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)

Four cases of hepatic angiosarcoma are reported with a review of 99 other cases in the English literature. Angiosarcoma of the liver is associated with chronic exposure to thorotrast, vinyl chloride, arsenicals, radium and possibly copper and with chronic idiopathic hemochromatosis. Although 40% of patients have hepatic fibrosis or cirrhosis at autopsy, the nature of the association between chronic liver disease and hepatic angiosarcoma is unknown. The clinical presentation of hepatic angiosarcoma is nonspecific with abdominal pain, weakness and weight loss common complaints and with hepatomegaly, ascites and jaundice common findings. Liver function tests are usually abnormal but there is no one liver function test or set of tests specific for the tumor. The occurrence of thrombocytopenia and disseminated intravascular coagulation is characteristic of hepatic angiosarcoma and may be related to local consumption of clotting factors and formed blood elements in the tumor. Catastrophic intraabdominal bleeding is also characteristic and occurs in one-fourth of all cases. This complication is likely related to the high incidence of clotting abnormalities and the vascular nature of the neoplasm. Selective hepatic arteriogram and open liver biopsy are the foundations of diagnostic evaluation. Percutaneous liver biopsy should be avoided. Failure to appreciate the possibility of hepatic angiosarcoma in the proper clinical setting, leading to blind percutaneous biopsy, may result in failure to make the diagnosis at the cost of significant morbidity and mortality. Survival of patients with hepatic angiosarcoma is brief; only 3% live longer than 2 years. Treatment of the tumor to date is empirical. There are probably a few patients who might benefit from radical surgery with curative intent. For all others chemotherapy is indicated. Adriamycin is active against hepatic angiosarcoma, but optimal dose and mode of administration require further investigation. Further study is also required to delineate the cause of hepatic angiosarcoma in the 60% of cases without definite epidemiologic association.
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PMID:The clinical features of hepatic angiosarcoma: a report of four cases and a review of the English literature. 36 8

Mixed-typed cryoproteins, consisting of IgG and IgM, were demonstrated in the sera of four sisters. While the IgG component was polyclonal in every instance, in two of them the IgM component was found to be monoclonal with type chi light chains. Clinical diagnoses included the purpura-weakness-arthralgias syndrome, posthepatitis cirrhosis, congestive heart failure and mitral stenosis. The cryocrit differed in the four sisters, ranging from 3 to 16%; in addition, rheumatoid factor activity was consistently associated with both washed cryoprecipitates and their isolated IgM components. Endomembraneous deposits of IgG and IgM were revealed by immunofluorescent studies of the renal biopsy specimen from one patient. A genetic abnormality, possibly of the autosomal recessive type, is suggested in this instance of familial cryoglobulinemia.
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PMID:Cryoimmunoglobulinemia in four sisters. 41 43

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Because of its presumed serious clinical significance, we made an analysis of the evidence for and against the occurrence of spontaneous reversal of portal flow in cirrhosis of the liver. We examined the evidence obtained from manometric studies, radioactive tracer studies, radiologic studies, and actual measurements of magnitude and direction of portal blood flow. Concerning manometric studies, we introduced a physical analysis, based on first principles, which demonstrates that the occluded portal pressures cannot be used to construct a hydraulic gradient for portal flow. Similarly, we examined the weakness of the evidence derived from radioactive tracer and radiologic studies and, in the latter, the drastically opposite results reported by different investigators. Finally, we found that actual measurements of magnitude and direction of portal flow provide impressive evidence against the occurrence of spontaneous reversal of portal flow in cirrhosis. We conclude that unless new and convincing evidence is provided, it may not serve the best interests of medicine and of our patients to continue accepting spontaneous reversal of portal flow in cirrhosis as if it were a proven phenomenon.
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PMID:Spontaneous reversal of portal blood flow: the case for and against its occurrence in patients with cirrhosis of the liver. 109 86

This is the definitive review of the cardiovascular effects of liver disease. Physiologic and pathologic studies accomplished primarily in the 1950s and 1960s have been applied to a case of a 16-year-old boy with cirrhosis of the liver who presented with weakness, dyspnea, cyanosis, and clubbing. The probable mechanisms for his signs and symptoms are discussed in detail. The cause for the hyperkinetic circulation is unknown. By exclusion, the cyanosis is attributed to intrapulmonary shunting. Portapulmonary shunts are not quantitatively important. The suitability of the terms micronodular and macronodular cirrhosis is highlighted. Indications for various types of surgical portal shunts are discussed. The value of preoperative hemodynamic measurements of the portal circulation to the individual patient is debated. A liver transplant is considered in this case with no promising medical therapy and a very poor prognosis. The renal disease manifested by red cell casts in the urine is thought to be caused by an immunologic reaction in the kidney somehow related to his liver disease. This discussion is led by Dr. Jack Myers, but his opinions are correlated with those of a pathologist, radiologist, surgeon, and gastroenterologist. It is a clinical tour de force, although not all the predictions are confirmed by laboratory studies such as this patient's hepatic wedge pressure, pulmonary artery pressure, and cardiac fluoroscopy.
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PMID:Multidisciplinary Conferences in Gastroenterology. Cardiovascular effects of severe liver disease. 127 11

A clinical study and follow-up of 77 patients (63 males and 14 females) with hepatocellular carcinoma with age range from 22 to 80 years were collected from the Institute of Post Graduate Medicine and Research and eight private hospitals from Dhaka City. Past history of transfusion was present in 16 (20.8%), Jaundice in 20 (26%) and 13 (16.9%) patients had associated cirrhosis. HBs Ag was positive in 17 (33.33%) out of 51 patients and liver ultrasound suggested hypoechogenic lesion in 44 (57.2%) patients. CT was performed in 7 (9.1%) and in one MRI was done. Eight (50%) out of 16 patients had alphafetoprotein ranging from 1000-12000 ng/ml. Space occupying lesion was detected in 25 (71.4%) out of 35 cases by isotope scan and needle biopsy was confirmatory in 25 (32.5%). Commonest presentations were abdominal lump (96.2%), weakness (79.3%), weight loss (74%), and loss of appetite (78%). Fifty six (72.2%) patients were followed weekly till death (2.9 +/- 2.4 months). The mean survival was higher under 30 years (5.9 +/- 3.7 months; P less than 0.05). Serum bilirubin above 5 mg/dl with HCC also had poor prognosis (1.6 +/- 0.8 months; P less than 0.01) Those who had prothrombin time higher than 16 seconds died earlier (1.6 +/- 0.7 months; P less than 0.01). Survival was poor in those who had the tumour size over 7 cm (2.5 +/- 0.9 months; P less than 0.01).
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PMID:Clinical profile: prognostic index in hepatocellular carcinoma. 166 11

A 62-year-old woman with hepatitis-B-surface-antigen-positive hepatic cirrhosis presented with weakness and paresthesias over the distal part of the limbs in the course of adenine arabinoside 5'-monophosphate (ARA-AMP) treatment, and recovered spontaneously after several weeks of drug withdrawal. Electrophysiological and histological studies demonstrated axonal neuropathy. Although the patient received a relatively low total dose (120 mg/kg), her age and advanced liver disease may have played a role in the ARA-AMP neurotoxicity.
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PMID:Toxic neuropathy after adenine arabinoside treatment in chronic HBsAg-positive liver disease. 168 32

1. Chronic alcoholism may be complicated by proximal muscle weakness associated with a selective atrophy of type II skeletal muscle fibres. The histopathological findings are non-specific as identical changes are seen in proximal muscle weakness associated with various metabolic myopathies, including osteomalacia. 2. The maximum voluntary contraction (MVC) of the dominant quadriceps and plasma 25-hydroxycholecalciferol [25-(OH)D] were measured in male alcoholics and control subjects to determine whether vitamin D deficiency contributed to proximal muscle weakness. 3. In both groups MVC declined with age and was related to body build. The distribution of plasma 25-(OH)D was skewed in alcoholics, with the mean significantly lower than in control subjects. Seventeen per cent of patients (but none of the control subjects) had pronounced biochemical deficiency [plasma 25-(OH)D less than 10 nmol/l]. 4. Alcoholics were significantly weaker than control subjects, even after correcting for the effects of age, height and weight. The severity of associated liver disease (cirrhosis vs no cirrhosis) did not influence muscle strength. Variation in plasma 25-(OH)D and albumin made an insignificant contribution to the difference in MVC observed between patients and control subjects. 5. We conclude that proximal muscle strength is reduced in chronic alcoholism but that this is not due to associated vitamin D [25-(OH)D] deficiency or alcoholic cirrhosis.
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PMID:Vitamin D deficiency and muscle strength in male alcoholics. 276 57

A 67-year-old, non-alcoholic Japanese female case with liver cirrhosis, in the course of admission due to ascites and rupture of the rectal varix, was affected by an unusual type of acute progressive encephalopathy, presenting inattentiveness and slurred speech as initial symptoms. Her consciousness was increasingly clouded. Variable symptoms such as saccadic eye movement, nystagmus, weakness, hyperreflexia, dysmetria, adiadochokinesis and painful dysesthesia were also noted. Laboratory examination disclosed abnormal liver functions, hyponatremia, respiratory alkalosis and normal blood ammonia. Cerebrospinal fluid was xanthochromic and contained slightly increased protein. On CT scan, bilateral symmetrical low density areas were demonstrated in the diencephalon, brainstem and cerebellum. A week after the onset, she was comatose with rigidity of the extremities. Hyperbilirubinemia and severe hyponatremia developed. On the second CT, low density areas extended to the cerebral deep white matter. Her respiration became irregular, and she expired 16 days after the onset. Autopsy disclosed edematous lesions with dark brown discoloration in the medial basal ganglia, ventral diencephalon and mesencephalic tegmentum. Less severely affected lesions with pale yellow discoloration extended into the cerebral white matter, pontine and medullar tegmentum and cerebellar dentate nuclei. In the central lesions, diapedesis of erythrocytes and serum-plasma was marked, with necrosis of the neurons. In the peripheral lesions, diapedesis of less proteinaceous fluid was noted, with less severe neuronal damages. Neither capillary prominence nor gliosis was remarkable. The clinical and pathological features of the present case bore some similarity to those of Wernicke's and Leigh's encephalopathies. However, the patient's age, habitus or clinical course was atypical for the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute encephalopathy with symmetrical, widespread, edematous and necrotic lesions--an autopsy case report]. 280 34

In a study of 228 consecutive medico-legal autopsies, malignant disease was discovered in 19 cases. The malignant diseases are discussed as to their primary sites and histologic types, age groups in which they occurred, conditions with which they may have been associated, symptoms and signs which in some cases may have warned of malignant disease, and supposed reasons why the malignant diseases were not recognized while the deceased were still alive. It was found that undetected malignant diseases occur mainly in the elderly, that chronic renal disease with scarred kidneys and cirrhosis of the liver may be predisposing conditions in cancer development, and that malignant disease in the aged may be undetected because of confusion with general weakness or because of small size and obviously slow growth of the tumor with lack of symptoms.
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PMID:[Malignant diseases as secondary findings in forensic autopsies]. 291 26


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