Posts Tagged ‘Mucosa’

Gastroduodenal Crohns Disease

02.27.10

In anatomy, the gastroduodenal artery is a small blood vessel in the abdomen.It supplies blood to the pylorus (distal part of the stomach) and the proximal part of the duodenum.It arises from the common hepatic artery and terminates in a bifurcation, when it splits into the right gastroepiploic artery and the anterior superior pancreaticoduodenal artery.

Crohns disease involving the gastric outlet and proximal duodenum, resulting in gastric outlet obstruction. Image on the right shows a view of the stricture as seen through a translucent dilating balloon, which has been inflated in the stricture.

1. Melatonin protection against ethanol-induced gastroduodenal injury was investigated in duodenumligated rats.
2. Melatonin, injected i.p. 30 min before administration of 1 ml of absolute ethanol, given by gavage, significantly decreased ethanol-induced macroscopic, histological and biochemical changes in the gastroduodenal mucosa.
3. Ethanol-induced lesions were detectable as haemorrhagic streaks. Ethanol administration damaged 36% and 25% of the total gastric and duodenal surface, respectively.

Melatonin treatment reduced ethanol-induced gastric and duodenal damage to 14% and 8%, respectively. When indomethacin was given together with ethanol, the gastric damaged area was 44% of the total surface, while the duodenal damaged area was 35%; melatonin administration reduced the damage to only 13% of the total gastric surface and to 12% of total duodenal surface.

4. Both stomach and duodenum of ethanol-treated animals showed polymorphonuclear leukocyte (PMN) infiltration. The number of PMN increased more than 600 and 200 times in stomach and duodenum, respectively, following ethanol administration. Melatonin treatment reduced ethanol-induced PMN infiltration by 38% in the stomach and 20% in the duodenum. In indomethacin-ethanol-treated rats, the number of PMN increased by 875% compared to control group in the stomach and by 264% in duodenum. Melatonin administration reduced the indomethacin-ethanol-induced PMN rise by 57% in the stomach and 40% in the duodenum.

5. Gastroduodenal total glutathione (tGSH) concentration and glutathione reductase (GSSG-Rd) activity were significantly reduced following ethanol and indomethacin-ethanol administration. Melatonin ameliorated both the decrease in tGSH concentration as well as the reduction of GSSG-Rd activity elicited by ethanol both in the stomach and duodenum; melatonin was effective against indomethacin-ethanol-induced damage only in the stomach.

6. Ethanol-induced gastroduodenal damage is believed to be mediated by the generation of free radicals. Recently, a number of in vivo and in vitro experiments have shown melatonin to be an effective antioxidant and free radical scavenger; thus, we conclude that the protection by melatonin against ethanol-induced gastroduodenal injury is due, at least in part, to its radical scavenging activity.

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Colitis Ulcerosa

07.13.09

Ulcerative colitis (Colitis ulcerosa, UC) is a form of inflammatory bowel disease (IBD). Ulcerative colitis is a form of colitis, a disease of the intestine, specifically the large intestine or colon, that includes characteristic ulcers, or open sores, in the colon.

The main symptom of active disease is usually diarrhea mixed with blood, of gradual onset. Ulcerative colitis is, however, a systemic disease that affects many parts of the body outside the intestine. Because of the name, IBD is often confused with irritable bowel syndrome (“IBS”), a troublesome, but much less serious condition. Ulcerative colitis has similarities to Crohns disease, another form of IBD.

Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission.Ulcerative colitis is a rare disease, with an incidence of about one person per 10,000 in North America.

The disease tends to be more common in northern areas. Although ulcerative colitis has no known cause, there is a presumed genetic component to susceptibility. The disease may be triggered in a susceptible person by environmental factors. Although dietary modification may reduce the discomfort of a person with the disease, ulcerative colitis is not thought to be caused by dietary factors. Although ulcerative colitis is treated as though it were an autoimmune disease, there is no consensus that it is such.

Treatment is with anti-inflammatory drugs, immunosuppression (suppressing the immune system), and biological therapy targeting specific components of the immune response. Colectomy (partial or total removal of the large bowel through surgery) is occasionally necessary, and is considered to be a cure for the disease. Ulcerative colitis is a relatively uncommon, chronic, recurrent inflammatory disease of the colon or rectal mucosa. Often a lifelong illness, the condition has profound emotional and social impact on the affected individual. Ulcerative colitis is defined as continuous idiopathic inflammation of the colonic or rectal mucosa.

The rectum is involved in more than 95% of cases. Some authorities believe that the rectum is always involved in an untreated patient. Partial healing may occur in a patient treated with topical therapy, creating diagnostic confusion. Ulcerative colitis occurs more frequently in white people. The incidence of ulcerative colitis is reported to be 2-4 times higher in Jewish people. However, recent population studies in North America do not completely support this assertion. Ulcerative colitis seems to have a female preponderance. Ulcerative colitis affects 30% more females than males. The incidence of ulcerative colitis peaks in people aged 15-25 years and in people aged 55-65 years, although it can occur in people of any age.

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