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)

Many hepatic lesions, ranging from subcellular alterations to malignant tumors, have been attributed to the use of anabolic steroids (AS) and contraceptive steroids (CS). These lesions that have been attributed to AS and CS are discussed with focus on the following: biochemical changes; subcellular alterations; intrahepatic cholestasis; vascular complications (sinusoidal dilatation, peliosis hepatitis, Budd-Chiari syndrome); hyperplasia and neoplasia (diffuse hyperplasia, nodular transformation, focal nodular hyperplasia, hepatocellular adenoma, hepatocellular carcinoma, and miscellaneous malignant tumors); and miscellaneous effects (effects of preexisting liver disease, cholelithiasis, and pancreatitis). OCs have a number of physiologic effects on the liver. These include decreased bile flow, diminished secretion of organic anions, and decreased synthesis and secretion of bile acids. Retention of bromosulfophthalein has been noted with AS during late pregnancy and in the puerperium. It is well established that the CS can lead to elevations of serum ceruloplasmin and copper levels. Subcellular alterations have been reported in both humans and rats on AS or women on CS and involve multiple organelles of the several systems of the liver. Both AS and CS have been implicated in intrahepatic cholestasis. Jaundice usually develops after 2-5 months of therapy with AS or after 3 months of OC use. The lesions attributed to CS and AS can involve any of the systems of the liver. At times more than 1 system is affected simultaneously. Most of the steroid related lesions resemble similar ones caused by other etiologies. Some, such as peliosis hepatitis, are rarely related to other etiologies, but others can be termed steroid specific. A number of diseases associated with the CS or AS also occur in pregnancy. Acute fatty metamorphosis of pregnancy and the periportal hemorrhagic necrosis characteristic of eclampsia have not been reported in patients on CS. Spontaneous rupture of the liver during pregnancy has not been attributed to the CS.
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PMID:Hepatic lesions caused by anabolic and contraceptive steroids. 628 45

Oral contraceptive (OC) use is discussed as a factor in various diseases and disorders of internal medicine. Studies show a significant increase in the risk of developing thromboembolism, pulmonary embolism, cerebrovascular incidents, and coronary infarction among OC users. These problems are caused by changes in blood coagulation, hemodynamics, fibrinolysis, and the damaging of vascular walls, all of which are attributable to OC use. OC use leads to a minor hypertension in 1% of users during the first year of use and in 2.5% by the fifth year. This is initially caused by increased angiotensinogen production in the liver; later, sodium retention caused by the gestagen OC component, mineralocorticoid activity and vascular damage play a part in causing this hypertension. Glucose tolerance is reduced by OCs; lipid metabolism is affected in many ways: e.g. elevation of plasma triglyceride levels. OC users run an increased risk of developing hepatic tumors. Jaundice, Budd Chiari syndrome, gall stones, and pancreatitis have all been observed among OC users. Contraindications to OC use are listed.
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PMID:[Internal medicine problems regarding contraception. Part I]. 744 16

The anticardiolipin or antiphospholipid antibody syndrome is characterized by an increased incidence of venous and arterial thromboses. This syndrome may occur in association with systemic lupus erythematosus or independently. Gastroenterological manifestations have included Budd-Chiari syndrome, hepatic infarction, esophageal necrosis with perforation, intestinal ischemia and infarction, pancreatitis, and colonic ulceration. We report a 39-yr-old man with antiphospholipid antibody syndrome complicated by adrenal insufficiency secondary to bilateral adrenal infarction who presented with severe epigastric pain. Endoscopic evaluation disclosed progressive gastric ulceration with necrosis in the distal body. Angiography revealed no vasculitis. Because of intractable pain despite intravenous anticoagulation and narcotic analgesia, the patient was taken to surgery, and an antrectomy with Billroth II gastrojejunostomy was performed. Histological examination revealed widespread vascular occlusive disease involving veins, small arteries, and arterioles present in all layers of the stomach and the perigastric fat consistent with the vasculopathy of the antiphospholipid antibody syndrome. Treatment with high intensity oral anticoagulation and corticosteroids resulted in clinical and endoscopic improvement. This case report extends the gastroenterological manifestations of the antiphospholipid antibody syndrome to include giant gastric ulceration and emphasizes the importance of anticoagulation in treatment.
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PMID:Giant gastric ulceration associated with antiphospholipid antibody syndrome. 912 46

The antiphospholipid syndrome is an autoimmune hypercoagulability syndrome in which a wide variety of thromboembolic diseases may occur. Gastrointestinal manifestations associated with vascular occlusion include Budd-Chiari syndrome, hepatic and splenic infarction, pancreatitis, omental and intestinal infarction, and esophageal variceal bleeding due to portal vein thrombosis, but chronic mesenteric ischemia associated with mesenteric arterial thrombosis is very rare in this syndrome. We experienced a female patient with primary antiphospholipid syndrome with abdominal angina and splenic infarction associated with celiac trunk and mesenteric arterial thromboses. This is the first report describing chronic mesenteric ischemia and splenic infarction in a patient with primary antiphospholipid syndrome.
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PMID:Primary antiphospholipid syndrome presenting with abdominal angina and splenic infarction. 1211 Oct 88

Estroprogestational contraception is responsible for morphologic and physiologic changes on the hepatic cells, vascular walls, blood coagulation, and lipid metabolism; these changes, in turn, cause several problems, among which jaundice and cholestasis are the most common. Less common are peliosis, ischemic colitis and ulcerous colitis. Treatment of such accidents is surgical and urgent in all acute cases. Benign and malignant tumors are a rare occurrence. Thrombotic risk is strictly related to modifications in blood coagulation, and, when the liver is concerned, often lead to the Budd-Chiari syndrome. Much more serious, because irreversible, is intestinal infarctus, caused by arterial or by venous thrombosis. Abdominal pains during the first months of oral contraceptive use are often a sign of pancreatitis.
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PMID:[Acute damage to the digestive tract related to contraceptives (author's transl)]. 1231 Apr 4

The antiphospholipid antibody syndrome (APA) is characterized by an increased incidence of venous and arterial thrombosis. APA syndrome has some gastroenterological manifestations such as Budd-Chiari syndrome, hepatic infarction, esophageal necrosis, intestinal ischemia, pancreatitis and colonic ulceration. We report a 34-year-old man with APA syndrome complicated by hepatic venous thrombosis (Budd-Chiari) and colonic ulcers. The clinical and laboratory findings were compatible with APA syndrome that developed secondary to systemic lupus erythematosus. In order to initiate anticoagulant therapy, he was heparinized. Since lower gastrointestinal bleeding developed, heparin was discontinued and the patient was followed up with baby aspirin and steroids. This case report extends the gastroenterological manifestations of the APA syndrome to include colonic ulceration, which may outweigh the efficacy of initial anticoagulant therapy.
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PMID:A case of antiphospholipid antibody syndrome with Budd-Chiari and colonic ulcers complicated with gastrointestinal hemorrhage. 1533 24

Tumor metastasis to the pancreas is a rare but recognized cause of acute pancreatitis. Autopsy series have reported a 24-40% of pancreatic involvement in small cell lung cancer. However, only a very few cases of tumor-induced acute pancreatitis have been described. Budd-Chiari syndrome complicating lung cancer is a rarely reported condition. We report a 68-year-old woman with extensive small cell lung cancer with the unusual initial presentation of both acute pancreatitis and acute Budd-Chiari syndrome. This patient suffered from progressive epigastralgia for 3 weeks. Severe epigastralgia with radiation to back and progressive jaundice developed 2 days prior to admission. After admission, the liver enlarged rapidly and the ascites increased markedly. Chest roentgenogram showed a mass lesion over the left lower lung field. Poorly differentiated carcinoma cells were found in ascites and bone marrow. The patient died on the ninth day of hospitalization before chemotherapy was initiated. Prompt diagnosis of extensive-stage small cell lung cancer may allow early chemotherapy treatment which favorably influences recovery when the pancreatitis is mild. Although prolonged survival might have been expected had this patient recovered from pancreatitis and received chemotherapy, diagnosis was delayed due to difficulty in immunohistochemical diagnosis of the tumor and the unusual clinical presentation. The use of stains employing antibodies against neurofilament and neuron-specific enolase cell antigens is important for early diagnosis of poorly differentiated metastatic tumor cells.
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PMID:Acute pancreatitis combined with acute Budd-Chiari syndrome as the initial manifestation of small cell lung cancer. 1603 34

Drug-induced injury commonly affects the gastrointestinal and hepatobiliary systems because of the mechanisms of absorption and metabolism. In pill esophagitis, injury is frequently related to direct contact with the esophageal mucosa, resulting in small superficial ulcers in the mid esophagus. Nonsteroidal anti-inflammatory drugs can lead to gastrointestinal tract ulcers and small bowel mucosal diaphragms (thin weblike strictures). Injury to the pancreatic and hepatobiliary systems can manifest as pancreatitis, acute or chronic hepatitis, cholestasis, or steatosis and steatohepatitis (which may progress to cirrhosis). Various drugs may also insult the hepatic vasculature, resulting in Budd-Chiari and sinusoidal obstructive syndromes. Focal lesions such as hepatic adenomas may develop after use of oral contraceptives or anabolic steroids. Ultrasonography, computed tomography, and magnetic resonance imaging can aid in diagnosis of drug-induced injuries and often are necessary to exclude other causes.
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PMID:Imaging of Drug-induced Complications in the Gastrointestinal System. 2676 32

Hepatic sinusoidal dilatation refers to the enlargement of the hepatic capillaries. Most of the time this condition is caused by hepatic venous outflow obstruction, which results in vascular stasis and congestion of hepatic parenchyma. In this setting, hepatic sinusoidal dilatation can be related to pericardial disease, heart failure, compression or thrombosis of the hepatic veins or inferior vena cava (i.e., Budd-Chiari syndrome) or central veins/sinusoids involvement (i.e., sinusoidal obstruction syndrome). Nevertheless, some extrahepatic inflammatory conditions (such as pyelonephritis, cholecystitis, pneumonia, pancreatitis, intestinal bowel disease, and others) may be associated with hepatic sinusoidal dilatation without concurrent venous outflow obstruction. On contrast-enhanced cross-sectional imaging, hepatic sinusoidal dilatation is typically characterized by a mottled, reticular enhancement of the liver, usually referred to as "mosaic" pattern. Other hepatic and extrahepatic imaging features, such us the dilatation of the hepatic veins or the presence of ascites, can help in identifying the cause of sinusoidal dilatation.
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PMID:Hepatic sinusoidal dilatation. 2939 60