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Biomedical subjects

S Sherlock

Publications and source records attributed to S Sherlock.

At least 73 records · Page 4Linked to original sources
PubMed1987

Hepatic transplantation.

In this article hepatic transplantation is discussed with respect to selection of patients, indications and contraindications, the donor and recipient operation, complications, and results.

Child↗
PubMed1987

Hepatocellular carcinoma and the hepatitis B virus: a study of British patients.

We have examined the relationship between hepatitis B virus infection and hepatocellular carcinoma in a series of 50 British patients with histologically-proven hepatocellular carcinoma. Serum HBsAg was detected in 10 patients (20 per cent), and of the remainder, 21 per cent of those tested had serological evidence of past hepatitis B virus exposure. None of nine tumour specimens from serum HBsAg negative patients had detectable HBV-DNA integration into the tumour cell genome. The presence or absence of serum HBsAg was of no prognostic significance in British patients with hepatocellular carcinoma. Liver cell dysplasia, a possible pre-malignant lesion, was noted in 53 per cent of patients who had had liver biopsies before the diagnosis of hepatocellular carcinoma, and in 79 per cent of biopsies taken at the time of diagnosis of hepatocellular carcinoma. The presence of liver cell dysplasia was not more common in serum HBsAg positive patients.

Adolescent↗
PubMed1987

The natural history of hepatitis B.

Hepatitis B infection is acquired through contact with the blood of a person carrying the hepatitis B virus. The carrier rate of HBsAg varies world-wide. In many endemic areas, infection is largely acquired perinatally, while in other areas of high prevalence, transmission occurs during childhood, with intrafamilial spread being particularly important. Subclinical hepatitis B attacks are extremely frequent. The unusual clinical episode diagnosed in the adult tends to be more severe than that for virus A or non-A, non-B infection although the overall picture is similar. A fulminant course may be related to an enhanced immune response, and in such instances, HBsAg titres may be low or undetectable. About 10% of patients suffering an acute attack, more commonly males, will not clear the virus and will become chronic carriers. These may remain 'healthy' or suffer from various grades of chronic hepatitis and cirrhosis. Chronicity is related to impairment of humoral and cell-mediated immunity. There are two phases of hepatitis B infection, the replicative and the integrated, the former being recognized by the presence of hepatitis B viral DNA in serum. Relapses of chronic hepatitis B may be related to conversion from replicative to integrated stages, to spontaneous reactivation, or to super-added virus infection, especially with delta virus.

Hepatitis B↗
PubMed1986

The spectrum of hepatotoxicity due to drugs.

Drugs in common use can cause toxic effects on the liver which can mimic almost every naturally occurring liver disease in man. Drugs can have direct (metabolite-related) toxic effects; they can also cause deposition of microvesicular fat in hepatocytes; or they can provoke reactions resembling acute alcoholic hepatitis (phospholipidosis) or acute viral hepatitis. Hepatotoxicity can also be part of a general hypersensitivity reaction, or hepatic fibrosis or cholestasis can predominate. Drugs can lead to almost any type of vascular disease in the liver and to benign and malignant tumours.

Acute Disease↗
PubMed1986

Viral hepatitis.

Developments over the last four years in our understanding of viral hepatitis are analyzed. The molecular structure of hepatitis A has been established, and vaccines for prevention are under development. The recognition of the replicative and integrated stages of hepatitis B infection has allowed more rational approaches to therapy. Vaccines are of proven value. Delta virus infection has assumed an important role world wide as a cause of serious and fulminant liver disease in hepatitis B carriers. The agents for non-A, non-B virus hepatitis have eluded identification. These are important causes of chronic liver disease particularly in recipients of blood transfusion.

Carrier State↗
PubMed1986

Hepatobiliary fibropolycystic diseases. A clinical and histological review of 51 patients.

The clinical, radiological and hepatic histological features of 51 patients with hepatobiliary fibropolycystic disease were reviewed. Many of the patients had more than one of the diseases; the combination of both congenital hepatic fibrosis (CHF) and Caroli's disease was most striking. Twelve patients with CHF (50% male) presented at 6 +/- 2 years of age (mean +/- SEM) with hepatosplenomegaly or variceal bleeding. Their main problems were recurrent variceal bleeds and renal disease. Polycystic kidneys and renal stones were present in 79% and chronic renal failure in 30%. Six of the 8 patients with Caroli's disease were male (75%) and presented later (aged 37 +/- 8 years) with hepatomegaly or cholangitis. Recurrent cholangitis developed in most (7/8) and 2 had polycystic kidneys. Twelve patients had a combination of CHF and Caroli's disease presenting with hepatosplenomegaly, bleeding or cholangitis. As in Caroli's disease, most (83%) were male, but the age of presentation (15 +/- 4 years), and the incidence of polycystic kidneys (42%) and renal failure (8%) was intermediate between CHF and Caroli's disease. In these patients, bleeds always predated cholangitis. Histologically, acute cholangitis was superimposed on the changes of CHF. Adult polycystic liver disease (10 patients) presented later (43 +/- 3 years) in females (90%) with pain, a mass or incidentally; polycystic kidneys were present in 33%. Microhamartomas (10 patients), which were usually incidental findings, were diagnosed latest (50 +/- 6 years). Three choledochal cysts were seen. The hazard of cancer in these diseases was reflected by 2 bile duct cancers and 1 pancreatic cancer (incidence 6%). This study has confirmed that hepatobiliary fibropolycystic diseases form part of a family and are often associated together. However, the diseases are of greatly differing severity and the prognosis in an individual patient is determined by the fibropolycystic diseases present.

Adolescent↗
PubMed1986

Serum autoantibodies, ulcerative colitis and primary sclerosing cholangitis.

The aetiology of primary sclerosing cholangitis is unknown, but it is closely associated with ulcerative colitis. Serum anticolon antibodies, crossreacting with portal tracts, have been reported in patients with ulcerative colitis but no studies have been carried out in primary sclerosing cholangitis. The frequency of serum anticolon antibodies and portal tract antibodies have been measured in 24 patients with primary sclerosing cholangitis and ulcerative colitis; 15 patients with primary sclerosing cholangitis without ulcerative colitis; 77 patients without primary sclerosing cholangitis: 25 patients with Crohn's colitis; 10 patients with primary biliary cirrhosis; 22 patients with extrahepatic biliary obstruction and 20 normal controls. Serum anticolon and portal tract antibodies were detected using immunoperoxidase techniques on normal colon and obstructed human liver. Tissue typing was undertaken using a standard microcytotoxicity technique. The frequency of anticolon antibodies was markedly increased in primary sclerosing cholangitis patients with ulcerative colitis (62.5%) compared with patients with ulcerative colitis (17%) and Crohn's colitis (16%) (chi 2 = 17.9; p less than 0.001). The antibodies were almost entirely of IgG and IgA classes in all groups. Anticolon antibodies were not found in sera from any other group. Sera from eight of 15 patients with primary sclerosing cholangitis, ulcerative colitis and anticolon antibody reacted with portal tracts of human obstructed liver. This reaction was also seen in four of nine patients with ulcerative colitis and primary sclerosing cholangitis and in three of 15 patients with primary sclerosing cholangitis alone. Portal tract antibody was of IgG class and was not present in sera from any other groups. Unlike anticolon antibody, there was a close relationship between HLA-B8 phenotype and the portal tract antibody (p<0.02; chi 2 = 6.04). Absorption studies confirmed that the anticolon antibody is distinct from portal tract antibody.

Autoantibodies↗
PubMed1986

Cannon lecture. The impact of radiology on hepatology.

Because of remarkable advances in diagnostic imaging and the development of a variety of useful interventional techniques, radiology now plays a central role in the diagnosis and treatment of patients with hepatic disease. These include focal, vascular, and metabolic liver diseases, abnormalities of the biliary tract, and conditions associated with hepatic transplantation. Thus, optimal care of patients with liver disease now requires that there be close cooperation between the two specialties.

Angiography↗
PubMed1985

Treatment of chronic hepatitis due to hepatitis B virus.

A clearer view of the natural history of chronic hepatitis B virus (HBV) infection has permitted recognition of a phase of viral replication associated with progressive liver damage, and one of absent replication when the disease is inactive and when continued presence of hepatitis B surface antigen (HBs) is due to the integration of viral genes with the host genome. These two phases can be identified by HBe antigenaemia and anti-HBe, respectively. Several active antiviral drugs are available and may significantly benefit certain HBe Ag-positive groups. The antiviral activity of vidarabine and its analogues and of alpha-interferons is established, and insight is being gained into factors that predict response. In general, results depend on duration of infection, and integrity of the patient's immune response. Anti-HBe positive carriers usually need no treatment, but in those with continuing low-level HBV replication or delta superinfection antiviral therapy, although of unproven value, may be tried. In patients without HBV or hepatitis delta virus (HDV) replication who have signs of active disease, immunosuppressants may be tried with benefit.

Acyclovir↗
PubMed1985

The effect of liver disease on factors V, VIII and protein C.

The components of the factor VIII complex were estimated by immuno- and bioassays in 85 patients with liver disease. The plasma concentrations of the antigens were elevated in 65% (VIII:CAg) and in 76% (VIIIR:Ag) of patients while the biological activities were elevated in only 14% (VIII:C) and 15% (VIII:RiCof). There was no correlation with C-reactive protein, used as a measure of an acute phase reaction (X2 = 0.7; P = 0.1); or with severity of liver disease as judged by prothrombin ratio (P = 1.0) but highest values were observed in patients with cholestatic liver disease. Following parenteral vitamin K there was a significant fall in both the biological activity of VIIIC (36%) and of VIII:CAg (38%) in 13 vitamin K deficient patients (P less than 0.001) but no change in 23 vitamin K replete patients or in the VIIIR:Ag levels in either group. Factor V levels were lower in patients with parenchymal liver disease (0.54 +/- 0.1 units/ml, mean +/- SEM, n = 12; normal range 0.5-1.5 units/ml) than in patients with extrahepatic cholestasis who were vitamin K deficient (1.2 +/- 0.1 units/ml, P less than 0.0001). The levels of protein C antigen, the vitamin K dependent protease which inactivates factors VIII:C and V, was at the lower end of the range in both groups (0.7 +/- 0.1, mean +/- SEM, n = 18, normal range 0.74-1.4 units/ml). There was no significant change in either protein C antigen or factor V following vitamin K. The discrepancy between the biological activity of factor VIII and the antigen levels could represent accumulation of partially degraded factor VIII or production of a hypoactive form. There is no evidence that the reduction in VIIIC and VIII:CAg following vitamin K was mediated by protein C.

Adolescent↗
PubMed1985

Acute and chronic viral hepatitis revisited.

Hepatitis A is an acute fecal-spread disease without chronicity. Gamma immunoglobulin is preventative. Eventually a vaccine will be used for those in developed countries, who have not acquired antibody in childhood. Hepatitis B is a blood-borne disease which can lead to chronic hepatitis, cirrhosis, and liver cancer. It is carried worldwide by many millions, especially in South-East Asia, the Pacific, Africa, and Southern Europe. Australian Aboriginals have a very high carrier rate. It also affects drug abusers, many partner homosexuals, and hospital workers in contact with blood. A safe vaccine is effective and particularly valuable for babies born to carrier mothers. Treatment of chronic hepatitis depends on whether the patient is in the replicative ('e' antigen positive) stage, where anti-viral therapy might be considered, or in the integrated ('e' antibody positive) stage where a trial of corticosteroids may be justifiable. Non-A, non-B hepatitis is a diagnosis of exclusion. There is no diagnostic test and no proven therapy. There are probably at least four types, parenteral short and long incubation and enteric sporadic and epidemic.

Acute Disease↗