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 167 consecutive patients with various types of neuropathy, the amplitude of the sensory potential and the maximum conduction velocity along the sural nerve were compared with conduction in other sensory nerves, and were related to structural changes revealed by nerve biopsy. Electrophysiological findings in the sural nerve were similar to those in the superficial peroneal and the median nerve, though the distal segment of the median nerve was normal in 20 per cent of the patients when it was abnormal in the sural nerve. Quantitation of histological findings was a more sensitive method than the electrophysiological study in that two-thirds of 33 patients with normal electrophysiology in the sural nerve showed mild loss of fibres or signs of remyelination in teased fibres. The amplitude of the sensory potential was grossly related to the number of large myelinated fibres (more than 7 micrometer in diameter). Considering the 95 nerves from which teased fibres were obtained, maximum conduction velocity was abnormal in half. In 18 of these nerves, slowing in conduction was due to axonal degeneration: the velocity was as to be expected from the diameter of the largest fibres in the biopsy ("proportionate slowing"). In 9 nerves slowing was severe and more marked than to be expected from loss of the largest fibres ("disproportionate slowing"); these nerves showed paranodal or segmental demyelination in more than 30 per cent of the fibres. In 16 nerves from patients with neuropathy of different aetiology neither loss of fibres nor demyelination could explain the moderate slowing. The cause of slowing in these nerves is unknown; other conditions are referred to in which slowing in conduction cannot be attributed to morphological changes. Finally, electrophysiological and histological findings are reported in some patients with neuropathy associated with malignant neoplasm, with rheumatoid arthritis, with polyarteritis nodosa, with acute intermittent porphyria and with cirrhosis of the liver.
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PMID:Sensory action potentials and biopsy of the sural nerve in neuropathy. 21 63

Liver enzymes were followed in 99 patients treated with D-penicillamine for rheumatoid arthritis. In six abnormalities were found which consisted of elevated levels of lactic dehydrogenase. ALAT/ASAT, alkaline phosphatases or combinations of these. The changes were reversible on stopping the drug with one possible exception. No evidence of biliary cirrhosis, chronic active hepatitis or HBag-associated hepatitis was found. Liver biopsy was performed in 4 cases--one was taken 2 months after the treatment was discontinued, and was normal. One biopsy showed mild inflammatory changes, whereas in two histologic evidence of toxic liver necrosis was present. Liver damage should be included among possible complications of D-PA treatment.
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PMID:Liver abnormalities in penicillamine treated rheumatoid arthritis. 28 88

Regencrative nodular hyperplasia (RHN) is a rare condition, the diagnosis of which is based upon histological findings. It is seen in Felty's syndrome with portal hypertension (PHT), as was the case in the patient reported here. This was a 72-year-old man, with long standing rheumatoid arthritis, hepatosplenomegaly, a neutrophil leucopaenia and oesophageal varices responsible for recurrent haematemeses. Despite a portocaval anastomosis, the patient died from postoperative acute hepatic failure. Histological study revealed changes in the hepatocytes and the reticulin system typical of RNH without cirrhosis. The relationship between Felty's syndrome and RHN, as well as the mechanism of the hypertension, are discussed in the light of cases from the literature.
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PMID:[Anatomo-clinical study of a case of regenerative nodular hyperplasia of the liver with Felty's syndrome and portal hypertension]. 54 55

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66

A reaction of the RES with its organs (lymph nodes, spleen, bone marrow and Kupffer's cells) is not uncommon in rheumatoid arthritis. Although these manifestations are pronounced in Felty's syndrome, reviewing articles about Felty's do not mention liver manifestations. This paper summarises the publications about liver findings in Felty's syndrome. Hepatomegaly, abnormal bromsulfalein tests, raised alkaline phosphatase and transaminases have been stated in many case reports. Among 34 patients, the frequency of hepatomegaly was 68%, of abnormal bromsulfalein tests 27%, of alkaline phosphatase 23% and of transaminases 18%, respectively (52). Alkaline phosphatase and transaminases were raised in almost all of 12 patients (3). The histological correspondence is an infiltration with lymphocytes of sinusoids and portal fields, a portal fibrosis and occasionally a cirrhosis. These histological abnormalities, as well as enlarged lymph nodes and splenomegaly, have to be considered as organic manifestations of rheumatoid arthritis. If the nodular regenerative hyperplasia of the liver, which has been reported also after use of contraceptives, is a manifestation of Felty's syndrome, remains unresolved.
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PMID:[Liver findings in Felty's syndrome. A review]. 69 99

The, in non-thyroidal illnesses, frequently occurring changes in the serum concentrations of peripheral thyroid hormones, are shown in patients with acute myocardial infarction, compensated and decompensated cirrhosis of the liver, renal insufficiency and in rheumatoid arthritis. The observed changes, (pathological) low total triiodothyronine, low or normal total thyroxine, and normal thyrotrophine), can make the diagnosis of hyperthyroidism impossible. Only in control measurements, after cessation of the simultaneous non-thyroidal illness, the peripheral thyroid hormone concentrations are found to be in the hyperthyroid range. The only way to establish the diagnosis, (or confirm the clinical suspicion), is to prove non-responsiveness of the pituitary to a TRH-stimulus. TRH-tests have, however, no diagnostic value in illnesses that affect pituitary function directly, such as terminal renal insufficiency. The diagnosis of hypothyroidism can be established by measurement of the basal thyrotrophine serum concentration (elevated) or by measurement of the serum concentrations of 3,3'5'-triiodothyronine (reverse T3), which is, according to a recent report, observed to be significantly decreased.
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PMID:[Evaluation of thyroid function in non-thyroid diseases]. 75 17

Evaluation of stored iron by means of DFOX-induced sideruria in 101 subjects with various degree of hyposideraemia with or without anaemia, is reported. Three groups were examined: 49 patients with chronic loss of blood and malabsorption and urinary iron values up to 1 mg/24hr; 43 with non-bleeding neoplasia, collagen disease, lymphoma, cirrhosis of the liver etc. and values of 1-2mg/24 hr; 9 with rheumatoid arthritis and cirrhosis of the liver and values over 2 mg/24 hr. The reasons why hyposideraemia may accompany incipient of frank tissue hypo-, normo- or hypersiderosis are discussed.
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PMID:[Desferrioxamine in the diagnosis of hypo-, normo-, and hypersiderotic hyposideremia]. 84 86

Oxphenisatin is known to induce liver damage and is suspected to cause or perpetuate chronic liver disease. In order to evaluate the hepatotoxic effect of long-term therapy with oxyphenisatin 26 consecutive patients with rheumatoid arthritis were investigated for the presence of liver disease. In all cases, liver biopsy, biochemical liver function tests and determination of Hepatitis-B antigen were performed. Ten patients showed no pathological changes in the liver biopsy and a further 2 had only non-specific changes. Seven patients had fatty liver, 5 passive congestion, one haemosiderosis and only one had cirrhosis of the liver. No correlation was found between the activity of rheumatoid arthritis, and duration of the disease, the drug therapy given, and the liver damage.
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PMID:Morphological changes in liver biopsies from patients with rheumatoid arthritis. 93 24

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

A case of upper gastrointestinal tract hemorrhage secondary to esophageal varices in a patient with Felty's syndrome prompted a review of the pathogenesis and treatment of this condition. Six previously reported cases of this association were found. The clinical picture is that of long-standing rheumatoid arthritis with severe articular and extraarticular manifestations including splenomegaly, depression of the blood elements, mild liver function abnormalities, portal hypertension without cirrhosis or portal vein obstruction, an elevated splenic blood flow, and a reduction in portal hypertension by simple splenectomy. The presence of portal hypertension with varices may be another indication of splenectomy in patients with Felty's syndrome.
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PMID:Esophageal varices in Felty's syndrome: A case report and review of the literature. 108 37


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