Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The assumption that tetracycline HCl can cause acute pancreatitis has been accepted since reports began to appear implicating it as a cause of fatty liver in pregnancy with associated pancreatitis. It is listed as an etiologic factor for acute pancreatitis in reference articles and standard medical textbooks without good documentation of this association in the absence of fatty liver. This report describes a documented case of tetracycline HCl-induced acute pancreatitis without associated overt liver disease.
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PMID:Tetracycline-induced pancreatitis. 645 64

The prevalence with which alcoholic pancreatitis is associated with alcoholic liver disease is unclear. To investigate this association further, we have reviewed the autopsy findings of 1022 patients who died from alcoholic liver disease and compared these findings with those from 352 patients who died from cardiac or pulmonary disease. All patients who died from liver disease had a history of chronic alcoholism with clinical and biochemical evidence of severe liver damage. Death resulted from hepatic coma, gastrointestinal bleeding, or infection. Liver disease patients were classified into two groups: (1) those with cirrhosis (77%) and (2) those without cirrhosis but with acute and/or chronic sclerosing hyaline necrosis (23%). Anatomic and histopathologic changes characteristic of chronic pancreatitis were found in 203 patients in approximately the same frequency (20% and 18%, respectively) in both groups. Acute pancreatitis without chronic lesions was observed in 8% and 10% of both groups, respectively. In the control group of 352 autopsies (122 cardiac and 230 pulmonary patients), the overall prevalence of pancreatitis, at 2.6%, was significantly (P less than 0.001) lower than that observed in the alcoholic liver disease groups. A total of 22 cases (50%) dying from acute or chronic sclerosing hyaline necrosis had severe chronic calcifying pancreatitis compared to 29 patients (18%) (P less than 0.001) dying from cirrhosis. By contrast, dense fibrosis was significantly (P less than 0.001) more commonly observed in patients with cirrhosis. We conclude that pancreatitis occurs frequently in patients dying from alcoholic liver disease but is an uncommon finding in patients dying from other causes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pancreatitis associated with alcoholic liver disease. A review of 1022 autopsy cases. 673 67

Results of measurement of serum lipase activity as determined by a UV-test described by Myrick and a titrimetric assay as described by Rick were compared as far as sensitivity and specificity in diagnosis of pancreatitis is concerned. Sensitivity of the UV assay is low (45% falsely normal values), and specificity as well (falsely pathological values in 55.5% of patients with liver disease and 9% of normal persons). In the UV assay lipoproteinlipases are measured as well as hepatic esterases: in 17 samples from persons having received heparin lipase activity was increased 3-8 fold. In a total of 99 samples no correlation was found between the results of the 2 assays. As a consequence it can be stated that the UV-test as described by Myrick has no relevance in diagnosis of pancreatitis; the commercially available assay kit is withdrawn in the meantime.
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PMID:[Clinical studies using a photometric method for determining serum lipase activity]. 673 89

The test for pancreatic exocrine function using N-benzoyl-L-tyrosyl-p-aminobenzoic acid (BTP test) does not require duodenal intubation, but misleadingly abnormal results often occur in patients with liver or bowel disease because the p-aminobenzoic acid (PABA) released by chymotrypsin hydrolysis of the peptide either is not conjugated or is malabsorbed. This study evaluated a modified BTP test, using a tracer dose of 14C-PABA to eliminate misleading results, to assess exocrine function from a single six-hour collection of urine. The test clearly distinguished all patients with pancreatic steatorrhoea from normal subjects and identified patients with less severe pancreatitis as often as did the Lundh test. Furthermore, in patients with bowel or liver disease the misleadingly abnormal results of the unmodified BTP test were eliminated by the modified test in all but one case. These findings suggest that the modified BTP test provides a practical alternative to conventional tests of pancreatic function that entail duodenal intubation.
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PMID:Preliminary evaluation of a single-day tubeless test of pancreatic function. 678 6

Excessive weight gain occurred in a patient who was taking sodium valproate and phenytoin. The sodium valproate was therefore withdrawn but the rapid weight loss that ensued led to phenytoin intoxication. Hence a retrospective analysis was conducted of 100 children with epilepsy treated with sodium valproate. Fit control improved in 77 and was best in children with generalised epilepsy. None of the reported severe side effects, such as acute liver disease and pancreatitis, were encountered. Milder but troublesome side effects, however, occurred in 65 patients. The commonest was increased weight gain, which occurred in 44 cases. Others were transient gastrointestinal disturbances (20), lassitude (nine), transient hair loss (six), transient enuresis (seven), and aggressive behaviour (four).
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PMID:Effects of sodium valproate in 100 children with special reference to weight. 679 86

The endoscopic retrograde cholangiogram and pancreatogram of 22 patients with primary biliary cirrhosis, 33 patients with other forms of chronic liver disease and 28 'normal' controls were compared. The incidence of radiological intrahepatic duct abnormality is similar in patients with primary biliary cirrhosis and in other forms of liver disease, but is present in only a minority of both groups. A 'notch' or smooth indentation on the extrahepatic bile ducts at the porta hepatis was present in 58% of patients with primary biliary cirrhosis but in none in either of the other two groups. Three out of seven patients with sclerosing cholangitis showed minimal-change pancreatitis. Pancreatic abnormalities were otherwise infrequent.
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PMID:The endoscopic retrograde cholangiogram and pancreatogram in chronic liver disease. 687 47

The clinical and epidemiological literature is reviewed as to metabolic effects of oral contraceptives (OCs). Both the estrogens and the progestins in OCs cause biochemical alterations which have metabolic consequences. Changes in glucose, lipid, and protein metabolism suggest that the dosage of both estrogens and progestins should be minimized as much as possible. All studies with OCs show no changes in glucose tolerance, but all do consistently show elevated plasma insulin levels as a result of OC usage. This occurs because the pill causes a decrease in insulin sensitivity in healthy women. Increases in age and weight, regardless of OC usage, will also cause an increase in glucose tolerance. Oral glucose tolerance deteriorates in all OC user groups, the greatest deterioration being in the high-dose estrogen users. Women with a history of gestational diabetes or impaired glucose tolerance should be considered high-risk pill users. Lipid abnormalities as a result of pill usage are primarily due to estrogen content. Fasting triglyceride levels are increased in all estrogen users. High-risk factors to be considered in OC prescription are: moderate obesity; diabetes; history of gestational diabetes; hypertension; history of pancreatitis, gallbladder or liver disease; physical evidence of xanthomatosis; age over 30 and smoker; age over 35; family history of hyperlipidemia; and family history of early atherosclerotic vascular disease. Many of the pill-induced protein synthesis changes are similar to those which occur during pregnancy. These, too, are due to estrogen content.
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PMID:Metabolic effects of the birth control pill. 702 12

In order to assess the incidence and possible predisposing and contributing factors in the development of acute pancreatitis after liver transplantation, we reviewed the medical records of all 1832 adult patients who underwent 2161 orthotopic liver transplantation (OLTx) procedures in our center between January 1987 and September 1992. Of these patients, 55 (3% incidence) developed clinical pancreatitis and 247 (13.4% incidence) developed hyperamylasemia (biochemical pancratitis). Overall mortality in cases of clinical pancreatitis was 63.6%. The mortality in cases of hyperamylasemia was similar to that found in the general liver transplant population (i.e., 23%). A strong correlation was found between pancreatitis after liver transplantation and end-stage liver disease due to hepatitis B (30% of the cases, P = 0.00001). Extensive surgical dissection around the pancreas (P < 0.05), the type of biliary reconstruction following liver transplantation (P < 0.05), and the number of liver grafts received by the same patient (P = 0.00001) appeared to be possible contributing factors as did the duration of venovenous bypass and the quantity of IV calcium chloride administered intraoperatively.
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PMID:Acute pancreatitis after liver transplantation: incidence and contributing factors. 753 81

Focal and multilobular biliary cirrhosis are considered pathognomonic of cystic fibrosis (CF) and almost invariably have been reported in patients with steatorrhea. In contrast, patients with pancreatic sufficiency and normal absorption are considered less likely to develop liver or biliary tract problems. The authors report three patients with CF and pancreatic sufficiency, presenting with recurrent abdominal pain (unrelated to pancreatitis). All had common bile duct disease, one with multilobular cirrhosis and portal hypertension. Pancreatic sufficiency was proven by quantitative pancreatic stimulation tests, 3-day fecal fat analyses, and serum pancreatic isoamylases. All three patients had mild lung disease. Two were homozygous for the common delta F508 mutation, and the other, a delta F508 compound heterozygote. Hepatobiliary structure and function were determined by serial hepatobiliary scintigraphy, percutaneous transhepatic cholecystography, and biochemical liver function tests. Patients 1 and 3 had mild hepatomegaly, normal liver biochemistry, and distal common bile duct strictures. Patient 2 had a firm nodular liver with splenomegaly, abnormal liver biochemistry, and a cholangiographic appearance of sclerosing cholangitis. All have undergone operative treatment for persistent abdominal pain. These cases confirm the occurrence of common bile duct pathology and liver disease in patients with CF and pancreatic sufficiency. They demonstrate that liver and biliary tract disease can occur independently of the underlying disease severity and the presence of steatorrhea. Further, they suggest that obstruction of the biliary tract may be an additional factor in the evolution of liver disease in CF.
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PMID:Hepatobiliary disease in cystic fibrosis patients with pancreatic sufficiency. 753 38

The human cytochrome P4502E1 gene (P4502E1), coding for an ethanol-inducible nitrosamine-metabolizing P-450, is involved in the metabolism of ethanol and many known carcinogens. Recently, restriction fragment length polymorphisms (RFLPs) within the P4502E1 have been suggested as genetic markers of susceptibility to alcohol-induced liver disease but the previous studies disagree whether alcoholics with c1 or c2 allele are more susceptible to alcohol-induced liver diseases. Using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, we determined the RsaI and PstI polymorphism of P4502E1 in 77 Chinese alcoholic patients (54 with alcohol-induced cirrhosis and 23 with acute alcohol-induced pancreatitis) and 164 non-alcoholics and compared them with previously published data. The PCR-RFLPs showed three P4502E1 genotypes: type A, homozygote c1/c1; type B, heterozygote c1/c2; and type C, homozygote c2/c2. The RsaI and PstI polymorphism of P4502E1 were completely linked in both Chinese alcoholics and nonalcoholic controls. The rare allele (c2) occurs at similar frequency of 0.232 and 0.234 (P > .05) in nonalcoholic controls and alcoholics, respectively. The genotype distributions of P4502E1 between Chinese alcoholics and nonalcoholics are not significantly different. The genotype and allele frequencies of P4502E1 for Chinese are significantly different from those of Swedes, European-Americans, and African-Americans, respectively (P < .00001), but very similar to Japanese (P > .05). In conclusion, ethnic variations exist between Asians and Caucasians and between Asians and African-Americans. No allelic variants at loci associated with RsaI/PstI RFLPs result in phenotypes displaying greater susceptibility to alcohol-induced cirrhosis or alcoholism in Chinese populations, which contradicts previous reports from Japanese groups.
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PMID:An investigation of whether polymorphisms of cytochrome P4502E1 are genetic markers of susceptibility to alcoholic end-stage organ damage in a Chinese population. 759 Jun 56


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