IBD - Inflammatory Bowel Disease

2008-03-09T00:40:00.000-08:00

Inflammatory bowel disease
From Wikipedia, the free encyclopedia

Classification & external resources
DiseasesDB
31127
eMedicine
med/1169 emerg/106 oph/520
MeSH
D015212
In medicine, inflammatory bowel disease (IBD) is a group of inflammatory conditions of the large intestine and, in some cases, the small intestine. It should not be confused with IBS, Irritable Bowel Syndrome (IBS), which is less severe.

Forms
The main forms of IBD are Crohn's Disease and Ulcerative Colitis (UC).
Accounting for far fewer cases are other forms of IBD:

Collagenous colitis
Lymphocytic colitis
Ischemic Colitis
Diversion colitis
Behçet's disease
Infective Colitis
Indeterminate colitis (Colitis which has not been determined Crohn's Or Ulcerative Colitis)

The main difference between Crohn's disease and UC is 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. [1]

Microscopically, ulcerative colitis is restricted to the mucosa (epithelial lining of the gut), while Crohn's disease affects the whole bowel wall.

Finally, Crohn's Disease and Ulcerative Colitis present with extra-intestinal manifestations (such as liver problems, arthritis, skin manifestations and eye problems) in different proportions.
Rarely, a definitive diagnosis of neither Crohn's disease nor ulcerative colitis can be made because of idiosyncrases in the presentation. In this case, a diagnosis of indeterminate colitis may be made. Although a recognised definition, not all centres refer to this.

Diagnosis
Although very different diseases, both may present with any of the following symptoms: abdominal pain, vomiting, diarrhea, hematochezia, weight loss, weight gain and various associated complaints or diseases (arthritis, pyoderma gangrenosum, Primary Sclerosing Cholangitis PSC). Diagnosis is generally by Colonoscopy with biopsy of pathological lesions.

Treatment
Depending on the level of severity, IBD may require immunosuppression to control the symptoms. such as azathioprine, methotrexate, or 6-mercaptopurine. More commonly, treatment of IBD requires a form of mesalamine. Often, steroids are used to control disease flares and were once acceptable as a maintenance drug. In use for several years in Crohns disease patients and recently in patients with Ulcerative Colitis, biologicals has been used such as the intravenously administered Remicade. Severe cases may require surgery, such as bowel resection, strictureplasty or a temporary or permanent Colostomy or ileostomy. Alternative medicine treatments for bowel disease exist in various forms, however such methods concentrate on controlling underlying pathology in order to avoid prolonged steroidal exposure or surgical excisement[2].

Usually the treatment is started by administering drugs with high anti-inflammatory affects, such as Prednisone. Once the inflammation is successfully controlled, the patient is usually switched to a lighter drug to keep the disease in remission, such as Asacol, a mesalamine. If unsuccessful, a combination of the aforementioned immunosurpression drugs with a mesalamine (which may also have an anti-inflammatory effect) may or may not be administered, depending on the patient.

Prognosis
While IBD can limit quality of life due to pain, vomiting, diarrhea, and other socially unacceptable symptoms, it is rarely fatal on its own. Fatalities due to complications such as toxic megacolon, bowel perforation and surgical complications are also rare.

While patients of IBD do have an increased risk of Colorectal Cancer (Colon 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.

After treatment, the patient is usually switched to a lighter drug with fewer 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.

Recent findings
A recent hypothesis posits that some IBD cases are caused by an overactive immune system attacking various tissues of the digestive tract because of the lack of traditional targets such as parasites and worms. The number of people being diagnosed with IBD has increased as the number of infections by parasites, such as roundworm, hookworm and human whipworms, has fallen, and the condition is still rare in countries where parasitic infections are common. This is similar to the hygiene hypothesis applied to allergies.[citation needed]

Initial reports (Summers et al 2003) suggest that "helminthic therapy" may not only prevent but even cure (or 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.

Prebiotics and probiotics are showing increasing promise as treatments for IBD (Furrie, 2005) and in some studies have proven to be as effective as prescription drugs (Kruis, 2004).
More recently, research (Hue et al 2006) has shown that IL-23 is overexpressed in tissues taken from Mouse models of IBD. The group showed that knocking out IL-23 (heterodimer of IL-12p40 and IL-23p19) severely reduced inflammation of the bowel, both in terms of cells and proinflammatory cytokine production. Also, they found that a novel group of CD4+ T lymphocytes, Th17 T cells, are highly upregulated in bowels of diseased mice. Taken together, the group shows that IL-23 but not IL-12 (IL-12p40 and IL-12p35; share a subunit) drives innate and T cell mediated intestinal inflammation.

In 2005 New Scientist published a joint study by Bristol University and Bath University 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. 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. 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 diarrhoea. The team also discovered another cannabinoid receptor, CB2, in the guts of IBD sufferers, which was not present in healthy guts. 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 moping up excess cells.[citation needed]

References
Furrie, E. Biotic Therapy Cuts Inflammation in Ulcerative Colitis. Gut 2005;54:242-249.
Kruis, W., P Fric, J Pokrotnieks, M Lukás, B Fixa, M Kascák, M A Kamm, J Weismueller, C Beglinger, M Stolte, C Wolff, and J Schulze. Maintaining remission of ulcerative colitis with the probiotic Escherichia coli Nissle 1917 is as effective as with standard mesalazine. Gut 2004; 53: 1617-1623.

Summers RW, Elliott DE, Qadir K, Urban JF Jr, Thompson R, Weinstock JV. Trichuris suis seems to be safe and possibly effective in the treatment of inflammatory bowel disease. Am J Gastroenterol 2003;98:2034-41. PMID 14499784.

Hue S, Ahern P, Buonocore S, Kullberg MC, Cua DJ, McKenzie BS, Powrie F, Maloy KJ. Interleukin-23 drives innate and T cell-mediated intestinal inflammation. J. Exp. Med. 2006; 203:2473-2483. [3]

External links
An Overview of Crohn's Disease and Ulcerative Colitis
IBD Forum A website designed for use by Doctors and other healthcare professionals specialising in the management of Inflammatory Bowel Disease
ColitisBlog.com is an information portal for Colitis Sufferers.

Support organizations
IBD Support Foundation
Crohn's and Colitis Foundation of America
European Federation of Crohns and Colitis Associations has member associations in most European countries.
Children and youngster group within the European Federation of Crohns and Colitis Assiciations
IBDCure International

v • d • e Digestive system - Gastroenterology

Click here for information on another diseases

Collagenous colitis

2007-12-31T01:26:00.000-08:00

Collagenous colitis
From Wikipedia, the free encyclopedia

Collagenous colitis is an inflammatory colonic disease with peak incidence in the 5th decade of life, affecting women more than men. Its clinical presentation involves watery diarrhea, usually in the absence of rectal bleeding. It is often classified under the umbrella entity microscopic colitis, along with a related condition, lymphocytic colitis.

Diagnosis
On Colonoscopy, the mucosa of the colon typically looks normal, but biopsies of affected tissue usually show deposition of collagen in the lamina propria, which is the area of connective tissue between colonic glands. Radiological tests, such as a Barium X-rays are typically normal.

Treatment
Treatment of collagenous colitis is often challenging, and many agents have been used therapeutically:

Bismuth agents, including Pepto-Bismol
5-aminosalicylic acid
Budesonide
Immunosuppressants, including azathioprine
Corticosteroids

Disease associations
An association between collagenous colitis and Celiac Disease has been reported, but there is no evidence that dietary restrictions used in celiac disease management are of benefit in collagenous colitis therapy.
There have also been reports of an association between collagenous colitis and lymphoma.

See also
Colitis
Lymphocytic colitis

References
Abstract of Cochrane Review on therapy
Abstract of review on collagenous colitis
Retrieved from "http://en.wikipedia.org/wiki/Collagenous_colitis"
Categories: Gastroenterology

Lymphocytic colitis

2007-12-30T03:09:00.000-08:00

Lymphocytic colitis
From Wikipedia, the free encyclopedia

Lymphocytic colitis, a subtype of microscopic colitis, is a rare condition characterized by chronic non-bloody watery diarrhea. The colonoscopy is normal but the mucosal biopsy reveals an accumulation of lymphocytes in the colonic epithelium and connective tissue (lamina propria). Collagenous colitis shares this feature but additionally shows a distinctive thickening of the subepithelial collagen table. The peak incidence of lymphocytic colitis is in persons over age 50; the disease affects women more than men.

Causes
No definite etiology has been determined. Some reports have implicated long-term usage of NSAIDs, antidepressants, and other drugs; and overactive immune responses are also suspected.

Treatment
Over-the-counter antidiarrheal drugs are effective for many people with lymphocytic colitis. Anti-inflammatory drugs, such as salicylates may also help. Corticosteroids or Mesalazines may be prescribed for people who do not respond to other drug treatment. The long-term prognosis for this disease is not clear.

See also
Colitis
Collagenous colitis

External links
Collagenous Colitis and Lymphocytic Colitis
Diseases Database
GPNotebook
eMedicine.com
Merck Manual

References
Gasteroenterology and Hepatology Resource Center, Johns Hopkins Medical Institutes
Retrieved from "http://en.wikipedia.org/wiki/Lymphocytic_colitis"
Categories: Gastroenterology Inflammations Digestive diseases

Ischemic Colitis

2007-12-29T23:30:00.000-08:00

Ischemic colitis
From Wikipedia, the free encyclopedia

Classification & external resources
ICD-10
K 55.9
ICD-9
557.9
DiseasesDB
34162
MedlinePlus
000258
eMedicine
radio/180

This article concerns ischemia of the large bowel.

Ischemic colitis (Ischaemic Colitis - British English) is a medical condition in which inflammation and injury of the large intestine result from inadequate blood supply. 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 via endoscopy. 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 ill.[5]
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[6] or chronic colitis.[7]

Causes and epidemiology
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.[8] 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.[8]

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.

Non-occlusive ischemia
In hemodynamic instable patients (i.e. shock) the mesenteric perfusion may be compromised. This condition is commonly asymptomatic, and usually only apparent through a systemic inflammatory response.

Occlusive ischemia
Mostly the result of a thromboembolism. Commonly the embolism is caused by atrial fibrillation, valvular disease, myocardial infarction, or cardiomyopathy.

Pathophysiology

Colonic blood supply
The colon receives blood from both the superior and inferior mesenteric arteries. The blood supply from these two major arteries overlap, with abundant collateral circulation. However, there are weak points, or "watershed" areas, at the borders of the territory supplied by each of these arteries. These watershed areas are most vulnerable to ischemia when blood flow decreases, as they have the fewest vascular collaterals.

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.

Development of ischemia
Under ordinary conditions, the colon receives between 10% and 35% of the total cardiac output.[9] 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.[10] 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.

Pathologic findings
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.[8] With more severe ischemia, a pathologic picture resembling inflammatory bowel disease (i.e. chronic ulcerations, crypt abscesses and psuedopolyps) may be seen.[11] 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.[8] Following restoration of normal blood flow, reperfusion injury may also contribute to the damage to the colon.[12]

Diagnosis
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.

Signs and symptoms
Three progressive phases of ischemic colitis have been described:[13][14]
A hyperactive phase occurs first, in which the primary symptoms are severe abdominal pain and the passage of bloody stools. Many patients get better and do not progress beyond this phase.
A paralytic phase can follow if ischemia continues; in this phase, the abdominal pain becomes more widespread, the belly becomes more tender to the touch, and bowel motility decreases, resulting in abdominal bloating, no further bloody stools, and absent bowel sounds on exam.
Finally, a shock phase can develop as fluids start to leak through the damaged colon lining. This can result in shock and metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion. Patients who progress to this phase are often critically ill and require intensive care.

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.[15] The sensitivity of findings among 73 patients were:[16]

abdominal pain (78%)
lower digestive bleeding (62%)
diarrhea (38%)
Fever higher than 38°C (34%) (38°C equals approximately 100.4°F)
Physical examination[16]
abdominal pain (77%)
abdominal tenderness (21%)

Diagnostic tests
There are no specific blood tests for ischemic colitis. The sensitivity of tests among 73 patients were:[16]

The white blood cell count was more than 15,000/mm3 in 20 patients (27%)
The serum bicarbonate level was less than 24 mmol/L in 26 patients (36%)
Plain X-rays are often normal or show non-specific findings.[17] In a series of 73 patients, plain abdominal radiography (56%) showing colic distension in 53% or a pneumoperitoneum in 3%.[16]
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.[18][19][20]
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.

Treatment
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.

Antibiotics are sometimes given in moderate to severe cases; the data supporting this practice date to the 1950s,[21] 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.[22][23][24] 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.[25]

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.

Prognosis
Most patients with ischemic colitis recovery 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.

Non-gangrenous ischemic colitis, which comprises the vast majority of cases, is associated with a mortality rate of approximately 6%.[26] 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.[27]

Long-term complications
About 20% of patients with acute ischemic colitis may develop a long-term complication known as chronic ischemic colitis.[28] 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.

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,[29] although endoscopic dilatation and stenting have also been employed.[30][31]

References

^ Higgins P, Davis K, Laine L (2004). "Systematic review: the epidemiology of ischaemic colitis.". Aliment Pharmacol Ther 19 (7): 729-38. PMID 15043513.
^ Brandt LJ, Boley SJ (2000). "AGA technical review on intestinal ischemia. American Gastrointestinal Association". Gastroenterology 118 (5): 954-68. PMID 10784596.
^ American Gastroenterological Association (2000). "American Gastroenterological Association Medical Position Statement: guidelines on intestinal ischemia". Gastroenterology 118 (5): 951-3. PMID 10784595. http://www.guideline.gov/summary/summary.aspx?ss=15&doc_id=3069&nbr=2295
^ Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed., 2002 Saunders, p. 2332.
^ Medina C, Vilaseca J, Videla S, Fabra R, Armengol-Miro J, Malagelada J (2004). "Outcome of patients with ischemic colitis: review of fifty-three cases.". Dis Colon Rectum 47 (2): 180-4. PMID 15043287.
^ Simi M, Pietroletti R, Navarra L, Leardi S (1995). "Bowel stricture due to ischemic colitis: report of three cases requiring surgEsophageal dilatationery.". Hepatogastroenterology 42 (3): 279-81. PMID 7590579.
^ Cappell M (1998). "Intestinal (mesenteric) vasculopathy. II. Ischemic colitis and chronic mesenteric ischemia.". Gastroenterol Clin North Am 27 (4): 827-60, vi. PMID 9890115.
^ a b c d Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed., 2002 Saunders, p. 2332.
^ UpToDate, Colonic ischemia, accessed 2 September 2006.
^ Rosenblum J, Boyle C, Schwartz L (1997). "The mesenteric circulation. Anatomy and physiology.". Surg Clin North Am 77 (2): 289-306. PMID 9146713.
^ Brandt LJ, Boley SJ, Goldberg L, et al: Colitis in the elderly. Am J Gastroenterol 76:239, 1981.
^ Granger D, Rutili G, McCord J (1981). "Superoxide radicals in feline intestinal ischemia.". Gastroenterology 81 (1): 22-9. PMID 6263743.
^ Boley, SJ, Brandt, LJ, Veith, FJ. Ischemic disorders of the intestines. Curr Probl Surg 1978; 15:1.
^ Hunter G, Guernsey J (1988). "Mesenteric ischemia.". Med Clin North Am 72 (5): 1091-115. PMID 3045452.
^ Greenwald D, Brandt L, Reinus J (2001). "Ischemic bowel disease in the elderly.". Gastroenterol Clin North Am 30 (2): 445-73. PMID 11432300.
^ a b c d Huguier M, Barrier A, Boelle PY, Houry S, Lacaine F (2006). "Ischemic colitis". Am. J. Surg. 192 (5): 679-84. doi:10.1016/j.amjsurg.2005.09.018. PMID 17071206.
^ Smerud M, Johnson C, Stephens D (1990). "Diagnosis of bowel infarction: a comparison of plain films and CT scans in 23 cases.". AJR Am J Roentgenol 154 (1): 99-103. PMID 2104734.
^ Alpern M, Glazer G, Francis I (1988). "Ischemic or infarcted bowel: CT findings.". Radiology 166 (1 Pt 1): 149-52. PMID 3336673.
^ Balthazar E, Yen B, Gordon R (1999). "Ischemic colitis: CT evaluation of 54 cases.". Radiology 211 (2): 381-8. PMID 10228517.
^ Taourel P, Deneuville M, Pradel J, Régent D, Bruel J (1996). "Acute mesenteric ischemia: diagnosis with contrast-enhanced CT.". Radiology 199 (3): 632-6. PMID 8637978.
^ PATH, EJ, McCLURE, JN Jr. Intestinal obstruction; the protective action of sulfasuxidine and sulfathalidine to the ileum following vascular damage. Ann Surg 1950; 131:159.
^ Plonka A, Schentag J, Messinger S, Adelman M, Francis K, Williams J (1989). "Effects of enteral and intravenous antimicrobial treatment on survival following intestinal ischemia in rats.". J Surg Res 46 (3): 216-20. PMID 2921861.
^ Bennion R, Wilson S, Williams R (1984). "Early portal anaerobic bacteremia in mesenteric ischemia.". Arch Surg 119 (2): 151-5. PMID 6696611.
^ Redan J, Rush B, Lysz T, Smith S, Machiedo G (1990). "Organ distribution of gut-derived bacteria caused by bowel manipulation or ischemia.". Am J Surg 159 (1): 85-9; discussion 89-90. PMID 2403765.
^ Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed., 2002 Saunders, p. 2334.
^ Longo W, Ballantyne G, Gusberg R (1992). "Ischemic colitis: patterns and prognosis.". Dis Colon Rectum 35 (8): 726-30. PMID 1643995.
^ Parish K, Chapman W, Williams L (1991). "Ischemic colitis. An ever-changing spectrum?". Am Surg 57 (2): 118-21. PMID 1992867.
^ Cappell M (1998). "Intestinal (mesenteric) vasculopathy. II. Ischemic colitis and chronic mesenteric ischemia.". Gastroenterol Clin North Am 27 (4): 827-60, vi. PMID 9890115.
^ Simi M, Pietroletti R, Navarra L, Leardi S (1995). "Bowel stricture due to ischemic colitis: report of three cases requiring surgery.". Hepatogastroenterology 42 (3): 279-81. PMID 7590579.
^ Oz M, Forde K (1990). "Endoscopic alternatives in the management of colonic strictures.". Surgery 108 (3): 513-9. PMID 2396196.
^ Profili S, Bifulco V, Meloni G, Demelas L, Niolu P, Manzoni M (1996). "[A case of ischemic stenosis of the colon-sigmoid treated with self-expandable uncoated metallic prosthesis]". Radiol Med (Torino) 91 (5): 665-7. PMID 8693144.

External links
Endoscopy images of ischemic colitis (German site)
[show]
v • d • e Digestive system - Gastroenterology (primarily K20-K93, 530-579)
Esophagus
Esophagitis - GERD - Achalasia - Boerhaave syndrome - Nutcracker esophagus - Zenker's diverticulum - Mallory-Weiss syndrome - Barrett's esophagus
Stomach/duodenum
Peptic (gastric/duodenal) ulcer - Gastritis - Gastroenteritis - Duodenitis - Dyspepsia - Pyloric stenosis - Achlorhydria - Gastroparesis - Gastroptosis - Portal hypertensive gastropathy
Hernia
Inguinal (Indirect, Direct) - Femoral - Umbilical - Incisional - Diaphragmatic - Hiatus
Noninfectiveenteritis & colitis
Inflammatory bowel disease (IBD, Crohn's disease, Ulcerative colitis) - noninfective gastroenteritis
Other intestinal
vascular (Abdominal angina, Mesenteric ischemia, Ischemic colitis, Angiodysplasia) - Ileus/Bowel obstruction (Intussusception, Volvulus) - Diverticulitis/Diverticulosis - Irritable bowel syndrome (IBS)other functional intestinal disorders (Constipation, Diarrhea, Megacolon/Toxic megacolon, Proctalgia fugax) - Anal fissure/Anal fistula - Anal abscess - Rectal prolapse - Proctitis (Radiation proctitis)
Liver/hepatitis
Alcoholic liver disease - Liver failure (Acute liver failure) - Cirrhosis - PBC - NASH - Fatty liver - Peliosis hepatis - Portal hypertension - Hepatorenal syndrome
Accessorydigestive
Gallbladder (Gallstones, Choledocholithiasis, Cholecystitis, Cholesterolosis, Rokitansky-Aschoff sinuses)
Biliary tree (Cholangitis, Cholestasis/Mirizzi's syndrome, PSC, Biliary fistula, Ascending cholangitis)Pancreas (Acute pancreatitis, Chronic pancreatitis, Pancreatic pseudocyst, Hereditary pancreatitis)
Other/general
Appendicitis - Peritonitis (Spontaneous bacterial peritonitis)
Malabsorption (celiac, Tropical sprue, Blind loop syndrome, Whipple's)
postprocedural: Gastric dumping syndrome - Postcholecystectomy syndromebleeding: Hematemesis - Melena - Gastrointestinal bleeding (Upper, Lower)
See also congenital
Retrieved from "http://en.wikipedia.org/wiki/Ischemic_colitis"
Categories: Gastroenterology

Diversion colitis

2007-12-29T00:05:00.000-08:00

Diversion colitis
From Wikipedia, the free encyclopedia

Diversion colitis is an inflammation of the colon which can occur as a complication of ileostomy or colostomy, often occurring within the year following the surgery. It can also occur in a neovagina created by colovaginoplasty, sometimes several years after the original procedure. In many milder cases after ileostomy or colostomy, diversion colitis is left untreated and disappears naturally. If treatment is required, possible treatments include short-chain fatty acid irigation, steroid enemas and mesalazine.[1]

References
^ Diversion colitis: histological features in the colon and rectum after defunctioning colostomy.. www.pubmedcentral.nih.gov. Retrieved on 2007-12-27.
Retrieved from "http://en.wikipedia.org/wiki/Diversion_colitis"
Categories: Gastroenterology

Behçet's disease

2007-12-28T17:13:00.000-08:00

Behçet's disease
From Wikipedia, the free encyclopedia

Classification & external resources
ICD-10
M 35.2
ICD-9
279.4
OMIM
109650
DiseasesDB
1285
eMedicine
med/218 ped/219 derm/49 oph/425
MeSH
D001528
Behçet disease (Behçet's syndrome, Morbus Behçet, silk road disease) is a chronic condition due to disturbances in the body’s immune system. This system, which normally protects the body against infections through controlled Inflammation, becomes overactive and produces unpredictable outbreaks of exaggerated inflammation. This extra inflammation affects blood vessels, usually the small ones. As a result, symptoms occur wherever there is a patch of inflammation, and can be anywhere where there is a blood supply.

History
Behçet disease is named after Hulusi Behçet (1889-1948), the Turkish dermatologist and scientist who first recognized the syndrome in one of his patients in 1924 and reported his research on the disease in Journal of Skin and Venereal Diseases in 1936.[1][2] The name (Morbus Behçet) was formally adopted at the International Congress of Dermatology in Geneva in September 1947.

Symptoms of this disease may have been described by Hippocrates in the 5th century BC, in his 3rd Epidemion-book.[3] Its first modern formal description was published in 1922.[1]
Some sources use the term "Adamantiades’ syndrome" or "Adamandiades-Behçet syndrome", for the work done by Benediktos Adamantiades.[4] However, the current World Health Organization/ICD-10 standard is "Behçet's disease".
In 1991, Saudi Arabian medical researchers discovered "neuro-Behcet's disease",[5] a neurological involvement in Behcet's disease, considered one of the most devastating manifestations of the disease.[6]

Diagnosis
There is no specific pathological test for Behçet disease at present. It is diagnosed clinically by specific patterns of symptoms and repeated outbreaks. Other causes for these symptoms have to be ruled out before making the diagnosis. The symptoms do not have to occur together, but can have happened at any time.

There are three levels of certainty for diagnosis:

International Study Group diagnostic guidelines (very strict for research purposes)
Practical clinical diagnosis (generally agreed pattern but not as strict)
Suspected' or 'Possible' diagnosis (incomplete pattern of symptoms)

International Study Group diagnostic guidelines
Must have:

Aphthous ( Mouth Ulcers ) (any shape, size or number at least 3 times in any 12 months),
along with 2 out of the next 4 "hallmark" symptoms:

genital ulcers (including anal ulcers and spots in the
genital region and swollen testicles or epididymitis in men),
skin lesions
(papulo-pustules, folliculitis, erythema nodosum, acne
in post-adolescents not on corticosteroids),
eye inflammation (iritis, uveitis, retinal vasculitis,
cells in the vitreous),
pathergy reaction (papule >2 mm dia. 24-48 hrs or
more after needle-prick).

Practical clinical diagnosis
Must have:

mouth ulcers,
along with 1 of the 4 hallmark symptoms above and with 2 of the symptoms below:

arthritis/arthralgia,
nervous system symptoms,
stomach and/or bowel inflammation,
deep vein thrombosis,
superficial thrombophlebitis,
cardio-vascular problems of inflammatory origin,
inflammatory problems in chest and lungs,
problems with hearing and/or balance,
extreme exhaustion,
changes of personality, psychoses,
any other members of the family with a diagnosis of Behcet disease.

'Suspected' or 'Possible' diagnosis
Usually given when someone does not have mouth ulcers or has mouth ulcers but does not have 1 of the 4 hallmark symptoms but has other symptoms and signs of inflammation and other causes for these have been ruled out.

Causes
No one knows why the immune system starts to behave this way in Behçet disease. It is not because of any known infections, it is not hereditary, it does not have to do with ethnic origin, gender, life-style, or age, where someone has lived or where they have been on holiday. It is not associated with cancer, and links with tissue-types (which are under investigation) are not certain. It does not follow the usual pattern for autoimmune diseases.

Treatment
Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. Anti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the disease.[7][8] Another Anti-TNF agent, Etanercept, may be useful in patients with mainly skin and mucosal symptoms.[9]

Interferon alfa-2a may also be an effective alternative treatment, particularly for the genital and oral ulcers[10] as well as ocular lesions.[11] Azathioprine, when used in combination with interferon alfa-2b also shows promise,[12] and Colchicine can be useful for treating some genital ulcers, erythema nodosum, and arthritis in women, and arthritis in men.[13]
Thalidomide has also been used due to its immune-modifying effect.[14] Dapsone and rebamipide have been shown, in small studies, to have beneficial results for mucocutaneous lesions.[15][16]

A different orientation could be explored in Behçet Disease, especially with genetic linkage to HLA-B51 antigen, just like the prevalence of HLA-B27 in Ankylosing Spondylitis. Ankylosing spondylitis is not due to an 'oveactive' immune system; instead it is a true autoimmune disease caused by molecular mimicry of the Osp (outer surface protein) with the Klebsiella pneumoniae germ (2 enzymes produced by this normally non-virulent pathogen), which is always present as a sub-clinical infection, typically at the ileocecal junction. The combination of antibiotics targeted to this specific germ, and dietary controls (elimination or severe restriction of all starches) could therefore potentially provide the most effective treatments, but such treatments have not yet been proven or generally approved. At the current time, a similar infectious origin has not yet been confirmed that leads to Behçet disease, but certain strains of Streptococcus sanguis has been found to have a homologous antigenicity.

Epidemiology
Behçet disease is considered more prevalent in the areas surrounding the old silk trading routes in the Middle East and in Central Asia. Thus, it is sometimes known as Silk Road Disease. However, this disease is not restricted to people from these regions.

An estimated 15,000 to 20,000 Americans have been diagnosed with this disease. In the UK, it is estimated to have about 2 cases for every 100,000 people.

Globally, males are affected more frequently than females. In the United States, more females are affected than males.

Pronunciation note
Because Hulusi Behçet was Turkish, the correct pronunciation is with a hard "ch", as in "choice", with "e" (both first and second e letters) as in "end" and with the terminal "t" sounded: "Beh-chet". Because it contains a cedilla, "Behçet" is frequently wrongly assumed to be French in origin and pronounced with a sibilant "s" sound (as in "satsuma") or soft "ch" (as in "shoe"), with the "e" incorrectly like "i" (as in see), with the "t" incorrectly silenced: "Beshay".

References
^ a b synd/1863 at Who Named It
^ H. Behçet. Über rezidivierende, aphtöse, durch ein Virus verursachte Geschwüre am Mund, am Auge und an den Genitalien. Dermatologische Wochenschrift, Hamburg, 1937, 105(36): 1152-1163.
^ Johns Hopkins Vasculitis Center (2004). Johns Hopkins Vasculitis Center Discusses Behcets Disease. Retrieved September 9, 2005.
^ B. Adamandiades. Sur un cas d'iritis à hypopyon récidivant. Annales d'oculistique, Paris, 1931, 168: 271-278.
^ Ravi Malhotra (2004), "Saudi Arabia", Practical Neurology 4: 184-185.
^ S. Saleem (2005), Neuro-Behcet's Disease: NBD, Neurographics, Vol. 4, Issue 2, Article 1.
^ Sfikakis PP, Theodossiadis PG, Katsiari CG, Kaklamanis P, Markomichelakis NN (2001). "Effect of infliximab on sight-threatening panuveitis in Behcet's disease". Lancet 358 (9278): 295-6. PMID 11498218.
^ Sfikakis PP (2002). "Behcet's disease: a new target for anti-tumor necrosis factor treatment". Ann Rheum Dis 61 Suppl 2: ii51-3. PMID 12379622.
^ Melikoglu M, Fresko I, Mat C, Ozyazgan Y, Gogus F, Yurdakul S, Hamuryudan V, Yazici H (2005). "Short-term trial of etanercept in Behcet's disease: a double blind, placebo controlled study". J Rheumatol 32 (1): 98-105. PMID 15630733.
^ Alpsoy E, Durusoy C, Yilmaz E, Ozgurel Y, Ermis O, Yazar S, Basaran E (2002). "Interferon alfa-2a in the treatment of Behcet disease: a randomized placebo-controlled and double-blind study". Arch Dermatol 138 (4): 467-71. PMID 11939808.
^ Kotter I, Zierhut M, Eckstein AK, Vonthein R, Ness T, Gunaydin I, Grimbacher B, Blaschke S, Meyer-Riemann W, Peter HH, Stubiger N (2003). "Human recombinant interferon alfa-2a for the treatment of Behcet's disease with sight threatening posterior or panuveitis". Br J Ophthalmol 87 (4): 423-31. PMID 12642304.
^ Hamuryudan V, Ozyazgan Y, Fresko Y, Mat C, Yurdakul S, Yazici H (2002). "Interferon alfa combined with azathioprine for the uveitis of Behcet's disease: an open study". Isr Med Assoc J 4 (11 Suppl): 928-30. PMID 12455182.
^ Yurdakul S, Mat C, Tuzun Y, Ozyazgan Y, Hamuryudan V, Uysal O, Senocak M, Yazici H (2001). "A double-blind trial of colchicine in Behcet's syndrome". Arthritis Rheum 44 (11): 2686-92. PMID 11710724.
^ Hamuryudan V, Mat C, Saip S, Ozyazgan Y, Siva A, Yurdakul S, Zwingenberger K, Yazici H (1998). "Thalidomide in the treatment of the mucocutaneous lesions of the Behcet syndrome. A randomized, double-blind, placebo-controlled trial". Ann Intern Med 128 (6): 443-50. PMID 9499327.
^ Matsuda T, Ohno S, Hirohata S, Miyanaga Y, Ujihara H, Inaba G, Nakamura S, Tanaka S, Kogure M, Mizushima Y (2003). "Efficacy of rebamipide as adjunctive therapy in the treatment of recurrent oral aphthous ulcers in patients with Behcet's disease: a randomised, double-blind, placebo-controlled study". Drugs R D 4 (1): 19-28. PMID 12568631.
^ Sharquie KE, Najim RA, Abu-Raghif AR (2002). "Dapsone in Behcet's disease: a double-blind, placebo-controlled, cross-over study". J Dermatol 29 (5): 267-79. PMID 12081158.

External links
Behçet's Disease Resource Guide from the National Eye Institute (NEI).
Behcet disease - MedLink Neurology Clinical Summary
Signs & Symptoms of Behçet's disease (with pictures)
American Behçet's Disease Association
Behçet's Syndrome Society (UK)
International Society for Behçet's Disease
DermNet systemic/behcet

v • d • eDiseases of the musculoskeletal system and connective tissue (M, 710-739)
Arthropathies
Arthritis (Septic arthritis, Reactive arthritis, Rheumatoid arthritis, Psoriatic arthritis, Felty's syndrome, Juvenile idiopathic arthritis, Still's disease) - crystal (Gout, Chondrocalcinosis) - Osteoarthritis (Heberden's node, Bouchard's nodes)
acquired deformities of fingers and toes (Boutonniere deformity, Bunion, Hallux rigidus, Hallux varus, Hammer toe) - other acquired deformities of limbs (Valgus deformity, Varus deformity, Wrist drop, Foot drop, Flat feet, Club foot, Unequal leg length, Winged scapula)
patella (Luxating patella, Chondromalacia patellae)Protrusio acetabuli - Hemarthrosis - Arthralgia - Osteophyte
Systemic connectivetissue disorders
Polyarteritis nodosa - Churg-Strauss syndrome - Kawasaki disease - Hypersensitivity vasculitis - Goodpasture's syndrome - Wegener's granulomatosis - Arteritis (Takayasu's arteritis, Temporal arteritis) - Microscopic polyangiitis - Systemic lupus erythematosus (Drug-induced) - Dermatomyositis (Juvenile dermatomyositis) - Polymyositis - Scleroderma - Sjögren's syndrome - Behçet's disease - Polymyalgia rheumatica - Eosinophilic fasciitis - Hypermobility
Dorsopathies
Kyphosis - Lordosis - Scoliosis - Scheuermann's disease - Spondylolysis - Torticollis - Spondylolisthesis - Spondylopathies (Ankylosing spondylitis, Spondylosis, Spinal stenosis) - Schmorl's nodes - Degenerative disc disease - Coccydynia - Back pain (Radiculopathy, Neck pain, Sciatica, Low back pain)
Soft tissue disorders
muscle: Myositis - Myositis ossificans (Fibrodysplasia ossificans progressiva)
synovium and tendon: Synovitis/Tenosynovitis (Calcific tendinitis, Stenosing tenosynovitis, Trigger finger, DeQuervain's syndrome) - Irritable hip - Ganglion cyst
bursa: bursitis (Olecranon, Prepatellar, Trochanteric) - Baker's cyst
fibroblastic disorders (Dupuytren's contracture, Plantar fasciitis, Nodular fasciitis, Necrotizing fasciitis, Fasciitis, Fibromatosis)
shoulder lesions: Adhesive capsulitis - Rotator cuff tear - Subacromial bursitis
enthesis: enthesopathies (Iliotibial band syndrome, Achilles tendinitis, Patellar tendinitis, Golfer's elbow, Tennis elbow, Metatarsalgia, Bone spur, Tendinitis)other, NEC: Muscle weakness - Rheumatism - Myalgia - Neuralgia - Neuritis - Panniculitis - Fibromyalgia
Osteopathies
disorders of bone density and structure: Osteoporosis - Osteomalacia - continuity of bone (Pseudarthrosis, Stress fracture) - Monostotic fibrous dysplasia - Skeletal fluorosis - Aneurysmal bone cyst - Hyperostosis - Osteosclerosis Osteomyelitis - Avascular necrosis - Paget's disease of bone - Algoneurodystrophy - Osteolysis - Infantile cortical hyperostosis
Chondropathies
Juvenile osteochondrosis (Legg-Calvé-Perthes syndrome, Osgood-Schlatter disease, Köhler disease, Sever's disease) - Osteochondritis - Tietze's syndrome
See also congenital conditions (Q65-Q79, 754-756)
Retrieved from "http://en.wikipedia.org/wiki/Beh%C3%A7et%27s_disease"
Categories: Autoimmune diseases Dermatology Words of Turkish origin

Infective Colitis

2007-12-28T16:21:00.000-08:00

Colitis
From Wikipedia, the free encyclopedia

Classification & external resources
ICD-10
K 50. - K52
ICD-9
558
OMIM
191390
DiseasesDB
31340
MedlinePlus
001125
eMedicine
ped/435
MeSH
C06.405.205.265

Colitis is a digestive disease characterized by inflammation of the colon.[1]

Signs and symptoms
Signs and symptoms of colitis include pain, tenderness in the abdomen, fever, swelling of the colon tissue, bleeding, erythema (redness) of the surface of the colon, rectal bleeding, blood in stool, rapid weight loss, aches and pains within the joints, and ulcerations of the colon. Common tests which reveal these signs include X-rays of the colon, testing the stool for blood and pus, Flexible Sigmoidoscopy , and Colonoscopy . Additional tests include stool cultures and blood tests, including blood chemistry tests. A high erythrocyte sedimentation rate (ESR) is one typical finding in acute exacerbations of colitis.

Types
Types of colitis include Ulcerative Colitis, Crohn's Disease, Diversion colitis, Ischemic Colitis, infectious colitis, fulminant colitis, chemical colitis, microscopic colitis, Lymphocytic colitis , and atypical colitis.

A well-known subtype of infectious colitis is pseudomembranous colitis, which results from infection by a toxigenic strain of Clostridium difficile (c-diff).[2] Parasitic infections can also cause colitis.

Any colitis with a rapid downhill clinical course is known as fulminant colitis. In addition to the diarrhea, fever, and anemia seen in colitis, the patient has severe abdominal pain and presents a clinical picture similar to that of septicemia, where shock is present. Approximately half of these patients require surgery.

Irritable Bowel Syndrome (IBS), a separate disease, has been called spastic colitis or spastic colon. This name causes confusion, since colitis is not a feature of irritable bowel syndrome.

Treatment
Treatment of colitis may include the administration of antibiotics and general anti-inflammatory medications such as Mesalamine or its derivatives, steroids, or one of a number of other drugs that ameliorate inflammation. Surgery is sometimes needed, especially in cases of fulminant colitis. Surgery usually entails removing the colon and bowel and creating a "pouch" with portions of the small intestine.

Changes in diet can be effective at treating the symptoms of colitis and easing the side effects. These can include reducing the intake of carbohydrates, lactose products, soft drinks and caffeine. This approach has been championed by Elaine Gottschall.

Notes
The following footnotes can include source references:
^ a b The term "colitis" is pronounced as "co-LIE-tiss" in reference to the word colon.
^ "Clostridium Difficile Colitis - Overview", WebMD from Healthwise, September 2006, webpage: WebMD-clostridium-difficile-colitis.

External links
Crohn's & Colitis Foundation of Canada
Crohn's & Colitis Foundation of America
The National Association for Colitis and Crohn’s Disease (UK)
Colitis at GPnotebook
[show]
v • d • e Digestive system - Gastroenterology (primarily K20-K93, 530-579)
Esophagus
Esophagitis - GERD - Achalasia - Boerhaave syndrome - Nutcracker esophagus - Zenker's diverticulum - Mallory-Weiss syndrome - Barrett's esophagus
Stomach/duodenum
Peptic (gastric/duodenal) ulcer - Gastritis - Gastroenteritis - Duodenitis - Dyspepsia - Pyloric stenosis - Achlorhydria - Gastroparesis - Gastroptosis - Portal hypertensive gastropathy
Hernia
Inguinal (Indirect, Direct) - Femoral - Umbilical - Incisional - Diaphragmatic - Hiatus
Noninfectiveenteritis & colitis
Inflammatory bowel disease (IBD, Crohn's disease, Ulcerative colitis) - noninfective gastroenteritis
Other intestinal
vascular (Abdominal angina, Mesenteric ischemia, Ischemic colitis, Angiodysplasia) - Ileus/Bowel obstruction (Intussusception, Volvulus) - Diverticulitis/Diverticulosis - Irritable bowel syndrome (IBS)other functional intestinal disorders (Constipation, Diarrhea, Megacolon/Toxic megacolon, Proctalgia fugax) - Anal fissure/Anal fistula - Anal abscess - Rectal prolapse - Proctitis (Radiation proctitis)
Liver/hepatitis
Alcoholic liver disease - Liver failure (Acute liver failure) - Cirrhosis - PBC - NASH - Fatty liver - Peliosis hepatis - Portal hypertension - Hepatorenal syndrome
Accessorydigestive
Gallbladder (Gallstones, Choledocholithiasis, Cholecystitis, Cholesterolosis, Rokitansky-Aschoff sinuses)
Biliary tree (Cholangitis, Cholestasis/Mirizzi's syndrome, PSC, Biliary fistula, Ascending cholangitis)Pancreas (Acute pancreatitis, Chronic pancreatitis, Pancreatic pseudocyst, Hereditary pancreatitis)
Other/general
Appendicitis - Peritonitis (Spontaneous bacterial peritonitis)
Malabsorption (celiac, Tropical sprue, Blind loop syndrome, Whipple's)
postprocedural: Gastric dumping syndrome - Postcholecystectomy syndromebleeding: Hematemesis - Melena - Gastrointestinal bleeding (Upper, Lower)
See also congenital
Retrieved from "http://en.wikipedia.org/wiki/Colitis"
Categories: Inflammations Digestive diseases Conditions diagnosed by stool test Gastroenterology

Leaky Gut Sydrome

2005-03-12T12:52:00.000-08:00

Leaky gut syndrome

From Wikipedia, the free encyclopedia

Leaky gut syndrome is proposed condition of altered or damaged bowel lining. The term is used by some alternative medicine practitioners, but the syndrome is not a recognized diagnosis.[1] It is hypothesized to be caused by increased permeability of the gut wall resulting from toxins, poor diet, parasites, infection, or medications.[2] The leaky gut then allows substances such as toxins, microbes, undigested food, waste, or larger than normal macromolecules leak through an abnormally-permeable gut wall. Proponents variously propose that these out of place substances affect the body directly or initiate an immune reaction.[3]

Contents1 Hypotheses
2 Controversy
3 Autism
4 Proposed Treatment
4.1 Autism
5 References
6 See also
7 External links

Hypotheses
Health care practitioners who diagnose this syndrome explain that intestinal inflammation which may originate from intestinal dysbiosis or other sources of irritation, widens the junctions between the cells of the intestinal lining, allowing endotoxins and incompletely digested particles to be partially absorbed. These are targeted by antibodies, forming immune complexes which cause a semi-infectious state and can be carried by the bloodstream to distant sites where they may stimulate the release of cytokines. Low grade fever, transient gut pain, and a sense of inability to absorb nutrients are some reported symptoms in otherwise undiagnosed patients.[4][5].

Controversy
While many practitioners maintain that leaky gut syndrome is a bona fide physiological condition, the area of "gut problems" lies between conventional and alternative medicine, and includes other diagnoses such as small bowel bacterial overgrowth syndrome or small intestine bacterial overgrowth (SIBO), and yeast syndrome or systemic candidiasis, and remains controversial and scientifically unsettled.[6]

Some alternative practitioners believe that leaky gut syndrome is a possible starting point or connection with many disorders such as asthma, diabetes, autoimmune diseases like lupus, diseases like scleroderma, internal colitis, long term disorders like rheumatoid arthritis, severe illnesses like multiple sclerosis and chronic fatigue syndrome and Crohn's disease. [7]

Autism
Andrew Wakefield has proposed a condition called Autistic enterocolitis to describe a condition where bowel disorders can contribute to autism,[8]. However 10 of the 13 authors of the paper have since retracted its interpretations[9], and the British General Medical Council (GMC) has ruled that Wakefield suppressed and falsified data[10][11].

Parents have reported gastrointestinal (GI) disturbances in autistic children, and several studies have investigated possible associations between autism and the gut.[12] The disputed Wakefield et al. paper also suggested that some bowel disorders may allow antigens to pass from food into the bloodstream and then to contribute to brain dysfunction.[8] Although Wakefield later proposed the term autistic enterocolitis, his studies' methodology has been criticized, their results have not been replicated by other groups,[13] and Wakefield has been accused of manipulating patient data and misreporting results.[14]

There is no research evidence that autistic children are more likely to have GI symptoms than typical children.[12] In particular, design flaws in studies of elimination diets mean that the currently available data are inadequate to guide treatment recommendations.[15] A 2008 study found that children with autism had no more peptides in their urine than typical children, casting doubt on the proposed mechanism underlying the leaky-gut theory.[16]

In another example, a 1998 study of three children with ASD treated with secretin infusion reported improved GI function and dramatic improvement in behavior, which suggested an association between GI and brain function in autistic children, although the low number of patients is statistically insignificant.[17] After this study, many parents sought secretin treatment and a black market for the hormone developed quickly.[12] However, later studies found secretin ineffective in treating autism.[18]

Autism
A review looked at the treatment of autism using an approach based on dietary manipulation used to alter the effects of so-called 'leaky gut'. It concluded that these treatments are cumbersome and not proven to be efficacious. [19]

Proposed Treatment
Leaky gut syndrome theories inspired several dietary treatments, including gluten-free diets, casein-free diets, antifungal diets, low-sugar diets, as well as supplements that include nystatin, B12, and probiotics.

References
1.^ http://www.quackwatch.org/01QuackeryRelatedTopics/fadindex.html
2.^ Liu Z, Li N, Neu J (April 2005). "Tight junctions, leaky intestines, and pediatric diseases". Acta Paediatr. 94 (4): 386–93. doi:10.1111/j.1651-2227.2005.tb01904.x. PMID 16092447.
3.^ Kiefer D, Ali-Akbarian L (2004). "A brief evidence-based review of two gastrointestinal illnesses: irritable bowel and leaky gut syndromes". Altern Ther Health Med 10 (3): 22–30; quiz 31, 92. PMID 15154150.
4.^ Leaky Gut Syndromes: Breaking the Vicious Cycles. Galland L. Townsend Letter for Doctors, August/September 1995, p. 63.
5.^ http://www.mdheal.org/leakygut.htm Galland 1995 fulltext article
6.^ Pizzorno, JE, Murray, MT, (November 2005) Textbook of Natural Medicine, 3rd edition, Churchill Livingstone, pp 167, 584, 1527 ISBN 0-443-07300-7
7.^ Leaking Gut Syndrome
8.^ a b Wakefield A, Murch S, Anthony A et al. (1998). "Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children". Lancet 351 (9103): 637–41. doi:10.1016/S0140-6736(97)11096-0. PMID 9500320. http://briandeer.com/mmr/lancet-paper.htm. Retrieved 2007-09-05.
9.^ McKee, Maggie (2004-03-04). "Controversial MMR and autism study retracted". New Scientist. http://www.newscientist.com/article.ns?id=dn4743. Retrieved 2007-08-10.
10.^ Fitzpatrick M (2007-07-04). "'The MMR-autism theory? There's nothing in it'". spiked. http://spiked-online.com/index.php?/site/article/3562/. Retrieved 2008-01-22.
11.^ "MMR scare doctor 'acted unethically', panel finds". BBC News. 2010-01-28. http://news.bbc.co.uk/2/hi/health/8483865.stm. Retrieved 2010-01-28.
12.^ a b c Johnson TW (2006). "Dietary considerations in autism: identifying a reasonable approach". Top Clin Nutr 21 (3): 212–25.
13.^ MacDonald TT, Domizio P (2007). "Autistic enterocolitis; is it a histopathological entity?". Histopathology 50 (3): 371–9. doi:10.1111/j.1365-2559.2007.02606.x. PMID 17257133.
14.^ Deer B (2009-02-08). "MMR doctor Andrew Wakefield fixed data on autism". Sunday Times. http://www.timesonline.co.uk/tol/life_and_style/health/article5683671.ece. Retrieved 2009-02-09.
15.^ Christison GW, Ivany K (2006). "Elimination diets in autism spectrum disorders: any wheat amidst the chaff?". J Dev Behav Pediatr 27 (2 Suppl 2): S162–71. doi:10.1097/00004703-200604002-00015. PMID 16685183.
16.^ Cass H, Gringras P, March J et al. (2008). "Absence of urinary opioid peptides in children with autism". Arch Dis Child 93 (9): 745–50. doi:10.1136/adc.2006.114389. PMID 18337276. Lay summary – BBC News (2008-03-17).
17.^ Horvath K, Stefanatos G, Sokolski KN, Wachtel R, Nabors L, Tildon JT (1998). "Improved social and language skills after secretin administration in patients with autistic spectrum disorders". J Assoc Acad Minor Phys 9 (1): 9–15. PMID 9585670.
18.^ Sturmey P (2005). "Secretin is an ineffective treatment for pervasive developmental disabilities: a review of 15 double-blind randomized controlled trials". Res Dev Disabil 26 (1): 87–97. doi:10.1016/j.ridd.2004.09.002. PMID 15590241.
19.^ Johnson TW (2006). "Dietary considerations in autism: identifying a reasonable approach". Top Clin Nutr 21 (3): 212–25.

See also
Autistic enterocolitis
Leaky gut
[edit] External linksWhat is Leaky Gut Syndrome, Reprinted from AIA Newsletter No.18 (Summer 1997)
Breaking the Vicious Cycle by Leo Galland, M.D.
Article outlining the effects of LGS from Medical Laboratory Observer
Be Wary of "Fad" Diagnoses
Retrieved from "http://en.wikipedia.org/wiki/Leaky_gut_syndrome"
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This page was last modified on 8 March 2011 at 01:38.