Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oesophageal varices are abnormally dilated veins that develop beneath the mucosa of the lower oesophagus and upper stomach and cause profound gastrointestinal haemorrhage associated with a high mortality. Varices develop in the presence of protal hypertension, which, in Europe and the USA, is most commonly due to alcoholic cirrhosis of the liver. Alcoholic cirrhosis develops in 10-20% of chronic ethanol abusers as a result of prolonged hepatocyte damage, leading to centrilobular inflammation and fibrosis. The net effect on the portal venous system is an elevation of resistance, and/or increase of inflow, producing portal hypertension, and the development of collateral channels in the form of varices. Such parenchymal liver disease also causes ascites, clotting deficiencies, secondary malnutrition and hepatic encephalopathy, all of which contribute to the high mortality associated with variceal haemorrhage. Variceal bleeding is more likely to occur when the varices are large, long and numerous, with surface red markings, and may be precipitated to respiratory tract infection, non-steroidal anti-inflammatory drugs, alcohol, or may occur spontaneously. Once identified by endoscopy, the aims of management are to control the haemorrhage, to prevent recurrent haemorrhage, and to treat the underlying cause of portal hypertension. Attention to nutrition and long-term rehabilitation are particularly important in those alcoholic cirrhotic patients who survive.
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PMID:Alcohol and oesophageal varices. 855 40

Surgical porto-caval anastomosis and percutaneous intrahepatic porto-caval shunt are effective in the management of bleeding esophageal varices but are associated with liver failure and a high incidence of encephalopathy. The neurochemical consequences of ammonia detoxification may be important with regard to the development of hepatic encephalopathy. Maintenance of splanchnic venous hypertension leads to less post-shunt hepatic encephalopathy because of diminished absorption of ammonia. Results of medical treatment of hepatic encephalopathy are contradictory. However, mortality and controversial results of surgical treatment in hepatic encephalopathy restrict its indications to a small number of patients. Prevention of hepatic encephalopathy begins with the selection of patients for surgical or percutaneous shunting.
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PMID:[Physiopathology and surgical treatment of hepatic encephalopathy after porto-caval anastomosis]. 857 64

We report a case of splenic vein aneurysm (SVA) that was enlarged during a 17-month follow-up. A 62-yr-old female with liver cirrhosis was followed up in our hospital. Real-time ultrasonography initially detected aechoic space at the middle part of the splenic vein, confirmed as SVA by contrast-enhanced computed tomography, magnetic resonance imaging and angiography. Magnetic resonance imaging showed the stagnation of blood flow in SVA, which suggests the presence of hypertension in the portal venous system. Moreover, SVA enlarged in parallel with the development of esophageal varices. These observations suggest that the persistent stagnation of blood flow in the portal venous system may have played a major role in the increase in size of the SVA in this case.
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PMID:Enlarging splenic vein aneurysm associated with stagnation of splenic venous blood flow. 860 14

Possible hepatic effects of oral contraceptives (OCs) include tumors, intrahepatic cholestasis, and less well known vascular lesions such as Budd-Chiari syndrome and peliosis, a disseminated pseudocystic dilatation of the sinusoid capillaries of the liver. A 29-year-old woman with a history of 4 pregnancies, hypertension and diabetes both requiring daily medication, and use since April 1983 of an oral contraceptive (OC) containing .15 mg levonorgestrel and .03 mg of ethinyl estradiol complained in March 1984 of epigastric pain and increased abdominal volume. Ascitis was diagnosed and the patient was hospitalized. She had experienced a generalized pruritus for several months and had lost weight. The bilirubin, alcaline phosphatase, and Gamma GT levels were slightly elevated. Sonography showed a hypertrophied liver. Incipient esophageal varices were seen with gastric fibroscopy. The small subhepatic venous branches had a cloudy aspect. The peliosis hepatis was diagnosed by a transjugular puncture biopsy of the liver. With discontinuation of the OCs, the ascites did not reappear after puncture and the perturbations of the liver functioning normalized. On follow-up in April 1985, slight hepatomagaly persisted but the patient reported no further symptoms. She continued her medication for hypertension and diabetes. Peliosis hepatis was 1st described in 1964 and several cases related to OC use have been reported since 1972. Peliosis has the aspect of multiple small congestive cavities of 1-3 mm in diameter in the parenchyma. The lesions consist of areas of hepatocellular necrosis secondarily filled with blood. The cysts may be voluminous and subcortical, creating a risk of hemoperitoneum. The lesions may also be associated with a benign or malignant liver tumor. Regression of the lesions is possible with termination of the etiologic agent. Clinically, hepatomegaly, painful or not, sometimes associated with splenomegaly, is often found with peliosis. Moderate jaundice is very frequent. Ascites or edema of the legs are observed. Hyperbilirubinemia and augmentation of phosphatases and Gamma GT are the main laboratory findings. Transaminases may be slightly elevated, and the rate of prothrombin may be diminished. The condition is sometimes diagnosed with laparoscopy, celiomesenteric arteriography, or phlebography, but hepatic puncture biopsy usually establishes the diagnosis. The contition may improve if the etiologic agent is removed or it may worsen because of liver failure or a complication such as hemoperitoneum or an associated tumor.
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PMID:[Peliosis hepatis and oral contraceptives: a case report]. 1228 Oct 5

Splenic venous hypertension (or 'left-sided portal hypertension') is a rare underlying cause of gastro-oesophageal varices. Ovarian carcinoma recurring beyond 10 years, following primary treatment with no interval disease, is also a rare occurrence. We report an unusual case of bleeding gastric varices secondary to splenic venous obstruction as a result of metastatic ovarian carcinoma. This occurred 21 years following surgery and adjuvant chemotherapy for primary ovarian carcinoma. To our knowledge, until now, there have been no reported cases of splenic venous hypertension due to ovarian carcinoma. This case report illustrates the successful emergency management of this condition by splenectomy, with complete resolution of varices confirmed endoscopically at 6 weeks. It is followed by a brief discussion regarding varices due to splenic venous hypertension.
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PMID:Bleeding gastric varices--a rare complication of ovarian cancer. 1570 76

We present the case of a 9-year-old boy with portal hypertension who died suddenly and unexpectedly due to pulmonary hypertensive crisis during a routine endoscopic procedure. He had known portal hypertension with esophageal varices but had no preceding clinical symptoms suggestive of significant pulmonary hypertensive disease despite postmortem histological evidence of advanced pulmonary vascular changes. Portopulmonary hypertension is a well-described and distinct clinical syndrome that is rare in childhood and is associated with a relatively poor prognosis. Occasional patients with histologically advanced disease may remain asymptomatic but present with pulmonary hypertensive crisis. Children with portopulmonary hypertension should be considered at high risk for surgical procedures, and pulmonary hypertensive complications should be excluded as a cause of death in all children dying suddenly in the setting of portal hypertension.
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PMID:Portopulmonary hypertension in childhood presenting as sudden death. 1680 32

The treatment of portal hypertension in children has undergone considerable evolution in the past decade. The treatment offered depends on the cause of the hypertension and the underlying health of the liver. The diagnosis of portal hypertension often can be made by the history and physical examination. Upper gastrointestinal bleeding in the presence of splenic enlargement is pathognomonic for portal hypertension. Bleeding and hypersplenism are the principal symptoms. Treatment of bleeding starts with confirming the diagnosis with esophageal and gastric endoscopy. The patient is admitted to an intensive care unit and started on intravenous octreotide. Banding or sclerosis of esophageal varices will result in cessation of the bleeding but not a permanent cure. A careful investigation for the cause of the portal hypertension should be done. This includes imaging studies of intra-abdominal arteries and veins, a liver biopsy, and liver function tests, including coagulation studies. For patients with extrahepatic portal vein thrombosis, early consideration should be given to surgical treatment with a meso-Rex bypass. Patients with liver disease should be treated for the underlying disorder and undergo regular endoscopic monitoring for recurrence of varices. Patients with well-compensated cirrhosis should be considered for selective surgical shunting, and those with advanced disease for liver transplantation. The benefit of long-term beta blockers in children has not been proven by clinical trials.
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PMID:Medical and surgical management of portal hypertension in children. 1694 69

Authors present a case report of a 51 years old man, with a past history of peptic ulcer, arterial hypertension and dislipidemia. Three weeks before hospitalization he did a upper endoscopy that revealed a duodenal ulcer and oesophageal varices (grade II/III). During etiologic investigation, hepatic disease and portal hypertension were excluded. He had a goiter that invaded the anterior mediastinum. After thyroidectomy the oesophageal varices disappeared.
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PMID:[Portal pseudo-hypertension]. 1698 49

Portal vein thrombosis secondary to protein C deficiency is a rare finding. Diagnosing a portal vein thrombosis itself is difficult due to nonspecific symptoms such as nausea, vomiting, anorexia, and weight loss. Proving that a protein C deficiency is the cause of a portal vein thrombosis is even more difficult as an extensive and thorough workup is required to rule out malignancies, myeloproliferative disorders, and hypercoaguable states which can all lead to thromboses. Patients require anticoagulation to prevent two dangerous complications of portal vein thrombosis; portal hypertension leading to esophageal varices with massive hemetemesis and extension of thrombus from the portal vein into the mesenteric veins leading to intestinal ischemia and death. In this case report, we present a patient with the complaint of painless jaundice who was found to have an incidental finding of portal vein thrombosis secondary to protein C deficiency. The different etiologies of portal vein thrombosis, along with diagnosis and treatment options will be discussed and highlighted.
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PMID:A rare incidental finding in a case of painless jaundice. 3071 33

While most long-term survivors of biliary atresia lead lives of good quality, some patients experience late complications. Cholangitis is a common complication even among 20-year survivors including some who develop ongoing liver dysfunction. Portal hypertension is another late complication. Endoscopic treatment for esophageal varices and partial splenic embolization for hypersplenism is effective as long as hepatic functional reserve is preserved. On the other hand, the treatment of secondary intrapulmonary vascular disorders including hepatopulmonary syndrome and portopulmonary hypertension is difficult. Early liver transplantation is recommended for these conditions. Pregnancy and delivery can be stressful events potentially leading to liver failure in female patients. Even very long-term survivors should be carefully monitored in terms of liver function, portal hypertension, and cholangitis.
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PMID:[Complications in long-term survivors of biliary atresia]. 1966 34


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