Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A suicidal 67-year-old woman with manic-depressive psychosis took an overdose of asprin, amitriptyline and diazepam. The initial effects were pyrexia, tachycardia, hyperpnea, metabolic acidosis, electrocardiographic changes, hypoprothrombinemia, gastritis, and pancreatitis. Four to six weeks later, she was examined because of persistent abdominal pain with mausea, anorexia anemia, and possibly a malabsorption syndrome. An exploratory laparotomy was performed. The surgeon found several previous adhesions, a small intestinal volvulus, and a nodular pancreas. This suggested previous perforation of the small bowel from enteritis, causing a "blind-loop" syndrone. The invilved section of the small bowel was resected. With appropriate treatment, the patient is well three months after operation.
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PMID:Unusual abdominal complications of a suicidal overdose of analgesic and psychotropic drugs in an elderly patient. 61 54

Ten episodes of massive transaminase increase with hepatic necrosis were observed in 7 patients after infusion of megluminioglycamide (Biligram). The patients were 3 men and 4 women aged 49 to 65 years with biliary tract disease (n = 1), recurrent pancreatitis (n = 1), hyperlipidaemia and minimal toxic liver damage (n = 1), pyelonephritis (n = 1), , arteriitis (n = 1), and pseudo-LE (n = 1). In 6 patients there was an increase of the alkaline phosphatase without icterus before the investigation and a slight increase of transaminases in 3 patients. After infusion of 100 ml of Biligram in 5 patients and of 200 ml in 2 patients there was an abrupt increase of GPT (98-2202 U/l) with a lesser increase of GOT. The alkaline phosphatase activity remained unchanged. Three patients showed symptoms such as upper abdominal pain, fever erythema, or conjunctivitis. Histologically all patients showed centrolobular necroses. Transaminases should be checked 2 days after intravenous cholangiograms. In patients with a definite increase reexposure should be avoided.
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PMID:[Hepatic necroses after infusion cholangiography (author's transl)]. 63 57

An analysis of 89 cases with chronic pancreatitis revealed 56% of chronic alcoholic pancreatitis (AP). The sex ratio was 47 males to 3 females and the mean age at onset was 42.4 years in AP and 49.3 years in chronic non-alcoholic pancreatitis (NAP). The 'total amount' of alcohol consumption was correlated to the onset. In AP, the abdominal pain was apt to relapse and severe in nature, furthermore painless pancreatitis was seen in 6%. The association with diabetes or calcification (38%) were more frequently seen in AP. The calcifications in AP appeared to be smaller in size and distributed diffusely or localized in cephalic portion. A striking frequency of liver dysfunctions (39 cases) were demonstrated, however, cirrhosis was rare in AP. The P-S test dysunctions in NAP were frequently reversible in the follow up study, while even some of chronic asymptomatic alcoholics developed clinical signs of pancreatitis during the observed period and proceeded to definite AP, of whom pancreatic dysfunctions showed fluctuation and eventual progression. In other words, even pain free intervals the pancreatic inflammation in susceptible persons may proceed to ultimated destruction of the pancreas. The fatality from chronic pancreatitis was rare (12.3%), which was related diabetes mellitus.
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PMID:A clinical investigation of chronic pancreatitis--comparative study between alcoholic pancreatitis and non-alcoholic pancreatitis--. 66 97

Information from 72 patients from 7 families in England and Wales confirms that hereditary pancreatitis is inherited as an autosomal dominant conditions with limited penetrance. The degree of penetrance is approximately 80%. These patients have had recurrent attacks of abdominal pain starting from childhood or young adult life. The mean age of onset in the 7 families studied was 13.6 years. There were two peaks, with maximum numbers at 5 years and 17 years. The second peak was thought to represent genetically susceptible individuals having pain brought on by alcohol rather than representing evidence of genetic heterogeneity. Five of the 7 families had members with both childhood and adult ages of onset. Only 4 patients out of 72 had life-threatening disease and in the majority of cases the attacks of pain were of nuisance value only. Hereditary pancreatitis was implicated in only 1 patient's death and this was not definite. Patients appear to get better after a period of symptoms usually as they approach middle age, or after a severe attack. In older patients alcohol, emotional upsets, and fatty food appear to precipitate attacks. Pancreatic insufficiency (5.5%), diabetes mellitus (12.5%), pseudocysts (5.5%), and haemorrhagic pleural effusion are uncommon complications. Portal vein thrombosis occurred definitely in 2 patients and was suspected in 3 others. Carcinoma of the pancreas was not found in any of 72 patients studied in detail; however, 2 members from a family not visited personally had chronic pancreatitis and malabsorption going on to carcinoma. They may have suffered from a different disease. Genetic linkage information was too slight for many definite conclusions. However, there was no suggestion of linkage with any of the markers tested.
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PMID:Hereditary pancreatitis in England and Wales. 67 83

A review of the pertinent radiologic findings of common alimentary tract disorders presenting with acute abdominal pain is presented. When the conventional plain abdominal films are not diagnostic, the use of special views and appropriate contract and ultrasound examinations on a urgent basis is encouraged. A more expenditious and accurate diagnosis of the cause of abdominal pain will inevitably reduce the morbidity and mortality of such entities as bowel perforation, infarction, and pancreatitis.
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PMID:Radiologic evaluation of acute abdominal pain arising from the alimentary tract. 68 7

Diverticula rarely occur within the lumen of the duodenum. They arise near the papilla of Vater and extend distally. The diverticulum is lined on both sides with duodenal mucosa, and its eccentric opening is usually proximal in the sac. The diverticulum results from incomplete recanalization of the intestinal lumen after the proliferative epithelial stage in the 7-week embryo and represents either a remnant of one of two channels formed during recanalization or a distal ballooning of a congenital duodenal diaphragm. Although the patient with a diverticulum may be asymptomatic, most patients present with abdominal pain and obstructive symptoms; pancreatitis and gastrointestinal bleeding may be associated with the diverticulum. Barium study shows a characteristic radiolucent halo that represents the wall of the diverticulum. Surgery should be approached with caution because injury to the papilla is a hazard, and in children, coexisting congenital anomalies may be present.
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PMID:Intraluminal duodenal diverticulum. Report of two cases and review of the literature. 80 22

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

Patients with abdominal pain resulting from pancreatitis are often misdiagnosed initially. There are no pathognomonic physical signs to implicate the pancreas as a source of chronic abdominal discomfort. Four patients seen consecutively (and one studied retrospectively) illustrate that erythema ab igne of the abdomen or low back may be a sign of pancreatitis. These patients had used heat on their abdomens or backs in attempts to relieve the pain. Using heat in this manner is common among patients with undiagnosed pancreatitis; the heat enhances the appearance of the erythema ab igne. The presence of pigmentation is a sign of organicity which should lead the physician to investigate the pancreas as a source of the patient's pain.
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PMID:Erythema ab igne, a sign of pancreatic disease. 85 Nov 10

A further Swiss family with hereditary chronic relapsing pancreatitis is reported. Five members definitely have the disease, while in 4 subjects the condition is suspected. The five proven cases are a mother and her four children. All suffer from recurrent attacks of abdominal pain which started between the 8th and 20th year of life, and in all of them exocrine pancreatic insufficiency and pancreatic calcifications can be demonstrated. The mother has had diabetes mellitus since the age of 40 and 3 of the 4 children also have the disease, with age of onset between 15 and 29. In 3 patients insignificant traces of aminoacids could be detected in the urine. At 16 years one male patient had a pseudocyst of the pancreas surgically removed. All the others are treated conservatively. Reports on approximately 25 families with this disease have been published so far. The condition is inherited as an autosomal dominant disorder. Typically, the clinical symptoms begin during childhood or early adolescent life. The pathogenesis is unknown. It is possible that an abnormal pancreatic juice is produced which causes the intracanalicular calcifications. The treatment is identical to that in the non-hereditary forms, i.e. generally conservative. Recently some authors have favored a more aggressive approach consisting of pancreatico-jejunostomy or partial resection of the pancreas.
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PMID:[Swiss family with chronic relapsing calcifying pancreatitis]. 89 47

A patient is described with acute pancreatitis which was probably caused by furosemide. Administration of furosemide on two separate occasions was associated with increases in serum amylase concentrations and recurrence of abdominal pain. This case is of further interest because of the presence of hyperlipemia in the absence of an underlying lipid abnormality. Following recovery from pancreatitis, the lipoprotein pattern evolved from type V to type III, type IIA, and finally to normal.
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PMID:Acute pancreatitis secondary to furosemide with associated hyperlipidemia. 90 Jan 1


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