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)

Lupus anticoagulant is an immunoglobulin that interferes with prothrombin conversion to thrombin and is manifested biochemically by prolongation of the partial thromboplastin time. Paradoxically, bleeding is rare in association with this anticoagulant, and deep leg vein thromboses, pulmonary emboli, and cerebrovascular accidents have been described in patients with this clotting inhibitor. This report describes the first case of Budd-Chiari syndrome associated with the lupus anticoagulant. The patient presented with abdominal pain and massive ascites. The Budd-Chiari syndrome was confirmed by liver biopsy and venography. No medical condition known to predispose to an increased thrombotic tendency could be identified, and the presence of the lupus anticoagulant in the patient's plasma may provide an explanation for his hypercoagulability and development of the Budd-Chiari syndrome.
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PMID:Budd-Chiari syndrome in a patient with the lupus anticoagulant. 641 18

A Budd-Chiari syndrome was observed in a 11 year-old girl who was admitted to hospital for abdominal pain and distension, soon followed by severe shock. X-ray investigations, surgery and autopsy showed partial stenosis of the common portion of the left hepatic veins associated with a complete obstruction of other hepatic veins but without alteration of the inferior vena cava.
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PMID:[Budd-Chiari syndrome caused by obstruction of the hepatic veins]. 665 54

We describe the clinico-pathological characteristics of hepatic injury associated with the toxic-epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic-epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd-Chiari syndrome. Serum gamma-glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug-induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine-induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatoxicity is a possible mechanism.
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PMID:Hepatic injury in the toxic epidemic syndrome caused by ingestion of adulterated cooking oil (Spain, 1981). 669 64

Hepatic vein thrombosis (Budd-Chiari Syndrome) is a rare disorder resulting from obstruction to the outflow of blood from the liver. The characteristic pathologic findings are intense congestion most pronounced around the terminal hepatic venules, cell necrosis, and a scant inflammatory reaction. Major clinical manifestations include hepatomegaly, right upper quadrant abdominal pain, and ascites. Disorders associated with hepatic vein thrombosis include those associated with a thrombotic tendency, such as polycythemia vera and paroxysmal nocturnal hemoglobinuria. Use of oral contraceptive agents probably increases tendency to develop hepatic vein thrombosis. Biochemical tests of the liver are of little value. The hepatic scan may be useful in suggesting the diagnosis with a marked decrease in uptake of isotope over affected areas of the liver. The diagnosis is confirmed by inferior vena caval and attempted hepatic venous catheterization. An associated thrombosis of the inferior vena cava is frequently found. Therapy in hepatic vein thrombosis is directed towards correction, in so far as possible, the underlying disorder, prevention of further extention of thrombosis, and management of ascites. Side-to-side portacaval or mesocaval shunt operation may convert the portal vein into an effective hepatic outflow vessel and reduce intrahepatic pressure and decrease injury. Mesoatrial shunts have proven useful in a few patients with hepatic vein thrombosis and either an inferior vena caval thrombosis or a marked pressure gradient from the abdomen to the thorax from ascites and an hypertrophied caudate lobe of the liver. For patients with extensive hepatocellular disease and portal hypertension, hepatic transplantation would seem to offer the best chance for survival.
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PMID:Hepatic vein thrombosis (Budd-Chiari syndrome). 669 73

A case is described wherein a 29 year old woman was admitted to the hospital because of the possibility of a hepatic tumor; symptoms included abdominal pain, diffuse hepatic enlargement and absence of uptake in an area of the right hepatic lobe. After a normal pregnancy and delivery 11 years earlier the patient used oral contraceptives (OCs) composed of norethindrone with mestranol until 8 years before entry; 5 years before admission she resumed use of an OC containing norethindrone and ethinyl estradiol. She smoked 1.5 packages of cigarettes and drank 1 glass of wine daily, and there was no history of nausea, vomiting, melena, jaundice, dark urine, light stools, hepatitis, or blood transfusions. Benign lesions which are known to be caused by OCs fall into 2 groups: designated focal nodular hyperplasia and liver-cell adenoma. The evidence linking the latter with OCs is more convincing since in case-controlled studies the risk of development of adenomas has been shown to increase with the estrogen strength of the OCs and duration of use; in women who have been taking OCs over 7 years the relative risk is 500 times that for matched control nonusers. The vascular complications of OC therapy include Budd-Chiari syndrome, peliosis hepatis, and periportal sinusoidal dilatation. The patient in this case was diagnosed to have periportal and midzonal hepatic sinusoidal dilatation association with OC medication. She underwent an operation on her liver which proved to be successful combined with cessation of OC use. The mechanism by which OCs cause these lesions is not known. In 5 of 13 cases similar to the one described here clinical and biochemical abnormalities resolved and 1 patient had a follow-up liver biopsy that revealed normal findings 10 months after cessation of OC therapy; there is no evidence to suggest that sinusoidal dilatation is irreversible.
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PMID:Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 40-1982. Tender hepatomegaly in a 29-year-old woman. 711 Feb 74

Case reports are presented that link the use of oral contraceptives (OCs) to liver disease, particularly to the Budd-Chiari syndrome. This syndrome is caused by occlusion of hepatic veins and although a causative relation between OC use and this syndrome is not proven, these facts support an association: 1) the known increased incidence of venous thrombosis in women using OCs; 2) data from a review of 164 cases of the syndrome showed that in 1959 men and women suffered the syndrome about equally, but since 1975 after the introduction of OCs another study reported women contracting the disease twice as often as men; 3) the syndrome is associated with pregnancy; and 4) since the 1975 study, association with the pill was found in 16 reported cases. Clinically, the average age of these 16 women with OC-associated Budd-Chiari syndrome was 32 years. Length of time before onset of symptoms after beginning OC therapy varied from 2 weeks to 8 years (mean 23.8 months). In most cases, abdominal pain, nausea, vomiting, and abdominal distension were present. Hepatomegaly and ascites were described in most cases and splenomegaly in less than half. Liver function abnormalities were nonspecific. Prognosis is not good, and management techniques for the syndrome have been largely unsuccessful. Metabolic alterations of steroids as they pass through the liver may account for the syndromes associated with OC use. 3 major diseases or effects are linked with OCs: hepatic dysfunction, cholestatic jaundice, and benign hepatic tumors and peliosis hepatis; these, however, are benigh complications compared with the severity of contracting Budd-Chiari syndrome, and the clinician should respect a woman's decision not to use the pill in the face of such disease-inducing possibilities.
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PMID:Oral contraceptives and liver disease. 726 Aug 2

Budd-Chiari syndrome following pregnancy is an extremely rare disease as reported in the literature. Reported here are 16 such cases in a total of 105 patients with Budd-Chiari syndrome seen at Postgraduate Institute of Medical Education and Research, Chandigarh, from 1963 to 1978. The clinical pointer to the diagnosis was sudden occurrence of abdominal pain and ascites following childbirth. Eleven patients had diuretic-resistant ascites. Percutaneous hepatography was valuable in detecting the site and the nature of the outflow block. The prognosis was uniformly bad, and eight patients died within one year from the onset of their illness. The various treatment schedules, including anticoagulant therapy, Rhodiascit ascitic fluid re-infusion and portasystemic shunt surgery, had no beneficial effect on the survival of these patients.
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PMID:Budd-Chiari syndrome following pregnancy. Report of 16 cases, with roentgenologic, hemodynamic and histologic studies of the hepatic outflow tract. 735 Jul 98

We report a unique case of Budd-Chiari syndrome caused by pacemaker leads-induced thrombosis. A 34 year old female patient was subjected to a permanent pacemaker insertion because of refractory paroxysmal supraventricular tachycardia attacks related to Wolff-Parkinson-White syndrome. Three years later, another pacemaker was re-implanted because of its dislodgement. Four episodes of skin infections at the implantation site were noted thereafter. The patient developed symptoms of abdominal pain and ascites 5 years after the second pacemaker implantation. Ultrasonography and computerized tomography of the abdomen revealed hepatomegaly with ascites and dilated inferior vena cava. An echocardiogram displayed thrombus formation in the superior vena cava, the right atrium and the inlet of the inferior vena cava into the right atrium. Inferior and superior venacavogram confirmed the above findings. With the impression that Budd-Chiari syndrome was caused by pacemaker-induced thrombus, we removed the pacemaker first and thoracotomy with thrombectomy was then performed. The clinical symptoms resolved after the operation. To our knowledge, this is the first case reported in the literature and this observation supported the thrombosis theory for membranous obstruction of inferior vena cava.
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PMID:Budd-Chiari syndrome due to pacemaker-induced thrombosis. 754 18

The Japanese Ministry of Health and Welfare Research Committee on Aberrant Portal Blood Flow carried out an epidemiological survey and clinical study on Budd-Chiari syndrome in 1990. In the primary survey for determining the prevalence of the disease, a questionnaire was sent to all major hospitals throughout Japan and 160 cases seen in 1989 were compiled. More epidemiological details were obtained in 87 of these 160 cases. The number of patients with Budd-Chiari syndrome in this country was estimated to be about 300 (prevalence of 2.4/million) with about 20 new cases occurring every year. In the clinical study, 157 authentic cases of Budd-Chiari syndrome studied in 15 years (1975-89) were analyzed. There were 87 males (average age, 36.4 years) and 70 females (46.5 years), and the average period from the likely onset to the first medical consultation was 6.6 years, suggesting that these patients were mostly chronic cases. The main clinical features were hepatomegaly, leg edema, ascites and venous dilatation over the trunk. Abdominal pain was recorded in only four (2.5%). There were 16 (10.2%) with known identifiable etiologies. Of the patients 93% showed an obstructing lesion of various thickness in the hepatic portion of the inferior vena cava. Only nine (5.7%) had hepatic vein obstruction without caval lesions. Thus, the majority of Budd-Chiari syndrome patients in Japan are idiopathic, having an obstructing lesion in the inferior vena cava. The main causes of 33 deaths (21%) were liver failure, variceal bleeding and hepatocellular carcinoma. Hepatocellular carcinoma occurred in 10 (6.4%) in the 15-year period. However, the incidence of Budd-Chiari syndrome among all cases of hepatocellular carcinoma was less than 1% in the survey made by the Liver Cancer Study Group of Japan.
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PMID:Epidemiological and clinical features of Budd-Chiari syndrome in Japan. 775 74

A 32-year-old male with Budd-Chiari syndrome and stenosis of the inferior vena cava presented to the hospital with severe abdominal pain. Two contiguous, 14 mm, overlapping (joined) Palmaz stents were placed across the area of stenosis in the inferior vena cava. The stents later embolized to the left pulmonary artery and were retrieved non-surgically over a Grollman balloon catheter with transesophageal echocardiographic assistance. This case report highlights the advantages and limitations of transesophageal echocardiographic assistance in such a procedure.
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PMID:Transesophageal echocardiography assisted retrieval of embolized inferior vena cava stent. 783 35


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