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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hispanics are the fastest growing minority in the United States. Typically, they are divided into five subgroups: Mexican American, Puerto Rican, Cuban American, Central or South American, and "other" Hispanics. Risk factors for morbidity and mortality vary among these subgroups. Use of health care services is affected by perceived health care needs, insurance status, income, culture, and language. Compared with whites, Hispanics are more likely to live in poverty, be unemployed or underemployed, and have little education and no private insurance. Hispanics are at an increased risk for certain medical conditions, including diabetes, hypertension, tuberculosis, human immunodeficiency virus infection, alcoholism, cirrhosis, specific cancers, and violent deaths. Proportionate to their representation in the population, there are few Hispanic health providers, emphasizing the need for all medical personnel to be knowledgeable about Hispanic health care needs.
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PMID:Hispanic health in the United States. Council on Scientific Affairs. 198 56

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

Previous studies strongly suggest that adenosine receptors on juxtaglomerular cells function to restrain the secretion of renin induced by a variety of stimuli. The clinical significance of this is that caffeine, a widely consumed adenosine receptor antagonist, could augment renin release responses to diseases such as renovascular hypertension, liver cirrhosis and heart failure and to therapeutic maneuvers such as salt restriction, diuretics and vasodilators. Caffeine may be particularly troublesome in this regard because this methylxanthine has central nervous system effects and intracellular actions that also might contribute to the overall ability of caffeine to potentiate renin secretion. The purpose of this study was to document the effects of caffeine on renin release responses to a vasodilator and to investigate what mechanisms were responsible for any augmentation of vasodilator-induced renin secretion. Accordingly, we compared the effects of caffeine vs. 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX; a xanthine that we documented in this study not to significantly enter the brain or penetrate cell membranes) on base-line and hydralazine-induced renin release in both normal and beta adrenoceptor-blocked (propranolol, 15 mg/kg) rats. Both xanthines (at a dose of 10 mg/kg plus 150 micrograms/min) attenuated adenosine-mediated hypotension and bradycardia, and DPSPX was at least as effective as caffeine in antagonizing peripheral adenosine receptors. Caffeine and DPSPX increased base-line plasma renin activity to a similar extent regardless of whether the animals were pretreated with propranolol. In rats with an intact beta adrenergic system, caffeine, but not DPSPX, increased the renin release response to low-dose hydralazine (1 mg/kg). Although both xanthines augmented the renin release response to high-dose hydralazine (10 mg/kg), caffeine was more efficacious in this regard. In beta adrenoceptor-blocked rats, neither caffeine nor DPSPX augmented the renin release response to low-dose hydralazine, whereas both xanthines equally potentiated the renin release response to high-dose hydralazine. These data demonstrate that caffeine increases base-line renin release primarily by blocking peripheral (most likely renal), cell-surface adenosine receptors; however, caffeine potentiates vasodilator-induced renin secretion in part by blocking peripheral (most likely renal), cell-surface adenosine receptors and in part by additional central nervous system and/or intracellular mechanism(s) that involve the beta adrenergic system.
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PMID:Caffeine potentiates vasodilator-induced renin release. 200 84

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

This article reports the first successful human orthotopic liver transplantation performed in Mexico. The recipient was a 41 year old white male, with a history of essential hypertension and hepatitis in 1975. The diagnosis of postnecrotic cirrhosis was made in 1985 by liver biopsy. The HBsAg was negative and the functional reserve of the liver was limited (Stage "C" of the Child-Pugh classification). A liver graft was obtained through the National Cadaver Organ Transplant Program on May 2, 1988 and an orthotopic liver transplantation was performed without incidents, using the portosystemic veno-venous bypass. Inmunosuppression was carried out with triple drug therapy, cyclosporine, azathioprine, and prednisone. His postoperative course was characterized by idiopathic cholestasis, one episode of acute rejerction, arterial hypertension, renal dysfunction, esophageal herpes and inguinal lymphocele, all of which resolved. Currently the patient is alive 22 months postransplantation with normal liver function and adequate quality of life.
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PMID:[Liver transplantation in Mexico. Report of the first successful case]. 206 9

This study examined the differences in mortality rate among the three ethnic groups aged 35 to 69: 1) Japanese living in Kawasaki city, 2) Koreans living in Kawasaki city, 3) Koreans living in Korea. Three different measures were used for analysis: 1) mortality rate by sex and age, 2) Mantel-Haenszel Rate Ratio (MHRR), 3) Standardized Proportional Mortality Ratio (SPMR). Major findings were as follows: 1) In terms of mortality rate by sex and age, Koreans in both Kawasaki and Korea showed higher mortality rates than Japanese in Kawasaki for both sexes and for all of the age categories. Koreans living in Kawasaki and Koreans living in Korea showed nearly identical levels of mortality rate for both sexes and for all of the age categories. 2) Calculation of MHRR utilizing a mortality rate for Japanese living in Kawasaki as 1 yielded the following: For all causes of death, MHRR of Korean males living in Kawasaki aged 35 to 59 was 2.59, and 2.37 for ages 60 to 69. For females MHRR for those age groups were 1.91 and 2.06 respectively. All of these MHRRs were statistically significantly high (p less than 0.05). 3) Among the causes for the high MHRR for Korean males living in Kawasaki aged 35 to 59 compared in Japanese living in Kawasaki were the following: all Malignant neoplasms (ICD 9, 140-208), Malignant neoplasm of liver (155), Hypertensive disease (401-405), Ischemic heart disease (410-414), Pneumonia (480-486), Liver Cirrhosis (571). For males aged 60 to 69, causes were Tuberculosis (010-018), all Malignant neoplasms, Malignant neoplasm of liver, Ischemic heart disease, Disease of the pulmonary circulation and other forms of heart disease (415-429), Cerebrovascular disease (430-438), and Liver Cirrhosis. In the case of females, Tuberculosis, Disease of the pulmonary circulation and other forms of heart disease, Malignant neoplasm of trachea, bronchus and lung were causes for high MHRR for Koreans in Kawasaki aged 35 to 59. All Malignant neoplasms, Malignant neoplasm of liver, Malignant neoplasm of trachea, bronchus and lung, Accidental causes of death except motor vehicle accidents (E800-807, E826-848, E850-949) were causes for females aged 60 to 69. 4) The mortality rates for ages 35 to 69 for both sexes are similar for both Koreans living in Kawasaki and in Korea.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A mortality study of middle-aged and elderly Koreans in Kawasaki City in comparison with Koreans in Korea and Japanese in Kawasaki City]. 213 81

This study evaluates the correlation between long-term weight history and health risks. One thousand three hundred and sixteen male subjects of normal weight (-5%(-)+5% by Broca's obesity index) at age twenty, were studied. The average age of the subjects was 43.7 +/- 6.5 (M. +/- S.D.) years old. According to their long-term weight history, the subjects were classified into four groups: weight lost (N = 35), weight stable (N = 502), mild weight gain (N = 187), severe weight gain (N = 592). Odds ratios for systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, uric acid, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, hyperperspiration, angina pectoris, and hypertension were significantly higher in the severe weight gain group than in the stable weight group. Stepwise logistic regression analysis was performed by choosing weight history, obesity index, age, and smoking and drinking habits as the independent variables. Weight history was shown to be a significant variable in systolic blood pressure, diastolic blood pressure, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, gamma glutamyl transpeptidase, fasting blood sugar, total cholesterol, triglyceride, shortness of breath, chronic hepatitis and liver cirrhosis. Odds ratios for factors suspected of promoting atherosclerosis were significantly higher in the severe weight gain group. Results of this study indicate that a weight gain of over 7 kilograms appears to be the critical level that is associated with health risks.
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PMID:[Health risk assessment of long-term weight history]. 213 52

The heart atrium, as well as under certain pathophysiological conditions the ventricle, synthesize and release ANP. Exerting natriuretic, diuretic and vasorelaxant effects, this peptide plays an important role in the body's blood volume and blood pressure homeostasis. Whereas the pharmacological actions of ANP have been quite convincingly demonstrated, its physiological and pathophysiological role is less well defined. ANP plasma levels tend to be increased in diseases with salt and water retention, such as essential hypertension, congestive heart failure, renal failure or liver cirrhosis. With regard to its hemodynamic effects, ANP seems to be beneficial in patients with hypertension. ANP appears to have little therapeutic potential as a diuretic in patients with congestive heart failure and liver cirrhosis, possibly due to the decreased renal responsiveness to ANP in these diseases. However, ANP might to be a valuable therapeutic agent in acute renal failure.
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PMID:[Atrial natriuretic peptide. II. Pathophysiology and possible clinical significance. Review]. 214 57

Plasma concentrations of the recently isolated potent vasoconstrictory peptide endothelin were measured in 382 patients. The investigations were performed by means of a sensitive radioimmunoassay specific for Endothelin-1, 2. The results from 110 healthy volunteers displayed a normal range of 44.67 +/- 3.51 pg/ml. Significantly raised levels were found in 33 patients with chronic end-stage renal failure both before and after hemodialysis. In contrast, 35 patients with compensated renal insufficiency did not differ from the normals. Sixty-five patients after kidney transplantation revealed significantly elevated levels, as did 27 patients with acute myocardial infarction, 8 after coronary bypass surgery, and 5 with liver cirrhosis. The mean values of 27 patients with untreated hypertension, 22 with secondary hypertension, of various causes and 16 with coronary artery disease were comparable to the normal population. The values were significantly decreased in 9 pregnant women with hypertension and proteinuria. A marked decline was found in 5 patients with systemic lupus erythematodes, while 20 patients with rheumatoid arthritis demonstrated only a slight decrease. The pathophysiological role of endothelin as a local or circulating hormone in regulating systemic blood pressure or release of other hormones remains to be determined.
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PMID:[Plasma endothelin in normal probands and patients with nephrologic-rheumatologic and cardiovascular diseases]. 221 2

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
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PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42


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