Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000727 (acute abdomen)
 3,084 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is presented that many of the enteric and systemic manifestations after jejunoileal bypass can be related to an inflammatory process within the bypassed small bowel rather than to the surgically induced sequelae of a short bowel syndrome with malabsorption. Invasion of the excluded segment by fecal flora was associated with a histologically demonstrable inflammatory response of the mucosa. The disorder was of variable severity and duration and occurred in the majority of 28 bypass patients. Progression to a clinical syndrome resembling an acute abdomen occurred in about 15% of the patients. Small bowel ileus and, in some patients, obstruction of the colon were suggested by physical signs and x-ray findings. Surgical exploration in such instances demonstrated an inflammaotry process of the excluded small bowel loops with severe distention of this segment and of the colon, but not organic obstruction. Pneumatosis cystoides intestinalis was a sequal in two patients. Exudative protein loss was documented in the severe cases. Most of the systemic sequelae are comparable to those seen with inflammatory diseases of the bowel such as Crohn's disease. Fever, excessive weight and lean tissue loss, and the involvement of skin, blood vessels, joints and possibly, the liver suggest an immune response as a common factor in the pathogenesis. The clinical improvement with antibiotics such as metronidazole or with restitution of normal bowel continuity indicates that the bacterial flora in the excluded small bowel segment or its byproducts are causally related to the systemic complications. Hyperoxaluria may be primarily the sequela of steatorrhea and not of the inflammatory process.
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PMID:Bypass enteropathy: an inflammatory process in the excluded segment with systemic complications. 83 42

Pancreas transplantation is usually performed in patients with denovo type I diabetes, who have advanced secondary complications. We report a case in which whole pancreaticoduodenal transplantation, with enteric drainage, was performed to correct both endocrine and exocrine deficiencies in a patient with hyperlabile diabetes and steatorrhea, unresponsive to oral enzyme replacement therapy, following staged total pancreatectomy for idiopathic or familial chronic pancreatitis. The transplant was performed one year after completion of native pancreatectomy and immediately established an insulin-independent euglycemic state, with normal oral and intravenous glucose tolerance test results and correction of steatorrhea. Beginning one year posttransplant, the patient had intermittent episodes of steatorrhea, associated with mild elevation of blood sugar levels, which were presumed to be due to rejection and, indeed, responded to antirejection treatment with antilymphocyte globulin and temporary increases in steroids dosages. At 20 months posttransplant, steatorrhea did not respond to antirejection treatment and an acute abdomen developed. Laparotomy revealed a perforated graft duodenum, which was resected; pathology showed transmural necrosis secondary to chronic rejection. The pancreas graft itself was left in situ, disconnected from the intestinal tract. The patient remained normoglycemic after graft duodenectomy but resumed oral enzyme replacement therapy in an attempt to combat recurrence of severe steatorrhea. However, his overall situation remained improved compared to pretransplant, since the exocrine deficiency was tolerable in the absence of a diabetic state. Ten months postgraft duodenectomy (38 months posttransplant), elevations in blood sugar levels were treated with another course of antirejection treatment and levels temporarily declined. At 14 months postgraft duodenectomy (42 months posttransplant), graft endocrine function again declined and exogenous insulin was resumed. Six months later, four years after the original transplant, a new enteric-drained pancreaticoduodenal graft was placed, once again resulting in an insulin-independent, steatorrheafree state. With improvements in immunosuppression, pancreas transplantation could be offered to selected patients with hyperlabile diabetes, following total pancreatectomy for benign disease; if the enteric drainage technique is used, in the absence of rejection, exocrine deficiency could be corrected as well.
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PMID:Pancreaticoduodenal transplantation with enteric drainage following native total pancreatectomy for chronic pancreatitis: a case report. 187 4

Isoamylase analysis by isoelectric focusing was performed in the serum of 30 healthy volunteers, 65 patients with acute or chronic pancreatic diseases, nine with acute abdomen, four with macroamylasemia, and four with duodenal duplication. In controls, up to four fractions (2 salivary, 2 pancreatic) were found; the pancreatic fractions were as a mean 44.7% (SD 8.6) of total. In chronic pancreatitis, only patients with steatorrhea showed a significant reduction of pancreatic isoamylase (p less than 0.001). In all patients with acute pancreatitis or pseudocysts, an additional fraction (similar to the so-called P3 fraction) was resolved. Moreover, additional isoenzymes were found in all patients with severe acute pancreatitis or pseudocysts, and not in controls or patients with mild forms, acute abdomen or duodenal duplication. A similar pattern was shown in a stored control serum after 10 mo at -20 degrees C. These fractions disappeared after successful surgical drainage. No specific alteration was found in pancreatic cancer. Amylase fractionation by isoelectric focusing can be used to confirm an acute pancreatitis, and to monitor patients with pancreatic pseudocysts and collections after surgical drainage.
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PMID:Isoamylase determination by isoelectric focusing in pancreatic disorders. A potential clinical aid. 203 21

Brown bowel syndrome is a rare condition characterized by deposition of lipofuscin in the smooth muscle cells of the gastrointestinal tract. The number of reported cases is small, but all are associated with malabsorptive states. Despite these small numbers, there is considerable evidence that vitamin E deficiency is important etiologically. We report here the case of a severely malnourished [body mass index 11.7 kg/m (2): normal range 20-25 kg/m (2)] 31-yr-old black male with a longstanding history of alcohol abuse, who was on anti-tuberculosis therapy. The patient presented with an acute abdomen and was found, at operation, to have a mid-ileal intussusception. Histological examination of the resected specimen demonstrated lipofuscin accumulation consistent with brown bowel syndrome, but no tumor. Subsequent investigations revealed no significant quantities of vitamin E in the blood and pancreatic steatorrhea. However, deficiency of other fat-soluble (vitamin A and D) and water-soluble vitamins (vitamin C and thiamine) also were detected. This report supports the association of brown bowel syndrome with vitamin E deficiency but cannot exclude the compounding effects of protein calorie malnutrition, multiple vitamin deficiencies, and chronic alcohol toxicity.
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PMID:Small bowel intussusception and brown bowel syndrome in association with severe malnutrition. 867 14