A 43-year-old woman with a solitary renal cyst developed polycythaemia. 21 well documented cases of this type have been previously published. In the majority of them a causal connection could be assumed between the renal cyst and polycythaemia: in 13 of the 15 cases (as in the reported one), the polycythaemia disappeared after surgical removal of the cyst. Measurement of serum erythropoietin can help in the differential diagnosis, but exclusion of polycythaemia vera may be difficult in the individual case.

Spontaneous cell-mediated cytotoxicity (SCMC), antibody-dependent cellular cytotoxicity (ADCC) and proliferative lymphocyte stimulation in alcoholic liver disease (ALD) were investigated. Peripheral blood lymphocytes (PBL) from eight patients with advanced ALD and nine normal controls were tested against hepatoma cells (PLC/PRF/5) as targets. Target cells were grown in either normal culture medium or medium supplemented with 1 and 5% ethanol, respectively, for 24 to 48 h. Ethanol-exposed hepatoma cells exhibited profound and characteristic morphological alterations. Ethanol preincubation, however, proved to be without effect on immune reactions. Provided that hepatoma cells are an appropriate model, we assume that the proposed immune reactions in ALD are based on metabolic interactions operative only in vivo but do not parallel morphological alterations of liver cells directly induced by ethanol.

Monoclonal antibodies have been raised against different antigenic determinants of normal rabbit hepatocytes. One antibody (2D3) recognized a liver-specific 43 kDa protein displayed exclusively on the basolateral portion of the hepatocellular membrane. Purified monoclonal antibodies were injected intravenously into rabbits. Following the injection of antibody 2D3, a dose-dependent increase of liver enzyme activities in sera was observed. Within 8 h, marked morphological alterations of the hepatocytes, including multiple cell necroses, could be demonstrated by light and electron microscopy. When isolated vital rabbit hepatocytes in culture were used as targets, cytotoxic effects of this antibody could also be observed. This indicates that liver cell damage was not due to antibody-dependent cellular cytotoxicity, but was mediated by the antibody itself. Control antibodies did not show these effects. Thus, our results clearly demonstrate that humoral immune reactions against particular liver membrane antigens may play a role in the development of liver diseases, and provide a useful experimental approach for the investigation of their specificity.

The effect of α-interferon treatment on serum levels of hepatitis B virus-encoded proteins was analyzed in eight patients with chronic type B hepatitis who participated in a pilot study of interferon therapy. Three individuals became HBsAg-negative, 4 lost HBeAg but remained HBsAg-positive and 1 remained positive for both HBsAg and HBeAg. Initiation of interferon treatment was rapidly followed by reduction or loss of hepatitis B virus DNA in the serum but by little immediate change in hepatitis B virus antigen levels. Changes in hepatitis B virus antigens were usually delayed. Loss of HBsAg from the serum was preceded by the sequential disappearance of pre-S-encoded proteins (pre-S1 and polymerized human serum albumin) and HBeAg. In patients who lost HBeAg but remained HBsAg-positive, serum levels of pre-S1 and polymerized human serum albumin usually, but did not always, decrease. The individual who remained HBsAg- and HBeAg-positive had unchanged serum levels of pre-S1, polymerized human serum albumin and HBsAg. These results suggest that α-interferon inhibits hepatitis B virus DNA replication but has little direct effect on synthesis of hepatitis B virus gene products.

Abstract. We describe twenty murine monoclonal antibodies directed against different antigenic determinants of human and rabbit liver‐specific protein LSP. Among them, nine were directed against liver‐specific epitopes as judged from immunohistological studies. Immunoelectronmicroscopy revealed that seven of these monoclonals recognized membrane determinants differing in staining of distinct areas of the hepatocellular surface. Eleven antibodies were directed against intracellular structures. Western blot analysis showed that the epitopes detected were displayed on either single or multiple protein bands with apparent molecular weights between 24 000 and 60 000. Further differences were observed with respect to the species specificity and (among the non‐organspecific antibodies) pattern of tissue cross‐reactivity. Our results demonstrate the presence of several liver‐specific determinants and membrane components within LSP. There are, however, a very much greater number of non‐organ‐specific epitopes and numerous determinants displayed on intracellular structures. This emphasizes the remarkable heterogeneity of the antigen preparation named LSP and warrants the use of clearly defined antigens in further studies dealing with auto‐immune phenomena in liver diseases.

Immunosuppressive therapy was stopped in 12 individuals positive for hepatitis Be antigen (HBeAg) and hepatitis B surface antigen (HBsAg) and in 4 individuals positive for HBsAg but negative for HBeAg. Discontinuation of immunosuppressive therapy in HBeAg-positive patients was always associated with a bout of hepatitis and elimination of HBeAg in 8/12 patients. One patient died from liver failure and 2 patients experienced a decompensation of their liver disease indicating that this approach might be harmful if used therapeutically. A bout of hepatitis was not noted in any of the individuals negative for HBeAg when the immunosuppressive therapy was stopped, implying that this event is not potentially harmful to the patient.

The production of monoclonal antibodies directed against surface structures of human T lymphocytes has provided unique probes to define discrete stages of T cell differentiation as well as individual T cell subpopulations that are programmed to perform regulatory and effector functions in the immune response (1–3). Importantly, besides their usefulness for phenotypic characterization of normal and malignant cells of the T lineage, these reagents have also been employed to characterize the physiologic role of their respective membrane molecules. For example, it was possible to identify by monoclonal antibodies the transferrin receptor (4), the receptor for interleukin-2 (5), and, more recently, the T cell antigen receptor (6). Moreover, on the basis of functional antibody effects in vitro, it was suggested that the subset restricted glycoproteins, T4 and T8, are themselves involved as associative recognition structures for constant portions of, respectively, class II or class I MHC gene products in effector—target cell interaction (7). This view originated from studies in which antibodies were utilized to block in vitro responses such as cytotoxicity or/and proliferation (8,9,10).

Glyceroltrinitrat (GTN) führt zur Erschlaffung der glatten Muskulatur von Blutgefäßen. Es wurde daher für möglich gehalten, daß es den Pfortaderhochdruck bei Patienten mit Leberzirrhose vermindern könnte. Mit der kürzlich beschriebenen endoskopischen Feinnadelpunktion von Ösophagusvarizen konnte der Einfluß von GTN auf den intravasalen Ösophagusvarizendruck (IOVD) gemessen werden. Drei Minuten nach sublingualer Gabe von 2.2 mg GTN fiel der IOVD bei 10 Patienten mit Varizen Grad III von 22.8 ± 2.0 mmHg auf 12.0 ± 0.4 mmHg (p◄0.005) und bei sechs Patienten mit Varizen Grad II von 16.3 ± 0.4 mmHg auf 10.0 ± 0.4 mmHg (p◄0.005). Unsere bisherigen Ergebnisse lassen vermuten, daß GTN zur Blutstillung bei der Ösophagusvarizenblutung geeignet sein könnte. Weitere Studien sollten darüber Aufschluß geben, ob Langzeitnitrate auch zur Prophylaxe der Varizenblutung geeignet sind.

A 42-year-old man of Croatian birth, with long-standing neurological symptoms, was found to have neurocysticercosis (a rare disease in Central Europe), as proven by positive antibody titres in serum and CSF and typical foci by computed tomography (CT). Ventriculo-cisternal drainage (after Torkildsen) controlled the acute symptoms of raised intracranial pressure. Postoperatively the CT revealed new low-density intracerebral foci, which responded to praziquantel.

During a period of 3 years we observed 5 patients with chronic active hepatitis B and 2 with hepatitis B virus-induced liver cirrhosis who cleared HBsAg from their sera after 2-14 years of HBsAg carriership. 4 of them developed anti-HBs. After HBsAg clearance there was no evidence of persisting inflammatory activity within their livers. 5 of the 7 patients had been treated for 1-39 months with prednisolone, sometimes in combination with azathioprine. This therapy, however, had been stopped more than 3 years before these patients terminated their HBsAg carriership. Our observations indicate that even after long-standing chronic active hepatitis B or hepatitis B virus-induced liver cirrhosis HBsAg may be eliminated in a considerable number of patients.

Cellular cytotoxicity of peripheral blood lymphocytes against autologous hepatocytes was studied in 9 patients with HBeAg positive and 8 patients with anti-HBe positive chronic hepatitis B. In the HBeAg positive group a greatly increased cytotoxicity of 41 +/- 7% (mean +/- SEM) was found, in contrast the moderately increased cytotoxicity in anti-HBe positive cases of 15 +/- 5% was clearly different (p = 0.005). The different cytotoxicity values could not be explained on the basis of the histological classification, but seemed to correlate at least to some degree to the aminotransferase levels. The cytotoxic activity resided in both T cell and non-T cell enriched lymphocyte compartments. Our findings may provide an explanation for the poor prognosis of HBeAg positive patients with chronic hepatitis B in contrast to their anti-HBe positive counterparts.