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)

A 62-year-old woman presented with uveitis and abnormal chest X-ray (bilateral hilar adenopathy). Skin biopsy in 1983 had revealed non-caseating epithelioid cell granuloma consistent with sarcoidosis. Her serum biochemical investigations and exploratory laparoscopy suggested nodular liver cirrhosis, but biopsy was not performed. Both blood urea nitrogen (BUN) and serum creatinine values were within normal limits. She received prednisolone therapy of 15 mg daily initially, and later a maintenance dose of 5 mg daily. In 1985, she complained of skin itching and her laboratory data revealed severe renal insufficiency (BUN 97 mg/dl, serum creatinine 12.2 mg/dl) and hypercalcemia (corrected serum calcium level: 11.5 mg/dl). Prednisolone treatment (40 mg daily) resulted in a dramatic improvement of renal function as well as other clinical abnormalities due to sarcoidosis, without any significant changes in liver function. She died of cerebral infarction in 1989. Autopsy showed interstitial nephritis with tubular calcinosis and hyalinized glomeruli. It is postulated that hypercalcemia due to sarcoidosis contributed to the renal failure in this patient. This case suggests that renal damage due to sarcoidosis may be reversible with appropriate corticosteroid therapy.
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PMID:[An autopsy case of sarcoidosis associated with renal failure]. 140 82

A case of multiple myeloma (Bence Jones, lambda) associated with alcoholic liver cirrhosis is reported. A 56-year-old Japanese male died of hepatic failure and hypercalcemia. Autopsy revealed alcoholic liver cirrhosis and plasma cell myeloma. Immunoelectrophoretic analysis of his reserved serum disclosed the presence of M component of lambda Bence Jones protein. IgA and lambda light chain were demonstrated in the cytoplasm of the myeloma cells. Complications such as generalized amyloidosis, metastatic calcification, myeloma kidney and hemorrhagic pancreatitis were noted. The coexistence of multiple myeloma and liver cirrhosis has rarely been reported. On the basis of a review of the reported cases, a possible association between both diseases was discussed.
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PMID:Multiple myeloma in alcoholic liver cirrhosis. 265 75

The authors report the clinical and biological features in 197 patients with hepatocellular carcinoma seen in two French hospitals. Mean age was 63 +/- 12 years. Eighty-nine per cent were men. Cirrhosis was present in 88 p. 100. Alcoholic liver disease was associated with hepatocellular carcinoma in 71.5 p. 100. At the time of diagnosis, ascites was present in 62 p. 100 of the patients, jaundice in 49 p. 100, encephalopathy in 20 p. 100 and gastrointestinal bleeding in 12.5 p. 100. Twenty patients (10 p. 100) did not have any of these complications. An increase in serum gammaglutamyl transpeptidase and ASAT was the most frequent biological abnormality observed in 96 and 94 p. 100 of patients respectively. Hypercalcemia and a high hematocrit were present in 5 and 6 p. 100 of patients respectively. Serum HBs Ag (RIA) was present in 17.5 p. 100 of patients, anti-HBc in 50 p. 100 and anti-HBs in 33.5 p. 100; 38.5 p. 100 of patients had no serum HBV marker. Serum alphafetoprotein levels were higher than 20 ng/ml, 250 ng/ml and 1,000 ng/ml in 76.5 p. 100, 43.5 p. 100 and 33 p. 100 of patients respectively. There were no relationships between the presence of serum markers of HBV or high alphafetoprotein levels and clinical and biological data. These results confirm that the clinical, biological and virological aspects of hepatocellular carcinoma in France are similar to those reported in other western countries.
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PMID:[Hepatocellular carcinoma in France. Clinical, biological and virological aspects in 197 patients]. 298 69

This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two. Bone x-ray films showed generalized osteoporosis in all patients. Renal function and arterial blood pH were within normal limits in every patient. The diagnosis of primary hyperparathyroidism in each patient was based on repeated demonstrations of hypercalcemia, hypophosphatemia, and markedly elevated serum immunoreactive parathyroid hormone concentrations. In all six patients, removal of the parathyroid adenoma resulted in disappearance of symptoms; normalization of serum calcium, phosphorus, and immunoreactive parathyroid hormone levels; and in four of the six, improvement in radiographic evidence of osteoporosis during follow-up of from 1 to 6 years. The association of cirrhosis, portacaval shunt, and primary hyperparathyroidism has not been documented previously. Our six patients with primary hyperparathyroidism constitute 3.4 percent of 174 survivors of emergency portacaval shunt in a series of 264 unselected, consecutive patients with cirrhosis and bleeding esophageal varices. Hepatic osteodystrophy is known to have occurred in only 11 of these 174 survivors. Primary hyperparathyroidism may be a more common cause of hepatic osteodystrophy than has been previously recognized, and should be considered in patients with cirrhosis in whom weakness, bone pain, and bone demineralization develop, particularly if they have a portacaval anastomosis.
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PMID:Hyperparathyroidism, cirrhosis, and portacaval shunt. A new clinical syndrome. 325 57

Various abnormalities of the renal tract can be detected from the renal images seen on 99Tcm methylene diphosphonate (MDP) bone scintigrams. Diffusely increased renal parenchymal activity has been associated with cytotoxic and other drug therapy, radiation nephritis, iron overload and cirrhosis. A further association--with hypercalcaemia--is reported here. In a retrospective study, 1950 bone scintigrams were reviewed and a significant relationship between high renal activity and hypercalcaemia was found. This was subsequently confirmed by a small prospective study. None of the patients whose bone scintigrams showed this association had evidence of nephrocalcinosis on X rays. It is postulated that in these hypercalcaemic patients there may be high tissue calcium in the kidneys which results in the high uptake of MDP, and it is suggested that serum calcium be measured in patients with previously unsuspected hypercalcaemia whose bone scintigrams exhibit the finding of high parenchymal renal activity.
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PMID:High renal activity on bone scintigrams. A sign of hypercalcaemia? 622 81

In order to elucidate a participation of intact parathyroid hormone (PTH(1-84)) in blood pressure (BP) and body fluid homeostasis, we studied fluctuations of PTH(1-84) during manipulations of BP in hyperparathyroid and healthy subjects, and during manipulations of blood volume in patients with glomerulonephritis or liver cirrhosis and in controls. Angiotensin II induced BP elevation was associated with increased values of PTH(1-84) both in healthy subjects (12-25 ng l-1, medians, p < 0.01), in patients with primary hyperparathyroidism (94-125 ng l-1, p < 0.01), in patients with low calcium due to end stage renal disease before requirement of dialysis (95-151 ng l-1, p < 0.02), and in patients with tertiary hyperparathyroidism (221-264 ng l-1, p < 0.05), but not in dialysis patients without hypercalcaemia (126-174 ng l-1, NS). The changes could not be attributed to reduction of serum calcium, but probably to the increase of plasma angiotensin II, which was positively correlated to the increase of serum PTH(1-84) in the healthy subjects (p = 0.619, n = 15, p < 0.05) and in the patients with primary hyperparathyroidism (p = 0.549, n = 18, p < 0.05). Noradrenaline induced BP elevation did not have a similar effect on PTH(1-84), and changes of PTH(1-84) were not related to changes of BP. Volume depletion after furosemide injection, also accompanied by increased levels of angiotensin II, resulted in elevation of PTH(1-84) in controls, cirrhotics, patients with glomerulonephritis without the nephrotic syndrome, but not in nephrotic patients. Volume depletion induced by bolus injection of atrial natriuretic peptide (ANP) was associated with decreased PTH(1-84) in healthy subjects (20-18 ng l-1, p < 0.02), but not in patients with nephrotic syndrome and liver cirrhosis. Volume expansion induced by albumin infusion caused increased plasma levels of ANP, but PTH(1-84) was unaltered. Thus, angiotensin II may be able to stimulate, and ANP to inhibit release of PTH(1-84), and PTH(1-84) may be involved in the regulation of BP and body fluid homeostasis. BP changes or changes in blood volume per se do not seem to influence PTH(1-84) levels.
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PMID:Parathyroid hormone in blood pressure and volume homeostasis in healthy subjects, hyperparathyroidism, liver cirrhosis and glomerulonephritis. A possible interaction with angiotensin II and atrial natriuretic peptide. 786 30

Administration of vitamins or metals may cause severe side effects. Retinoids (derivatives of vitamin A) used for the treatment of various skin disorders are teratogenic, hepatotoxic and may induce a substantial increase in serum lipids. A case report demonstrates that vitamin D supplementation in a patient under total parenteral nutrition can cause hypercalcemia. The isolated administration of vitamin B1, without concomitant vitamin B6 and nicotinamide may precipitate potentially life-threatening pellagra encephalopathy. Repeat blood transfusions may produce clinically overt organ hemosiderosis, e.g. cirrhosis of the liver, diabetes mellitus or myocardiopathy. The literature contains reports on a few cases of sarcoma associated with orthopedic metal implants. The controversial issue of the potential dangers of dental amalgams is briefly mentioned.
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PMID:[Vitamins and metals: possible hazards for humans]. 866 74

The histopathology and clinical picture of hepatocellular carcinoma (HCC) varies between individual patients and regions. These variations are perhaps due to differences in the genetic alterations that precede hepatocarcinogenesis. In this study, the clinicopathological features of HCC were compared between southern African blacks and Japanese, indicating large differences in the frequency of underlying cirrhosis, grade of cancer cell differentiation and clinical course. Intra-abdominal bleeding and febrile, rapidly progressive HCC are more common among blacks. Such a difference is accounted for, in part, by frequent encapsulation of the tumour which is well differentiated, and grows slowly in an expanding fashion in Japan. Encapsulated HCC was not seen among the black patients studied. Other distinct clinicopathological types discussed in this paper include diffuse-type HCC which is usually caused by multiple portal spread occurring almost simultaneously; the clinical course is fulminant. Sclerosing carcinoma is frequently associated with hypercalcaemia in the United States, but not in Japan. Fibrolamellar carcinoma is nearly non-existent in Asia, whereas it is common among young adults in the West. Its prognosis is generally better than ordinary HCC. Hepatocellular carcinoma has a strong propensity to invade vessel and duct systems. Portal invasion does not produce distinct clinical signs although it may aggravate portal hypertension. Patients with tumour occlusion in the major portal vein may give rise to ischaemic hepatitis when blood pressure drops suddenly in the preterminal stage. Liver parenchyma develops submassive necrosis and clinically there is an acute rise in alanine aminotransferase (ALT). Invasion into a major hepatic vein and the inferior vena cava also occurs, but less frequently compared with portal invasion. The patient can live even with a tumour thrombus in the atrium crossing the tricuspid valves. Intraductal invasion causes acute jaundice as well as an occasional haemobilia with pain. We recently found that a distinct pathological type called 'extrahepatic growth' or 'pedunculated HCC' develops as a result of fusion of right-sided adrenal metastasis of HCC and the liver, perhaps through the 'adreno-hepatic fusion' which is rather common in cirrhotic livers.
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PMID:Hepatocellular carcinoma: clinicopathological aspects. 940 52

Chronic pancreatitis (CP), a disease described only in 1946 by Comfort and colleagues is currently a global disease. Chronic alcoholism, albeit is the most frequent etiologic factor for the disease in most of the affluent nations, a form of CP of undetermined etiology, tropical calculous pancreatitis (nutritional pancreatitis, Afro-Asian pancreatitis, or tropical calculous pancreatopathy) has been recognized to be prevalent in many developing nations. Hereditary pancreatitis inherited as an autosomal dominant disease is reported from all parts of the world. A landmark is the recent discovery of a gene that transmits the disease. Nearly 10% of cases of CP are truly "idiopathic" with no identifiable cause. Recent studies indicate that the idiopathic variety of CP has two subsets--a juvenile form and a senile or late onset form, with distinct clinical features. It is extremely rare to see CP secondary to hyperlipidemia or hypercalcemia. These etiologic associations appear to be overemphasized. Epidemiological studies indicate that alcoholism is growing in incidence all over the world along with an increase in all alcohol-associated disorders such as cirrhosis of the liver or pancreatitis. A genetic predisposition to alcoholic pancreatitis is suspected based on population studies, but not proven. The influence of cigarette smoking in enhancing alcohol-induced injury to the pancreas underscores the health hazard associated with alcoholism and cigarette smoking--two habits that often coexist in many individuals. The recent finding that all forms of CP are premalignant further emphasizes the need to enforce preventive measures. The hope is that CP is a preventable disease. The despair is that alcoholism is increasing and spreads across geographic and religious boundaries.
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PMID:Chronic pancreatitis: a historical and clinical sketch of the pancreas and pancreatitis. 953 Nov 14

Amongst the principal metabolic situations that can require emergency attention in the oncology patient we find: hypercalcaemia, hyponatraemia, tumoural lysis syndrome, lactic acidosis, hyperuricaemia, renal failure, hyperammonaemia, hypermpotasaemia, etc. Hypercalcaemia is the most frequent metabolic complication in oncology, appearing in 10-30% of these patients. It has two main mechanisms, tumoural lysis and humoural hypercalcaemia mediated by PTHrP (a protein related to parathormone). The principal factor for its diagnosis is suspicion, since some symptoms are non-specific and can be attributed to other causes such as somnolence, constipation, etc. Treatment will be based on intensity and is started with calciuretic measures with an intense hydration with physiological serum and on some occasions with furosemide. Anti-reabsorptive measures include calcitonin, bisphosphonates, mithramycin, gallium nitrate and on occasions corticoids. Bisphosphonates such as pamidronate and zoledronate seem to be highly useful in these cases. Hyponatraemia is classified depending on plasmatic osmorality; when this is low we find ourselves facing an authentic hyponatraemia that can develop with an extra-cellular volume that is high (cardiac insufficiency, cirrhosis, nephrotic syndrome and renal insufficiency), low (renal and extra-renal sodium losses) and normal (principally SIADH, related to a high elimination of sodium in the urine with high urinary osmolarity in spite of this being low in blood). Several types of tumour and different chemotherapy drugs can produce this SIADH. Treatment will vary according to the type and intensity, but in general this is based on hydric restriction and the replacement of the sodium deficit, either through physiological serum or through hypertonic saline serums depending on the case, and on occasions furosemide for the elimination of excess water.
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PMID:[Metabolic emergencies in the oncology patient]. 1572 5


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