutic interventions for the disease have been treatments that incorporate  hematopoietic stem cell transplantation  into chemotherapy plus surgical (when needed to treat local bowel issues such as obstruction or perforation) regimens. [ 3 ]


MEITL has been seen more often in Asians and individuals of  Hispanic  descent, in males (male to female ratio of ~2 to 1), and in mature or elderly individuals (median age ~60 years). [ 2 ]  Patients may present with irregular bowel movements, abdominal pain,  hematochezia  (i.e. the anal passage of fresh blood), [ 2 ]   B symptoms  (i.e. fever,  night sweats , weight loss),  loss of appetite , [ 5 ]  and/or bowel  perforations  and/or  obstructions . [ 2 ]


The malignant T cells in MEITL can be identified by: their expression of  cluster of differentiation  (i.e. CD)  cell surface molecules   CD3 ,  CD8 , and  CD56 ; by their failure to express  CD4 ,  CD5 , or  CD30 ; and, in particular, by their overexpression of  megakaryocyte-associated tyrosine kinase . They are not infected with the  Epstein-Barr virus  and therefore do not express this virus's products (e.g.  EBER1 or EBER2 ). [ 3 ]  In most individuals with the disease, these T cells are  γδ rather than αβ T-cells  based on their expression of γδ rather than αβ  T-cell receptors . They also commonly express  cytotoxic T cell  activation markers such as  TIA1 ,  granzyme B , and  perforin  and therefore may have derived from or be related to  cytotoxic T cell  lymphocytes. However, in up to 25% of cases the malignant cells in MEITL also express markers of  B cell  lymphocytes. Detection of these " tumor marker " molecules on or in the lymphocytes of diseased tissues is critical for diagnosing MEITL; however, it does not clearly establish the original type of lymphocytes which became MEITL's malignant cells. This issue requires further studies. [ 8 ]