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)

The immunological disturbances occurring as a result of liver disease have been studied in an animal model of cirrhosis. The mononuclear phagocytic cells of the normal liver phagocytose large amounts of antigen irrespective of whether that antigen is injected directly into the portal or into the systemic circulations. The liver therefore acts as a filter 'in series' and 'in parallel' with the spleen and reduces the immunogenicity of antigens entering the organism by either of these routes. In rats with hepatic cirrhosis, there is a reduction in the capacity of the liver to phagocytose the flagellar antigen of Salmonella adelaide. This results in increased stimulation of splenic lymphoid tissue and in an increased antibody response to this thymus-independent antigen. The increased antigenic stimulus to the spleen may also be responsible for the increased suppressor-cell activity which has been demonstrated in these rats, and may be the mechanism of the diminished cell-mediated immune response both in this animal model of cirrhosis and in the human disease state. These studies suggest that many of the immunological disturbances associated with chronic liver disease may be the result of maldistribution of antigen occurring because of impaired hepatic phagocytic capacity.
Clin Exp Immunol 1976 Dec
PMID:The immune response in cirrhotic rats. Antigen distribution, humoral immunity, cell-mediated immunity and splenic suppressor cell activity. 1 99

In 4 patients with cirrhosis and ascites, diuretic therapy resulted in an impairment of renal function that was associated with a rise in plasma renin activity (PRA). In 3, this occurred in the absence of volume depletion. When diuretics were discontinued, renal function returned to normal. beta-adrenergic blocking drugs were then given to suppress renin secretion and diuretics restarted. On this occasion, impairment of renal function did not occur. In 2 further patients, administration of beta-adrenergic blockers during a period of diuretic-induced renal impairment resulted in an improvement in renal function. Although these findings may indicate that diuretic-induced renal impairment in cirrhosis is at least partly due to activation of the renin-angiotensin system, in another group of patients a diuretic-induced rise in PRA was not associated with a deterioration in renal function.
Postgrad Med J 1979 Dec
PMID:Diuretic-induced renal impairment without volume depletion in cirrhosis: changes in the renin-angiotensin system and the effect of beta-adrenergic blockade. 4 11

"e" is a serum antigen associated with type-B hepatitis. It is found only in hepatitis B surface antigen (HBsAg) positive sera, but is antigenically distinct from HBsAg. e antigen was not detected in the serum of any of 99 cases of acute type-B hepatitis who recovered normally. Its antibody, anti-e, was found in 14 (14%). The antibody usually appeared before clearance of HBsAg and before appearance of HBsAb. Serum e was not detected in any of 29 symptom-free carriers of HBsAg, but 21 (73%) showed anti-e. Serum e was found in chronic active hepatitis (44%) and chronic persistent hepatitis (31%). The antibody, however, was detected in only 2 of 79 patients with chronic active hepatitis but in 7 (44%) of chronic persistent hepatitis. Serum e was not found in 5 patients with primary liver-cell carcinoma or 5 with inactive HBsAg-positive cirrhosis. The antibody was, however, found in all 5 of those with inactive cirrhosis and in 4 of the 5 with primary cancer. These results suggest that the presence of e antigen is associated with active and usually continuing liver disease. Anti-e, however, is associated with inactive liver disease and asymptomatic carriage of HBsAg, and its presence must be regarded as a valuable sign in predicting those who will escape progressive chronic liver disease.
Lancet 1975 Dec 13
PMID:Incidence and clinical significance of e antigen and antibody in acute and chronic liver disease. 5 57

In a patient with liver cirrhosis and severe hypersplenism resistent to corticosteroids splenectomy was attempted but proved impossible. Embolisation of the splenic artery with tiny fragments of absorbable gelatin sponge induced gradual restitution of haematological function to normal after 6 wk. Abdominal pain, paralytic ileus of short duration, transient pyrexia, and pleural effusion ensued but were well tolerated. The patient has remained well, 2 1/2 mo later. It is suggested that this simple method may prove rewarding and could safely be used, if necessary, more than once in patients for whom other treatments are unsuitable or have failed.
Lancet 1976 Dec 11
PMID:Treatment of hypersplenism by embolus placement in the splenic artery. 6 45

Eight patients with diuretic-resistant ascites due to cirrhosis were treated by reinfusion of concentrated ascitic fluid. In 11 procedures, with a mean duration of 21.9 hours, weight loss averaged 14.8 kg. Complications during reinfusion included septicemia in 1 procedure, left-sided heart failure in 5, pyrexia in 7 and coagulation abnormalities in 10. Ascites recurred within 2 months after reinfusion in all but one patient. Although this technique is an efficient and inexpensive method of treatment of ascites, it does not appear indicated in patients with cirrhosis and resistant ascites in view of the possibly serious complications associated with reinfusion and the poor long-term results.
Can Med Assoc J 1977 Dec 03
PMID:Treatment of resistant ascites by continuous ultrafiltration--reinfusion of ascitic fluid. 7 94

Sixteen cases of alcoholic hepatitis with alcoholic hyaline (Group I) and 13 cases without alcoholic hyaline (Group II) have been collected since 1970. These were most frequently found in the fifth decade in both groups. One female was found in Group I. Cases of about two-thirds of both groups were comsumers of 110 g or more of alcohol per day. No significant differences except fever and erythrocyte sedimentation rate were found in clinical and laboratory changes between both groups. Fatty change in liver biopsy specimens were more frequently seen in Group I than in Group II. The wedged hepatic venous pressure was markedly elevated in alcoholic hepatitis with cirrhosis and moderately elevated in alcoholic hepatitis without cirrhosis. Wedged hepatic venography showed the main portal trunk and extrahepatic collaterals, namely, reversal of the portal flow or such tendency in 2 out of 5 patients of Group I.
Tohoku J Exp Med 1977 Dec
PMID:Alcoholic hepatitis with and without alcoholic hyaline. 7 93

The prevalence of serological markers of active of past hepatitis-B virus (H.B.V.) infection was determined in 80 Greek patients with primary hepatocellular carcinoma (P.H.C.), 160 age and sex matched controls and 40 patients with metastatic liver cancer (M.L.C.). The relative risk of the various patterns of H.B.V. serological markers for P.H.C. was calculated. Active H.B.V. infection, as indicated by positive tests for hepatitis-B surface antigen (HBsAg), or antibody to hepatitis-B core antigen (anti-HBc) without antibody to HBsAg) (anti-HBs), was associated with P.H.C. (relative risk 10.4) but not with M.L.C. (relative risk 1.2). Patients without markers and those who had recovered from hepatitis B (anti-HBs-positive) had approximately the same low risk for P.H.C. (relative risk 0.8). Active infection was more common in P.H.C. patients with co-existing cirrhosis than in those without cirrhosis (67% versus 26%). Thus the relationship between active hepatitis B and P.H.C. seen in African and Asian populations is now seen in a European Caucasian population with different racial, environmental, and dietary circumstances.
Lancet 1978 Dec 09
PMID:Hepatitis B and primary hepatocellular carcinoma in a European population. 8 32

Grossly raised levels of tumour related vitamin B12 binding protein, reflected by rises in serum vitamin B12 and unsaturated vitamin B12 binding capacity (UBBC), were found in three of 44 patients with hepatocellular carcinoma. All three were HBsAg negative and had normal serum alpha fetoprotein levels. The patients did not have underlying cirrhosis and the tumours contained characteristic intracellular inclusions. In the first patient the UBBC level fell during a partial remission induced by adriamycin therapy and in the second patient UBBC levels rose with progression of her disease. In the third patient serum B12 binding protein levels fell after tumour resection. Assay and subsequent monitoring of serum vitamin B12 and UBCC may prove valuable in the assessment and follow-up of some patients with hepatocellular carcinoma whose alpha fetoprotein levels are normal.
Gut 1978 Dec
PMID:Vitamin B12 binding protein as a tumour marker for hepatocellular carcinoma. 8 76

The relationships among collateral veins, gastroesophageal varices, extrahepatic shunting, and free portal pressure were studied by percutaneous transhepatic portography in 57 patients with cirrhosis of the liver. The size of esophageal varices was related to the size of the coronary and short gastric veins and to the portal pressure. The size of gastric varices was related to cephalad collaterals from the spleen and splenic vein, but not to portal pressure. Portosystemic shunting was associated with collaterals in the lower abdomen, but not with varices or portal pressure.
AJR Am J Roentgenol 1979 Dec
PMID:Percutaneous transhepatic portography. III. Relationships between portosystemic collaterals and portal pressure in cirrhosis. 11 3

A rise in plasma growth hormone (GH) after thyrotrophin-releasing hormone (TRH) and a striking reduction after dopaminergic drugs is present in acromegalic ('responder') patients. We have investigated the GH response to dopaminergic stimuli in two conditions of animals and man, which, like acromegaly, are characterized by a TRH-induced GH rise, i.e. rats with electrolytic lesions of the median eminence (ME) and patients with hepatic cirrhosis. In addition, we have studied the TRH-induced GH rise in rats with ME lesions, in the cirrhotic patients and in a group of 'responder' acromegalics before and after administration of dopaminergic drugs. In rats with ME lesions an infusion of dopamine (DA) neither modified baseline GH levels nor the TRH-induced GH rise. In five out of six cirrhotic patients oral administration of L-Dopa was followed by the usual rise in plasma GH. infusion of DA increased plasma GH levels in three out of seven cirrhotic patients and in four out of five subjects an earlier GH rise after TRH was seen. However, in the 'responder' acromegalics, the infusion of DA, besides lowering baseline plasma GH, was capable of reducing the TRH-induced GH rise. Collectively these data indicate that the TRH-induced GH rise emphasizes defects in the neurohormonal links between the central nervous system and the anterior pituitary. Instead, the paradoxical fall of GH after dopaminergic drugs appears to be a prerequisite of acromegaly and may be attributable to receptors for DA located on the tumorous tissue.
Clin Endocrinol (Oxf) 1979 Dec
PMID:Interaction between the thyrotrophin-releasing hormone-induced growth hormone rise and dopaminergic drugs: studies in pathologic conditions of the animal and man. 11 94


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