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Biomedical subjects

C M Leevy

Publications and source records attributed to C M Leevy.

At least 19 recordsLinked to original sources
PubMed1998

Viral hepatitis C.

Identification of a cDNA clone and the genome of hepatitis C virus in 1988-1989 allowed the development of clinical tests that are now used to detect and quantify hepatitis C virus. This has largely eliminated post-transfusion hepatitis C virus infection; however, the overall incidence of chronic hepatitis C and its complications has greatly increased because of its transmission by other means, lack of a protective vaccine, and inadequate virucidal therapy. Drug abuse is the most common cause of hepatitis C; an etiologic mechanism, however, remains unknown in one third of patients referred to the New Jersey Medical School Liver Center. Response to treatment depends on the viral subtype, immune reactivity of the host, and hepatic pathologic alterations. Many patients with hepatitis C improve or are cured by administering an interferon with or without ribavirin; patients refractory to these measures exhibit persistent elevation of serum cytokines and progressive liver disease. New measures, including protease inhibitors and adjunct immunotherapy, should increase effectiveness of therapy, diminishing hepatitis C virus-induced cirrhosis and hepatocellular cancer. Populations, including the underserved, who harbor and transmit hepatitis C virus require special assistance. This is best achieved by community support groups organized through medical schools, physician associations, and churches to help prevent, detect, and treat chronic hepatitis C.

Acquired Immunodeficiency Syndrome↗
PubMed1994

The founding and development of New Jersey Medical School.

The need to address the social and biological aspects of medicine was emphasized at the founding of New Jersey Medical School in 1954. This need has remained a major goal, as the sponsorship, name, and location of the Medical School have changed with the times.

Biology↗
PubMed1994

Alcoholic liver disease.

Alcoholism alone, or in combination with other etiologic factors, is a common cause of liver failure because of hepatitis, cirrhosis, and/or hepatocellular cancer. Encountered morphologic and functional alterations are due to immunologic reactivity to cell injury evoked by acetaldehyde, other noxious factors, and nutrient deficits. Less than 20% of subjects who consume over 90 g/d of ethanol for years develop progressive liver damage and cirrhosis. Alcoholism should be interrupted in patients with subclinical hepatic abnormalities. Although early alcoholic hepatitis and cirrhosis respond to abstinence and symptomatic therapy, available measures have little influence on functional and morphologic abnormalities in end-stage alcoholic liver disease. Resection is desirable for localized hepatocellular cancer, and liver transplantation should be considered for cirrhosis. Transplantation is appropriate for patients with uncomplicated end-stage alcoholic cirrhosis in whom evidence of liver failure can be controlled during a 6-month period of rehabilitation. Continuous psychosocial support is required to prevent recividism in the posttransplant immunosuppressed alcoholic.

Ethanol↗
PubMed1990

Excess vitamin A injures the liver.

Chronic vitamin A intoxication in a 56-year-old female is reported. Some abnormal blood chemistries included elevated transaminase and alkaline phosphatase, increased cerebrospinal fluid and portal pressure, and elevated vitamin A in blood and liver. A liver biopsy indicated histologic evidence of perisinusoidal collagen deposition and noncoalescent fat droplets in Ito cells. Caution against the misdiagnosis of alcoholic cirrhosis for vitamin A intoxication is recommended.

Diagnosis, Differential↗
PubMed1990

Use of a specific monoclonal antibody to detect Mallory bodies in liver disease.

Mallory bodies (MBs), which are common in alcoholic hepatitis, primary biliary cirrhosis and liver disease associated with Type II diabetes mellitus, are often difficult to find on liver biopsy specimens or to predict from clinical or biochemical studies. Immunofluorescence studies with anti-NMB-1, a Mallory body-specific monoclonal antibody, indicate that this is a sensitive method for recognizing Mallory bodies in cryostat sections of liver from griseofulvin-treated mice or patients with liver disease. Validity of the leukocyte migration test, which facilitates detection and monitoring of patients who harbor Mallory bodies, is confirmed by pretreatment of Mallory bodies with anti-NMB-1. Prevention of Mallory body-induced migration inhibition by addition of anti-NMB-1 indicates that this effect is not due to inactivation of leukocytes by a Mallory body contaminant. Anti-NMB-1, developed using standard hybridoma techniques, does not react with normal hepatocytes or other cells. Investigations with SDS polyacrylamide gel electrophoresis and western blotting reveal that it exhibits binding with 62, 55, 42 kd peptides, and four other bands in the range from 40 to 30 kd from the Mallory bodies. The NMB-1 epitope which facilitates morphologic and clinical detection of Mallory bodies is distinct from cytokeratin and appears to be responsible for its immunogenicity.

Animals↗
PubMed1989

Effect of peritoneo-venous shunt on portal pressure.

The cause of variceal bleed after a peritoneo-venous shunt is not known. Portal haemodynamic consequences of a peritoneo-venous shunt are poorly understood. The most critical period after a peritoneo-venous shunt is the early postoperative period when rapid mobilisation of peritoneal fluid occurs. Serial changes in the portal pressure during the early postoperative period have not been recorded. In the present study preoperative wedge hepatic vein (WHV), right atrial (RA) and pulmonary capillary wedged (PCW) pressures, cardiac index (CI), and plasma volume (PV) were measured in five alcoholic cirrhotic patients with tense ascites for up to 20 hours postoperatively. The longterm effect was assessed by repeating the intrahepatic and/or wedged hepatic vein pressures in three of the surviving patients after 10 to 20 months. A significant increase in the circulatory dynamics and portal pressure was seen within two hours after shunt placement. Wedged hepatic vein pressure increased from 27.6 (8.2) mmHg to 37.2 (9.2) mmHg (p less than 0.01), RA pressure increased from 6.8 (1.5) mmHg to 14.0 (4.3) mmHg (p less than 0.05), PCW increased from 7.2 (3.5) mmHg to 19.3 (5.7) mmHg (p less than 0.01), CI increased from 3.4 (0.27) lit/m2/min to 4.3 (0.85) lit/m2/min (p less than 0.05). This was accompanied by a 34% increase in the plasma volume from 1838.5 (142.1) to 2471.4 (210) ml/m2. These derangements were maintained up to 20 hours postoperatively. After 10 to 20 months, repeat measurements revealed a return to preoperative measurements. It is concluded that there is an acute increase portal pressure after a peritoneo-venous shunt attributed to increased circulation plasma volume, resulting from rapid mobilisation of ascitic fluid after the shunt. A sudden increase in portal pressure might be an important provoking factor for variceal bleeding after peritoneo-venus shunt.

Blood Pressure↗
PubMed1986

[Intrahepatic cholestasis: modulation by immunological factors?].

The mechanism of intrahepatic cholestasis in active liver disease has not yet been elucidated. Recent investigations in type II drug-induced hepatitis have suggested that lymphocytes produce a cholestatic factor. The authors' studies on lymphocyte cultures of patients with alcoholic hepatitis and acute viral hepatitis suggest that cellular immune phenomena may be of general significance in the pathogenesis of intrahepatic cholestasis. Supernatants of cultured lymphocytes of patients with alcoholic and acute viral hepatitis reduced bile flow and bile acid excretion in a rat model, provided that the lymphocytes had been previously stimulated by the appropriate antigen. An identical cholestatic effect was seen using sera of these patients. The pathogenetic mechanism of this lymphocytic factor is still unknown.

Animals↗
PubMed1986

Erythroderma with fulminant hepatitis: a possible association.

Exfoliative dermatitis or erythroderma may be a sign of systemic disease, usually a T-cell lymphoma, although other malignancies may also be associated. We observed two patients in whom severe hepatitis and an exfoliative dermatitis occurred simultaneously. We believe that this association has not been reported previously.

Adult↗
PubMed1984

Platelet-associated IgG in hepatitis and cirrhosis.

Increasing evidence is accumulating which indicates that immunological abnormalities contribute to the development of liver disease and its signs and symptoms. Platelet-associated IgG (PAIgG) levels were quantified in 42 patients with biopsy-proven liver disease of various etiologies to determine the relationship of thrombocytopenia to immunologic abnormalities in these disorders. Five of six nonthrombocytopenic patients with acute viral hepatitis B had elevated PAIgG. Six of ten patients with chronic active hepatitis had elevated PAIgG and thrombocytopenia. In contrast, only one of six patients with chronic persistent hepatitis had elevated PAIgG. Nine of ten patients with alcoholic hepatitis had elevated PAIgG; seven of the nine were thrombocytopenic. Seven of ten alcoholic patients with cirrhosis had elevated PAIgG; six of seven were thrombocytopenic. Thus the increase in PAIgG may be present without thrombocytopenia in acute liver injury, while patients with chronic persistent hepatitis do not usually exhibit this abnormality. Severe chronic active liver disease is accompanied by thrombocytopenia and an increase in PAIgG levels.

Biopsy↗
PubMed1984

Cardiac function in alcoholics with cirrhosis: absence of overt cardiomyopathy--myth or fact?

Cardiomyopathy in alcoholics is considered to be associated with a low incidence of hepatic cirrhosis. To evaluate cardiac hemodynamics in alcoholic liver disease, left ventricular function in 37 patients with hepatic cirrhosis (group II) was compared with that in 13 normal subjects (group I) matched for age, sex and cardiac size. These groups were contrasted with group III, comprising 32 alcoholics without cirrhosis who had cardiac symptoms but no cardiomegaly or heart failure. Patients with cirrhosis as a group did not differ from normal subjects (group I) in terms of left ventricular filling pressure and cardiac muscle and pump function (cardiac index). However, subgroup IIA (n = 21) had a stroke index significantly less than normal, while subgroup IIB had a significantly increased stroke index and myocardial cardial contractility with a diminished systemic arterial resistance. Similar hepatic abnormalities were present in both subgroups. In group III, left ventricular end-diastolic and aortic mean pressures were significantly elevated compared with values in normal subjects, while cardiac index and indexes of ventricular contraction and relaxation were abnormal. Further examination of patients with cirrhosis indicated that the responses to volume or pressure increments in terms of the level of stroke work for a given filling pressure were most abnormal in group IIA, approximating those of group III. Thus, although overt cardiomyopathy is infrequent in patients with cirrhosis, asymptomatic myocardial disease may assume clinical importance during volume or pressure overload.

Blood Pressure↗
PubMed1984

Studies of the influence of immunological and serological factors from patients with cholestasis due to alcoholic or viral hepatitis on biliary function in the rat.

Studies were undertaken to determine if cholestasis in alcoholic or viral hepatitis is related to immunologic hyperreactivity as suggested for cholestasis due to type-II drug-induced hepatitis, and evaluate possible mechanisms involved in lymphokine-induced cholestasis. Results indicate that a cholestatic factor exists in alcoholic and acute viral hepatitis. Supernatants of lymphocytes from patients with alcoholic hepatitis stimulated by an extract of alcoholic hyalin evoked a 28% +/- 7.3 SEM reduction in rat bile flow (P less than 0.03). Supernatants of lymphocytes from patients with acute viral hepatitis activated by liver-specific protein caused a reduction in rat bile flow of 24% +/- 5.9 SEM (P less than 0.03). A decrease in bile flow also occurred following injections of sera from patients with alcoholic or acute viral hepatitis. In contrast, injection of supernatants of non-stimulated lymphocytes or those from chronic active hepatitis or healthy subjects did not produce a significant change in bile flow. Supernatants of stimulated lymphocytes from tuberculin-sensitized guinea pigs caused a similar decrease in rat bile flow and reduced excretion of human secretory immunoglobulin A (IgA). Despite reductions in rat bile flow there were no alterations in liver morphology, liver plasma membrane Na-K-ATPase activity, microsomal cholesterol-7 alpha-hydroxylase activity or low-dose indocyanine green clearance during the period of observation.

Adult↗
PubMed1984

Hepatocellular carcinoma in the alcoholic.

The conversion of alcoholic hepatitis into cirrhosis and the eventual development of hepatocellular carcinoma (HCC) has been documented by serial biopsies in patients with uncomplicated alcoholism. Ethanol toxicity, nutritional deficiency and immunological abnormalities in a genetically predisposed individual appear to account for this sequence which can be accelerated by the hepatitis B virus and other noxious agents. Immune deficiency in malnourished alcoholics with liver disease diminishes response to the hepatitis B vaccine and may contribute to the development of HCC. Antigenic moieties in Mallory bodies appear to contribute directly to cytotoxicity and fibrosis in alcoholics, and may act like proto-oncogens. Available Mallory-body-specific monoclonal antibodies will hopefully facilitate diagnosis and treatment. Studies of DNA and collagen synthesis by in vitro perfusion of percutaneous liver biopsies provide information on precursor lesions of HCC. Abstinence, nutrient therapy and drug-induced anabolism lead to repair of liver damage and correction of immunological abnormalities, both of which may contribute to development of HCC in alcoholics with cirrhosis.

Carcinoma, Hepatocellular↗
PubMed1983

Hepatic proline after bile duct ligation in rats.

Since biliary hyperplasia of fascioliasis correlated with hepatic proline level, we examined the occurrence of a similar chemical stimulus during bile obstruction. Uptake of tritiated proline and glycine rose in both hepatocytes and a bile duct enriched cell fraction, following duct ligation in rats. The increased hepatic content of proline but not glycine suggests that proline has a role in post-obstructive biliary proliferation.

Animals↗