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)

Eighteen patients with alcoholic cirrhosis were examined, and parotid saliva was collected. Enlargements of the parotid glands were seen in eleven of the eighteen patients (61%). This percentage is in accord with the data previously reported. The salivary findings of increased flow rate, protein, and amylase levels indicate that hypertrophy and increased acinar function may be a component of the parotid enlargement and that, furthermore, a fatty replacement of functional gland tissue is probably not involved. In addition, the salivary electrolyte changes found, increased potassium with effectively decreased sodium excretion, suggest that the elevated aldosterone level commonly found in cirrhotic patients affects salivary secretions in these patients in much the same way as it does in patients with hypertension.
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PMID:Salivary studies in alcoholic cirrhosis. 106 47

Since its introduction into clinical practice in 1967, selective variceal decompression by means of a distal splenorenal shunt (DSRS) has become one of the more commonly performed portal-systemic shunting procedures in the treatment of variceal hemorrhage throughout the world. In addition to selective decompression of gastroesophageal varices, the DSRS provides the advantages of preservation of portal perfusion of the liver and maintenance of intestinal venous hypertension. Many large, uncontrolled series and the majority of controlled randomized studies have demonstrated a lower incidence of encephalopathy after the DSRS than after nonselective shunt procedures. A secondary advantage of the DSRS is that the hepatic hilum is avoided, thus making subsequent liver transplantation a less formidable procedure. None of the studies have shown an advantage to this shunt with respect to long-term survival in patients with alcoholic cirrhosis. However, some of the large, uncontrolled series have shown that survival is significantly improved in patients with non-alcoholic cirrhosis compared to nonselective shunt procedures in the same population. Controlled trials comparing the DSRS to endoscopic sclerotherapy have shown that chronic endoscopic variceal sclerosis is an appropriate initial therapy for most patients as long as shunt surgery is readily available if sclerotherapy fails.
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PMID:Selective variceal decompression: current status. 177 5

We investigated the occurrence of alcoholic autonomic dysfunction in patients with alcoholic cirrhosis in order to define its prevalence and relationship to renal sodium retention. Forty-seven alcoholics and 16 age-matched normal subjects were evaluated. Thirty-seven patients had liver disease (13 with and 24 without ascites), and 10 patients had normal hepatic function. Autonomic nervous system function was ascertained by skin sudomotor responses and the response of blood pressure and plasma norepinephrine concentration to upright tilt (sympathetic nervous system function), and by heart rate responses to deep breathing, Valsalva maneuver, and upright tilt (parasympathetic and sympathetic nervous system function). Heart rate responses to deep breathing and Valsalva maneuver were diminished, and skin sudomotor responses were significantly worse, in alcoholics than in control subjects. Alcoholic patients also had significantly lower supine mean arterial pressure (93 +/- 10 vs. 116 +/- 8 mm Hg, p less than or equal to 0.0001), and significantly greater increases in arterial pressure during passive upright tilt, than control subjects (mean increase 6.5 +/- 6.6 vs. 0.1 +/- 1.6 mm Hg, p = 0.0003). All of these findings were present to similar degrees in patients with and without liver disease and in cirrhotic patients with and without ascites. Supine heart rates, however, differed among the groups evaluated. Heart rate was significantly greater in patients with cirrhosis than in alcoholic patients without liver disease (83 +/- 11 vs. 71 +/- 13 bpm, p = 0.006), and in patients with ascites than in patients without ascites (88 +/- 12 vs. 80 +/- 10 bpm, p = 0.04). Plasma norepinephrine concentration was elevated in most patients with cirrhosis and was significantly higher in patients with ascites than in patients without ascites (789 +/- 238 vs. 388 +/- 185 pg/ml, p less than 0.0001; nl range: 65-320 pg/ml). Autonomic nervous system function is similarly impaired in alcoholics with and without liver disease. Patients with cirrhosis also have increased heart rate and elevated plasma norepinephrine concentration, abnormalities that are most pronounced in patients with sodium retention. Their is uncertainty as to the stimulus for norepinephrine release, and its source, in these patients. However, the similarity of supine blood pressure in patients with and without ascites and the occurrence of orthostatic hypertension rather than orthostatic hypotension following upright tilt suggest that arterial underfilling is not responsible.
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PMID:Autonomic dysfunction in alcoholic cirrhosis: relationship to indicators of synthetic activation and the occurrence of renal sodium retention. 202 44

The relative importance and behaviour of plasma and platelet plasminogen activator inhibitor (PAI-1) in disease has not hitherto been examined. In this study the concentration of PAI-1 in the plasma and platelets of patients with a variety of disorders was examined using a specific ELISA and a functional assay. Mean plasma PAI-1 was elevated in groups of patients with diabetes mellitus, hypertension, alcoholic cirrhosis, angina and myocardial infarction. Plasma PAI-1 was raised in the post-operative phase and the PAI-1 released after surgery was not derived from platelets. In all groups PAI-1 in the platelet pool reflected the platelet count, except in type II diabetes mellitus and chronic renal failure, where a reduced quantity of PAI-1 antigen per platelet was found. In severe chronic renal failure, abnormal platelets and diminished platelet PAI-1 may contribute to the haemorrhagic tendency sometimes seen in this disorder. Plasma PAI-1 represents a larger proportion of total circulating PAI-1 in disease than it does in healthy individuals; PAI-1 per platelet is abnormal only in a minority of disorders. Plasma and platelet pools of PAI-1 vary independently in disease and both merit consideration in evaluating the importance, if any, of PAI-1 in thrombosis or haemorrhage.
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PMID:The platelet and plasma pools of plasminogen activator inhibitor (PAI-1) vary independently in disease. 220 5

We describe 3 patients with painful intraarticular knee effusions composed of a viscous milky white suspension of monosodium urate crystals, in the absence of any cellular component. Two patients presented with acute bilateral knee pain. One patient presented with unilateral knee pain of gradual onset. All 3 patients had a history of ethanol abuse. Two patients had a history of gout. Two patients had chronic renal insufficiency, hypertension, and congestive heart failure. One patient had alcoholic cirrhosis. Two patients' pain responded to colchicine. One patient's discomfort was relieved only by repeated arthrocentesis. We conclude that intraarticular free urate can cause painful joints in the absence of an apparent inflammatory response.
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PMID:Intraarticular noninflammatory free urate suspension (urate milk) in 3 patients with painful joints. 235 87

Mesenteric varices can appear as massive, acute lower gastrointestinal bleeding. The small bowel or colon may be involved, varices usually developing at sites of previous surgery or inflammation in patients with portal hypertension. Two patients with alcoholic cirrhosis and protal hypertension presented with rectal bleeding. Tc-99m RBC studies demonstrated varices and extravasation into the adjacent bowel. The varices were documented by mesenteric angiography. Characteristic features of Tc-99m labeled RBC studies can identify mesenteric varices as the cause of intestinal bleeding and localize the abnormal vessels.
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PMID:Scintigraphic demonstration of gastrointestinal bleeding due to mesenteric varices. 238 39

Following insertion of a Leveen's valve after surgical portocaval anastomosis, a male patient with alcoholic cirrhosis developed dyspnoea with hypoxaemia. An interstitial syndrome was present in the lower lobes. Other findings were: polycythaemia (Hb 20 g/100 ml), subnormal spirometric values, decrease in CO transfer capacity, normal pulmonary compliance, absence of intracardiac shunt and pulmonary arterial hypertension and absence of bronchial or alveolar lesions on a surgical lung biopsy. Blood gas measurements and radioisotope explorations led to the conclusion that the patient had an anatomical shunt predominant in the lower parts of the lungs, associated with a shunt effect and a transfer disorder. The anatomical shunt was due to pulmonary arteriovenous microfistulae, some of which were visualized by superselective angiography. Catheterization of the portocaval anastomosis eliminated any shunt between the portal system and the pulmonary veins.
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PMID:[Dyspnea with hypoxemia in a case of cirrhosis with portal hypertension]. 293 68

Patients with portal hypertension of varying etiology may develop pulmonary artery hypertension. In the present autopsy study, pulmonary and hepatic tissue was studied in 12 patients in whom pulmonary and portal hypertension coexisted. Plexogenic pulmonary arteriopathy was present in 10 patients, 7 of whom had coexistent thromboembolic lesions. One patient had isolated medial hypertrophy, which may be an early stage in the plexogenic category, whereas isolated thromboembolic pulmonary vascular disease was observed in one subject. Hepatic disease was consistent with alcoholic cirrhosis in seven patients, cryptogenic cirrhosis in four and extrahepatic portal hypertension without cirrhosis in one. Thrombocytopenia was present in all 10 patients whose platelet count was determined. This study suggests that pulmonary hypertension associated with portal hypertension commonly has a plexogenic appearance on histologic examination. However, thrombosis (whether embolic or in situ) may also contribute to vascular obstruction.
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PMID:Coexistent pulmonary and portal hypertension: morphologic and clinical features. 368 Jul 90

A case of exogenous hypermineralocorticism secondary to absorption of an alcohol-free liquorice beverage is reported here. The patient was a 53 year old man with known alcoholic liver cirrhosis who had stopped drinking alcohol one year earlier. He was admitted to the hospital for fever and myalgia without hypertension. Laboratory tests showed severe hypokalemia (1.7 mmol/l), metabolic acidosis and enzyme abnormalities compatible with rhabdomyolysis. Urinary potassium excretion was high. Plasma renin activity and aldosterone levels were low. Symptoms were those of exogenous hypermineralocorticism. One month earlier, the patient had drunk 0,25 1 per day of an alcohol-free licorice beverage for two weeks. Clinical and biological symptoms disappeared with potassium loading alone. Three weeks later, when serum potassium levels remained normal, the ingestion of the same amounts of the same beverage produced an important decrease in serum potassium levels. Intoxication by liquorice is a well-known cause of pseudoprimary hyperaldosteronism. But the case reported here has some unique features. It is, to our knowledge, the first case reported in the literature, although a few cases have been brought to the attention of the poison center in Marseille. The amount of beverage ingested was small (0.35 g/day of glycyrrhizinic acid) as compared to the usual threshhold of toxicity (0.7 g/day). The toxic effects lasted two weeks after discontinuing ingestion. Cirrhotic patients may be more susceptible than others but the main consumers of this type of beverage are presumably ex-alcoholics.
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PMID:[Major hypokalemia with rhabdomyolysis secondary to the intake of a nonalcoholic aniseed aperitif]. 647 67

The authors report 2 cases of pseudohyperaldosteronism secondary to consumption of alcohol-free "pastis" in abstinent alcoholic cirrhotics. In both cases patients presented with ascites, edema, increased blood pressure and hypokalemic alkalosis. Except for hypokalemia, the disorders improved rapidly after withdrawal of the beverage. Glycyrrhizic acid, present in little amounts in the beverage, is presumably responsible for this syndrome. Patients with alcoholic cirrhosis would be particularly at risk. It is suggested that alcohol-free "pastis" could be responsible for ascites and edema in cirrhotic patients. This drinking habit should be looked for in abstinent cirrhotic patients with ascites, particularly in case of associated systemic hypertension.
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PMID:[Pseudohyperaldosteronism induced by alcohol-free aniseed aperitif in alcoholic cirrhotic patients]. 652 26


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