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

A total of 301 Black patients without rheumatic diseases was studied to estimate the prevalence and causes of positive rheumatoid factor. The latex slide test was positive in 25% of patients and 21% had a 'diagnostic' titre of 80 or more. A significant relationship between gamma-globulin levels and rheumatoid factor positivity was demonstrated. IgG appeared to be the most important in determining this relationship. The most common ailments among sero-positive patients were cirrhosis and tuberculosis.
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PMID:Rheumatoid factor in non-rheumatoid black patients. 6 47

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

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

The long-term clinical course of patients with primary Type II essential mixed cryoglobulinaemia is unclear as many reports fail to separate this group from patients with Type III disease. We have reviewed 13 patients with Type II essential mixed cryoglobulinaemia who presented to the Hammersmith Hospital between 1976 and 1990. All patients had a cryoglobulin level greater than 0.1 mg/ml (range 0.27-6.50 mg/ml), and characterization of the cryoglobulin in all cases revealed the presence of a monoclonal IgM kappa component with rheumatoid factor activity together with polyclonal IgG. All patients had evidence of activation of the classical pathway of complement with greatly reduced levels of C4, while C3 levels were moderately reduced in three patients. All patients had skin disease and joint symptoms were reported by nine patients, with erosive arthritis in one. Eight patients had peripheral sensorimotor neuropathy. Renal disease was observed in 10 patients, manifesting as raised creatinine level, proteinuria or haematuria. Renal tissue was examined in eight patients: in six the appearances were those of a mesangiocapillary glomerulonephritis Type I while in the other two patients there was a mesangioproliferative glomerulonephritis, in one diffuse and in the other focal and segmental. Glomerular capillary 'hyaline thrombi' were found in six biopsies, extracapillary proliferation was found in three and evidence of vasculitis was found in all eight. Liver biopsy showed macronodular cirrhosis in one patient, while a second with recurrent episodes of jaundice showed only chronic inflammatory changes. No patient was positive for hepatitis B surface antigen; however one patient had low titre anti-hepatitis B surface antibody. Normochromic normocytic anaemia was present in nine patients. Bone marrow examination was carried out in 13 patients at presentation to our unit: 10 showed no evidence of a lymphoproliferative disorder, while three suggested the presence of a non-Hodgkin's lymphoma (some years after original presentation in all three). Unusual clinical features included one patient with retinal vasculitis and one patient with severe pulmonary haemorrhage.
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PMID:Type II essential mixed cryoglobulinaemia: presentation, treatment and outcome in 13 patients. 162 Aug 12

A human B cell subpopulation identifiable by the expression of the cell surface antigen Leu-1(CD5) was examined in peripheral blood lymphocytes obtained from patients with various liver diseases by dual two-color fluorescence flow cytometry. A significantly high level of Leu-1 B cells in chronic hepatitis and in liver cirrhosis especially in hepatitis B surface antigen (HBsAg)-positive patients (hepatitis B virus carriers) was observed. However, there was no significant difference between the percentage in controls and those in patients with acute hepatitis and primary biliary cirrhosis. Moreover, we could not demonstrate a correlation between the incidence of these cells and positive IgM class rheumatoid factor in patients with liver diseases. The percentage of Leu-1 B cells in patients who had been receiving prednisolone at the time of this study was lower than that in healthy controls. These results suggested that Leu-1 B cells might be associated with the continuation of the HBsAg-positive state and that the presence of the Leu-1 B cell population might be modified by prednisolone administration.
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PMID:Leu-1(CD5) B cell subpopulation in patients with various liver diseases--special reference to hepatitis B virus carrier and to changes caused by prednisolone therapy. 246 4

The origin of leukocytoclastic vasculitis (LV) being often difficult to determine, we have undertaken since 1980 a prospective study of factors associated with LV. We selected 53 patients whose LV was clinically predominant, and excluded patients in whom LV was an expected phenomenon in a known autoimmune or infectious disease. Twenty-eight of the 53 patients presented with a typical Gougerot-Ruiter disease, 15 with a bullous or necrotic form of the disease and 10 with urticarial lesions. Detail of the prospective laboratory tests performed is given in table I. Correlations between laboratory values and LV-associated factors were significant with the decrease of complement but not with the presence of circulating immune complexes, rheumatoid factor, cryoglobulin or direct immunofluorescence test positivity. Most of the associated factors in our series were infectious agents (streptococci, hepatitis virus), immunological agents (rheumatoid factor, cryoglobulin) or drugs known to be potential LV-inductors; other factors were less common or quite recently described (enterovirus, Yersiniae, cirrhosis, primary liver cancer, Chlamydiae, refractory anemia with an excess of myeloblasts. We do not feel that a large series of laboratory tests should be performed in every case of LV. The clinical context and simple laboratory tests, such as blood cell count, complement assay, plasma electrophoresis and a search for rheumatoid factor should be enough to guide the clinician and help him decide whether further investigations are needed. However, it should be noted that in some cases without clinical pointers only full virological evaluation enabled us to determine that enteroviruses may be involved in the pathogenesis of LV.
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PMID:[Prospective study of factors associated with leukocytoclastic vasculitis]. 336 10

Serum Clq binding activity (ClqBA) is increased in diabetes mellitus with liver injury, carcinoma of gastrointestinal tract with metastatic liver and chronic liver disease (CLD). Significant elevations of ClqBA level are observed in the order of liver cirrhosis, chronic aggressive hepatitis and chronic persistent hepatitis. In CLD there are significant correlations between ClqBA and gamma-globulin, rheumatoid factor, anti-DNA-antibody, CH50, C3, C4, C3-activator and HBsAg.
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PMID:Studies on circulating immune complexes of the liver disease. 4. Clq binding activity. 615 28

beta 2 Microglobulin levels were measured by radioimmunoassay in the serum of 160 patients with liver disease and compared to 63 normal controls and 75 asymptomatic HBs-Ag carriers. All the latter subjects had normal values. Elevated serum beta 2 microglobulin levels were found in most of the other categories: acute viral hepatitis (35/45); chronic persistent (8/26) or active (35/41) hepatitis and liver cirrhosis (27/38). beta 2 Microglobulin values were significantly lower in chronic persistent hepatitis than in the three other groups (p less than 0.05). Steroid therapy was followed by reduction of serum beta 2m levels in 11/11 cases of chronic active hepatitis, eight of whom returned to normal value. Although linked to the course of the disease, variations of beta 2 microglobulin were independent of transaminases, bilirubin and gamma globulins. Elevated serum beta 2 microglobulin correlated with demonstration of rheumatoid factor but not with detection of circulating immune complexes, hepatitis B virus markers or autoantibodies. The results suggest that elevation of serum beta w microglobulin is encountered mostly in the active forms of inflammatory liver diseases.
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PMID:Elevation of serum beta 2 microglobulin in liver diseases. 616 10

Inhibition assay of 125I-C1q binding to IgG-p-azobenzamidoethyl Sepharose 6B (IgG-Sepharose) by immune complexes was developed for the detection of circulating soluble immune complexes in the liver disease and was compared with polyclonal rheumatoid factor (pRF) binding inhibition assay and with C1q binding assay. The C1q inhibition assay was proved to be very sensitive, reproducible and rapid. Sucrose density gradient ultracentrifugal analysis showed that the assay could detect aggregates of human IgG (AHGG) larger than 19s. C1q inhibition activity (C1qIA) correlated with severity of the liver disease, defined by histological criteria. The highest C1qIA was observed in sera of patients with primary biliary cirrhosis, followed by liver cirrhosis, fulminant hepatitis, chronic aggressive hepatitis (2B), lupoid hepatitis and hepatocellular carcinoma in the order. There were correlations of C1qIA with serum gamma-globulin levels, sero-positivity for rheumatoid factor and hepatitis B surface antigen, and significant correlations existed also among pRFIA, C1qIA and C1qBA. Ultracentrifugal analysis of sera from patients with the liver disease showed that ClqIA demonstrated two sizes of immune complexes, 7s and larger than 19s, while complexes larger than 8s were seen in pRFIA.
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PMID:Studies on circulating soluble immune complexes of the liver disease. 6. Comparative studies of 125I-pRF inhibition assay, 125I-Clq inhibition assay and 125I-Clq binding assay. 697 71

The clinical course of 40 patients with significant quantities of mixed cryoglobulins, but without lymphoproliferative, collagen-vascular or chronic infectious diseases, is presented. These cases comprise 51.3 percent of all mixed and 31.7 percent of all types of cryoglobulins evaluated by us over the period 1960--1978. A characteristic clinical syndrome, consisting of recurrent palpable purpura (100 percent), polyarthralgias (72.5 percent) and renal disease (55 percent), was seen. Biopsy specimens of skin lesions showed cutaneous vasculitis, and half had immune reactants in vessel walls. Seventy percent of patients had evidence of hepatic dysfunction, often subclinical, and more than 60 percent of those tested had serologic evidence of prior infection with hepatitis B virus. Hepatic lesions ranged from minimal triaditis to chronic active hepatitis and/or cirrhosis. All 22 patients in whom clinical renal disease developed had significant proteinuria; 63.6 percent had diastolic hypertension, 77.3 percent edema, 45.5 percent renal failure and 22.7 percent were nephrotic. Glomerular disease associated with deposition of immunoglobulin G, immunoglobulin M and complement, often with coexistent renal arteritis, was confirmed pathologically in 15 cases. All cryoglobulins had rheumatoid factor activity and consisted of IgM and polyclonal IgG; five also contained IgA. Thirteen had a monoclonal IgM kappa component. Serum protein electrophoresis was unremarkable or showed diffuse hyperglobulinemia. Striking depression of early complement components was noted but did not correlate well with the cryoprotein concentration, renal involvement or clinical course. Follow-up for periods up to 21 years from onset of symptoms revealed that renal involvement has a deleterious effect on prognosis. Postmorten examinations of nine patients demonstrated widespread vasculitis in addition to renal involvement. Preterminal infection was found in eight.
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PMID:Mixed cryoglobulinemia: clinical aspects and long-term follow-up of 40 patients. 699 82


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