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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

Pulmonary hypertension is a recognized but unusual complication of liver disease. It can complicate the perioperative course of liver transplantation. Mild to moderate pulmonary hypertension is generally well tolerated during the procedure and does not appear to contribute to mortality. Since the pulmonary vascular disease may progress rapidly, it may have advanced to the point of irreversibility at the time of surgery. So, patients with known moderate pulmonary hypertension should have pulmonary arterial catheterisation immediately prior to transplantation. If pulmonary artery hypertension has become severe, then a preoperative trial of vasodilators is warranted. If this fails, the procedure should be cancelled. We present a patient with alcoholic liver cirrhosis in whom a rapidly progressive pulmonary hypertension made liver transplantation impossible.
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PMID:Rapidly progressive pulmonary artery hypertension and end-stage liver disease. 890 71

Liver transplantation for alcoholic cirrhosis remains controversial at some transplantation centers. We compared resource utilization and outcome in alcoholic and non-alcoholic cirrhotic patients undergoing liver transplantation. From April 1990 to November 1994, 60 patients received orthotopic liver transplants for end-stage alcoholic liver disease, and 119 transplants were performed in 103 patients for non-alcoholic liver disease. No significant differences were noted in resource utilization of the variables examined. The outcome of liver transplantation (early graft function, frequency of sepsis, incidence of rejection, renal function, arterial hypertension...) was equivalent or better in alcoholic patients. Postoperative mortality was higher in non-alcoholic population (25.2% vs 16.7%). One-year and three year actuarial survival was not significantly different, but it was higher in the alcoholic group (77% vs 67% and 74% vs 64% respectively). The recurrence rate of alcohol in take has been 9.09%, with most patients drinking only socially. We conclude that liver transplantation for end-stage alcohol-related cirrhosis provides excellent results and resource utilization appears to be equivalent to that for patients undergoing transplantation for non-alcohol-related cirrhosis.
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PMID:[Orthotopic hepatic transplant in chronic hepatopathy of alcoholic origin]. 896 58

Although the underlying mechanisms no doubt differ, activation of the sympathetic nervous system is an important pathophysiological feature in primary arterial hypertension, in portal hypertension accompanying hepatic cirrhosis, and in heart failure, and is a logical therapeutic target for centrally acting sympathetic nervous system suppressant drugs. Portal hypertension: The sympathetic outflows to skeletal muscle vasculature, the heart, the kidneys and to the hepatomesenteric circulation are stimulated in patients with alcoholic cirrhosis of the liver, perhaps as a reflex response to the vasodilatation and vascular shunting present. Acute dosing with clonidine produces dose dependent reduction in noradrenaline spillover from visceral organs and reduction in hepatic vein wedge pressure, with preservation of hepatic blood flow and negligible fall in arterial pressure. These findings indicate the clinical potential of drugs such as clonidine, moxonidine and rilmenidine for chronically lowering portal venous pressure in cirrhosis. Arterial hypertension: Activation of the sympathetic outflow to the heart, kidneys and skeletal muscle vasculature is commonly present in younger (< 45 years) patients with essential hypertension. The sympathetic stimulation appears to have adverse consequences in hypertensive patients beyond blood pressure elevation. Neural vasoconstriction in skeletal muscle has metabolic effects by impairing glucose delivery, which is a basis for insulin resistance and hyperinsulinemia. Within the heart a trophic effect of sympathetic activation on cardiac growth, contributing to the development of left ventricular hypertrophy, and an arrhythmogenic effect are also likely. Cardiac failure: The cardiac sympathetic nerves are preferentially stimulated in severe heart failure, with norepinephrine release from the failing heart at rest being increased as much as 50-fold, similar to the level seen in healthy people during near maximum exercise. This preferential activation of the cardiac sympathetic outflow contributes to arrhythmogenesis and possibly to progression of the heart failure, and has been directly linked to mortality; a high rate of spillover of noradrenaline from the heart is a strong, independent predictor of poor prognosis in severe cardiac failure. The mechanisms underlying sympathetic nervous stimulation are not entirely clear. Increased intracardiac diastolic pressure seems to be one peripheral signal, and increased forebrain norepinephrine turnover an important central mechanism. Following the demonstration of the beneficial effect of the beta-adrenergic blocker, carvedilol, and with second generation centrally acting sympathetic suppressants now under clinical investigation, elucidation of the abnormalities in central nervous control of sympathetic outflow in heart failure has become clinically relevant.
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PMID:Increased sympathetic nervous system activity and its therapeutic reduction in arterial hypertension, portal hypertension and heart failure. 985 71

A 40-year-old normotensive man suddenly developed diplopia, tinnitus and a burning sensation on the left side of his body while driving a motorcycle. He did not complain of headache, nausea or vomiting. Neurologic examination revealed left trochlear nerve palsy and impaired pinprick, temperature and joint position sensation of the left limbs. There was no ptosis or motor deficit. He had a mild bleeding diathesis due to alcoholic liver cirrhosis. Computerized tomography and magnetic resonance image of the brain disclosed hemorrhages in the right midbrain tectum and the left temporal lobe. After nine months of observation, there was nearly complete recovery of symptoms, except for mild residual diplopia. From a literature review, only nine case of midbrain tectal hemorrhage involving the inferior colliculus have been reported. These patients had a unique clinical presentation. Diplopia due to trochlear nerve palsy, either unilateral or bilateral, was present in all of the cases. Tinnitus and sensory disturbance contralateral to the lesion side were very common. Only three patients had risk factors for hemorrhage, including bleeding diathesis, hypertension and vascular anomalies. In the majority of patients, no underlying causes were detected. The outcome was favorable with conservative treatment.
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PMID:Midbrain hemorrhage presenting with trochlear nerve palsy. 1067 25

Insulin resistance appears to be a common feature and a possible contributing factor to several frequent health problems, including type 2 diabetes mellitus, polycystic ovary disease, dyslipidemia, hypertension, cardiovascular disease, sleep apnea, certain hormone-sensitive cancers, and obesity. Modifiable factors thought to contribute to insulin resistance include diet, exercise, smoking, and stress. Lifestyle intervention to address these factors appears to be a critical component of any therapeutic approach. The role of nutritional and botanical substances in the management of insulin resistance requires further elaboration; however, available information suggests some substances are capable of positively influencing insulin resistance. Minerals such as magnesium, calcium, potassium, zinc, chromium, and vanadium appear to have associations with insulin resistance or its management. Amino acids, including L-carnitine, taurine, and L-arginine, might also play a role in the reversal of insulin resistance. Other nutrients, including glutathione, coenzyme Q10, and lipoic acid, also appear to have therapeutic potential. Research on herbal medicines for the treatment of insulin resistance is limited; however, silymarin produced positive results in diabetic patients with alcoholic cirrhosis, and Inula racemosa potentiated insulin sensitivity in an animal model.
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PMID:Insulin resistance: lifestyle and nutritional interventions. 1076 68

Because of the donor shortage, there are concerns for liver transplantation in patients with alcoholic cirrhosis. We therefore analyzed patients transplanted for alcoholic cirrhosis at our center with respect to patient and graft survival, recurrence of disease, and postoperative complications. Out of 1000 liver transplantations performed in 911 patients, 167 patients were transplanted for alcoholic cirrhosis; 91 patients received CsA- and 76 patients FK506-based immunosuppression. Recurrence was diagnosed by patient's or relative's declaration, blood alcohol determination, and delirium. Diagnosis and treatment of acute and chronic rejection was performed as previously described. One- (96.8% versus 91.3%) and 9-year patient survival (83.3% versus 80%) compared well with other indications. Five of 15 patients died due to disease recurrence. Recurrence of disease was significantly related to the duration of alcohol abstinence prior to transplantation. In patients who were abstinent for less than 6 months (17.1%), recurrence rate was 65%, including four of the five patients who died of recurrence. Recurrence rate decreased to 11.8%, when abstinence time was 6-12 months and to 5.5%, when the abstinence times was > 2 years. Next to duration of abstinence, alcohol relapse was significantly related to sex, social environment, and psychological stability. The incidence of acute rejection compared well with other indications (38.1%); CsA: 40.1% versus 33.3% in FK506 patients. In all, 18.2% of CsA patients experienced steroid-resistant rejection compared with 2.6% of FK506 patients. Seven patients (7.6%) in the CsA group and one patient (1.3%) in the FK506 group developed chronic rejection. A total of 57.1% developed infections; 5.7% were life-threatening. CMV infections were observed in 14.3% (versus 25% for other indications). New onset of insulin-dependent diabetes was observed in 8.6% and hypertension in 32.4%. In conclusion, alcoholic cirrhosis is a good indication for liver transplantation with respect to graft and patient survival and development of postoperative complications. FK506 therapy was favourable to CsA treatment. Patient selection is a major issue and established criteria should be strictly adhered to. Patients with alcohol abstinence times shorter than 6 months should be excluded, since recurrence and death due to recurrence was markedly increased in this group of patients.
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PMID:Liver transplantation for alcoholic cirrhosis. 1111 78

The case describes a 56-year-old man who had thymic cyst hemorrhage, followed by right hemothorax. There was a high possibility that his accompanying disease, an alteration in hemostasis due to alcoholic liver cirrhosis and hypertension, would induce thymic cyst hemorrhage. Thymic cyst hemorrhage should be included in possible causes of the sudden onset of mediastinal or intrathoracic hemorrhage, in addition to the rupture of aortic aneurysm or malignant mediastinal tumor.
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PMID:Spontaneous thymic cyst hemorrhage causing hemothorax. 1465 May 99

We report a 67-year-old man with rt. hand resting tremor and rigidity after lt. putaminal hemorrhage. He had hypertension and alcoholic liver cirrhosis as past history. When he was 62 years old, he realized rt. hemiplegia suddenly and admitted in Juntendo Urayasu hospital. Brain CT showed intracranial hemorrhage in lt. putamen. He was treated with neurosurgery operation for rejecting hemorrhage. Mild rt. hemiparesis remained but he could live independently. He was medicated sulpiride for depression after cerebrovascular accident. On 63 years old, resting tremor and rigidity appeared on his rt. hand. His doctor stopped sulpiride and treated with L-Dopa/Benserazide and trihexiphenidyl. His parkinsonism was stable with this treatment for four years. His doctor considered that he was Parkinson's disease or drug-induced parkinsonism. On 67 years old, he became akinetic-mutism state suddenly and admitted in the hospital. His consciousness turned alert soon and discharged after two weeks. This episode was considered as epilepsy. After one week from discharge, he was found cardio-pulmonary arrest and confirmed dead in the hospital. Post-mortem examination revealed necrosis in the posterior-lateral part of lt. putamen due to hemorrhage. However, there was no degenerative change of the striatum or the substantia nigra and no Lewy bodies in his brain. Other pathological changes were also not found. His parkinsonism might be caused putaminal pathology due to hemorrhage.
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PMID:[A 67-year-old man with rt. hand resting tremor and rigidity after lt. putaminal hemorrhage]. 1591 60

A 70-year-old man had been obese since youth. He had been treated for hypertension and diabetes mellitus. An abdominal ultrasound showed a mass in the liver. He was admitted to St Marianna University School of Medicine Hospital for further evaluation. There was no history of alcohol use, and hepatitis viral markers and autoantibodies were all negative. Several imaging studies showed overt hepatocellular carcinoma (HCC). Transcatheter arterial embolization was performed, followed by surgical resection. Histopathological examination revealed moderately differentiated HCC. The non-tumor areas had pseudolobules in a diffuse pattern similar to alcoholic cirrhosis. The histological findings in the ectopic liver tissue attached to the gallbladder, which was also resected during surgery, were that there was no cirrhosis, but fine fibrosis with inflammatory cell infiltration of sinusoids. These findings were consistent with non-alcoholic steatohepatitis (NASH). There was probably a progression of similar findings that had developed into cirrhosis. These findings confirmed a diagnosis of HCC, cirrhosis, and underlying NASH in this patient. The present case is important for investigation of the development into cirrhosis and carcinogenesis of NASH. The present case demonstrates the importance of evaluating obese patients with fatty liver for underlying NASH and ongoing follow up for development of cirrhosis and HCC.
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PMID:Hepatocellular carcinoma with silent and cirrhotic non-alcoholic steatohepatitis, accompanying ectopic liver tissue attached to gallbladder. 1639 79


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