Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 15 patients with cirrhosis of the liver, the pressures in a systemic artery, in the inferior vena cava and the portal vein, flows in the portal vein and the hepatic artery, and oxygen content and acid-base balance in the arterial, portal and hepatic venous blood were studied during operation before and after the construction of an end-to-side portacaval shunt. Portal pressure decreased from 23 to 13 millimeters of mercury. Portal flow increased from 660 mililiters per minute to the liver to 1,300 milliliters per minute through the shunt. Hepatic arterial flow increased from 230 to 480 milliliters per minute, but this did not fully compensate for the loss of portal blood flow to the liver. Accordingly, total hepatic blood flow was reduced. There was also a decrease in the oxygen transport to the liver, but in spite of this, there was no change in the oxygen content in the hepatic vein nor any production of acid metabolites. Possible implications of these findings on the preoperative investigation of patients with portal hypertension are discussed.
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PMID:Immediate changes in blood flow and oxygen metabolism of the cirrhotic liver following portacaval shunt operations. 84 2

A 68-year-old man, after having been diagnosed as having hepatic disease at about the age of 41 years, had been hospitalized frequently until his death. Blood sugar, iron, and copper had not increased during his illness. Although the diagnosis of liver cirrhosis had been made and he had been receiving therapy, various neurologic symptoms without disturbances of consciousness appeared six months before his death. Autopsy revealed hemochromatosis, liver cirrhosis, and pancreatic fibrosis. A large amount of iron had accumulated in the liver, the pancreas, and the thyroid gland, while considerable numbers of ceroid and lipofuscin pigment granules had accumulated diffusely in the brain. Abnormal astrocytes of the Alzheimer II type were diffusely distributed in the brain and contained no intranuclear glycogen which stained positive with the carmine stain. No spongy changes were seen in the deeper layers of the cerebral cortex. Chemical analyses for trace metals in the brain, liver, and kidneys revealed a large amount of iron and increased copper in the liver, and considerable quantities of copper, manganese, calcium, and mercury in the brain. Because of changes in the erythrocyte sedimentation rate and marked thymol turbidity seen before and after the occurrence of the neurologic symptoms, this man was suspected of having disorders of the trace-metal binding proteins and/or of their polymers.
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PMID:Hemochromatosis associated with brain lesions--a disorder of trace-metal binding proteins and/or polymers? 92 21

Porphyrin metabolism was investigated in a 63-year-old male patient who developed a subacute onset polyneuropathy with predominance of motor signs in the upper limb. The screening for lead, cadmium, mercury, aluminum and thallium was negative. The study of porphyrin metabolism showed remarkable abnormalities, particularly a very high level of plasmatic 5-aminolaevulinic acid contrasting with a normal level of porphobilinogen and a nearly complete loss of activity of aminolaevulinic acid dehydratase with no regenerative response to dithiothreitol or zinc ions. The other causes of aminolaevulinic acid dehydratase deficiency (tyrosinaemia, alcoholism, smoking, cirrhosis, renal insufficiency, diabetes mellitus) were ruled out. The diagnosis of primary aminolaevulinic acid dehydratase deficiency was proposed and confirmed by the familial study, which revealed the existence of several heterozygous members in this family.
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PMID:Biochemical diagnosis of an hereditary aminolaevulinate dehydratase deficiency in a 63-year-old man. 260 May 50

Fifty consecutive orthotopic liver transplants were performed without venous bypass in 41 recipients. Seven patients were transplanted twice and one patient received 3 transplants. The average age of the recipients was 37 years. The commonest indications for transplantation were primary biliary cirrhosis and cirrhosis from chronic active hepatitis. Fifty-eight percent of the recipients had undergone previous upper abdominal surgery. During the anhepatic period systolic blood pressure decreased by 21% to an average of 98 mm. of mercury. Cardiac output decreased by 52% to a mean (+/- SEM) of 3.89 +/- 0.21 L/min., and there was a doubling of the systemic vascular resistance. The hemodynamic alterations promptly returned to preclamping levels following hepatic revascularization. The average intraoperative transfusion requirements were 13 units of packed red blood cells, 9.6 units of platelets, 14.5 units of plasma and 6.6 L of crystalloid. Patients with previous surgery and retransplants required an average of 13 and 17 units of packed red blood cells, respectively. There was no deterioration in renal function in the postoperative period and no patient required hemodialysis. The 30 day survival was 87.8%. The 90-day and one-year actuarial survival is 80.5% and 68.8%, respectively. It is concluded that venous bypass is not necessary as a routine in orthotopic liver transplantation.
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PMID:Liver transplantation without venous bypass. 354 24

The main hepatic change in erythropoietic protoporphyria is the deposition of protoporphyrin. Brown deposits of this pigment occur in bile canaliculi and ductules, discretely in hepatocytes, and secondarily in macrophages and Kupffer cells. The pigment is deposited in a crystalline form. Under the fluorescence microscope with a mercury maximum pressure burner (HO 50) at a wave length of 380--500 nm, it shows a typical red fluorescence even after paraffin embedding. Its crystalline structure results in a characteristic double refraction under the polarising microscope. Light-microscopically, hepatocellular reactions are characterised mainly by discrete alterations in the ergastoplasm. However, cell damage is indicated by diffusely distributed, hyaline single cell necrosis and by cytolytic piecemeal necrosis at the peripheries of hepatic lobules. Numerous, often disturbed mitoses produce binuclear and multinuclear hepatocytes. The obligatory secretion of protoporphyrin into the bile ducts leads to an alteration in the canalicular and ductular excretion apparatus which involves distinct ductular proliferation and accompanying fibrosis. Piecemeal necrosis is a further consequence of this process. The resulting histological picture is similar to sclerosing cholangitis with which it also has in common the slowly progressive development of hepatic cirrhosis.
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PMID:[Hepatic reactions in erythropoietic protoporphyria (author's transl)]. 611 81

As the clinical significance of hemodynamic parameters remains controversial, the portohepatic gradient has been measured in 89 patients with cirrhosis by a transjugular approach. Relationships between portohepatic gradient and clinical, roentgenologic and prognostic patterns were studied with a maximum follow-up period of 36 months. Portohepatic gradient was not related to the rate of occurrence or rate of recurrence of digestive tract bleeding. Portohepatic gradient was related to the size of esophageal varices, p less than 0.01. Observation of large varices at endoscopy was associated with a higher risk of digestive tract bleeding. Portohepatic gradient was related to the number of portosystemic shunts opacified at portography, p less than 0.01. Portohepatic gradient was found to be related to these aspects of prognosis: the mean portohepatic gradient was higher in patients who died than it was in survivors, p less than 0.05. When patients were separated into two groups according to portohepatic gradient values--greater than or equal to 20.8, less than 20.8 millimeters of mercury--the actuarial survival rate was inversely related to portohepatic gradient at one, p less than 0.02, and at 12, p less than 0.02, months of follow-up study. This relationship could be demonstrated in the entire group of patients with cirrhosis and in the group of patients with digestive tract bleeding. This pattern seemed to be related to the risk of hemorrhage. In groups of patients and within a 24 month observation period, the survival rate was significantly related to the range of portohepatic gradient in each group.
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PMID:Clinical and prognostic significance of portohepatic gradient in patients with cirrhosis. 698 Dec 15

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

Within the past decade an entire family of membrane proteins--aquaporins--which function as transmembrane water channels has been identified; they occur throughout the plant, animal, and bacterial kingdoms. Several family members permit glycerol and urea permeability. Most aquaporins are inhibited by mercury. Constitutively expressed aquaporin 1 is the major permeability channel of the proximal tubule, descending thin limb of the loop of Henle, and it is also found in vasa recta. Aquaporin 2 is expressed in the principal cells of the collecting duct where it shuttles between intracellular vesicles and the apical membrane in response to vasopressin. Aquaporin 2 mutations cause nephrogenic diabetes insipidus; increased aquaporin 2 activity is implicated in the pathophysiology of heart failure, cirrhosis, and nephrotic syndrome. Aquaporins 3 and 4 provide basolateral membrane water channels in the collecting duct. These 4 channels and 6 others are also found elsewhere throughout the body. The physiological importance of several of the channels remains unknown. Aquaporin 1 inhibitors might induce useful diuresis, but humans who lack aquaporin 1 have no significant clinical disease. Inhibition of aquaporin 2 activity by vasopressin receptor antagonists may be useful in heart failure, cirrhosis, nephrotic syndrome, and the syndrome of inappropriate antidiuretic hormone (ADH) release.
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PMID:Aquaporin mediated water flux as a target for diuretic development. 1059 41

Chronic hepatitis B virus infection causes nearly all the deaths from this virus. As the initial infection occurs without symptoms and decades prior to the onset of cirrhosis and liver cancer, these consequences are rarely recognized as being caused by the virus. Consequently, its public health importance is under-recognized. Safe and effective vaccines have now been available for over 20 years. Concerns have been raised regarding the mercury preservative in vaccines leading to potential toxicity. But the evidence to date does not support any association of hepatitis B vaccine with serious adverse consequences. Protecting infants through immunization is the most effective control strategy. By 2005, over 80% of countries had implemented routine infant immunization. In countries with relatively low rates of hepatitis B virus infection, some have argued to defer immunization until later life. However, these arguments focus on the more visible acute infection. The possible future cost from a single infant infection argues for universal infant hepatitis B immunization--given the very high costs of treating its consequences (e.g., liver transplant) and the very low price of the vaccine.
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PMID:Should hepatitis B vaccine be used for infants? 1728 Apr 76

Palmar erythema (PE), an often overlooked physical finding, is due to several physiologic or systemic pathologic states. PE can exist as a primary physiologic finding or as a secondary marker of systemic pathology. Primary or physiologic PE can be due to heredity, occurs in at least 30% of pregnant women as a result of associated alterations in the function of the skin and its microvasculature, or may be a diagnosis of exclusion (i.e. idiopathic PE). Secondary PE from systemic pathology encompasses a wide range of disease states. Twenty-three percent of patients with liver cirrhosis, from varying causes, can manifest PE as a result of abnormal serum estradiol levels. Patients with a rare neonatal liver disease such as Wilson disease and hereditary hemochromatosis may exhibit PE along with the other systemic manifestations of the genodermatoses. PE has been reported to occur in >60% of patients with rheumatoid arthritis and is associated with a favorable prognosis. Up to 18% of patients with thyrotoxicosis and 4.1% of patients with diabetes mellitus can have PE. This cutaneous manifestation of diabetes occurs more often than the more classic diseases such as necrobiosis lipoidica diabeticorum (0.6%). PE can be seen in early gestational syphilis and among patients with human T-lymphotrophic virus-1-associated myelopathy. Drug-induced PE with hepatic damage has been documented with use of amiodarone, gemfibrozil, and cholestyramine, while topiramate and albuterol (salbutamol) have been reported to cause PE in the setting of normal liver function. Fifteen percent of patients with both metastatic and primary brain neoplasms may have PE. Increased levels of angiogenic factors and estrogens from solid tumors have been postulated as the cause of PE in such cases. Erythema ab igne can mimic PE, and patients with atopic diathesis are more likely to have PE than matched control subjects. Smoking and chronic mercury poisoning are environmental causes of PE.No treatment of primary PE is indicated. If medication is the cause of PE, the drug responsible should be discontinued if possible. Identification of PE related to underlying disorders should be followed by treatment of the underlying condition. In light of the numerous etiologies of PE, this article reviews the current literature and provides a framework to help guide the clinician in determining the cause of PE in patients presenting with this finding.
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PMID:Palmar erythema. 1803 17


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