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A total of 172 Swedish patients treated with interferon-alpha for at least 24 weeks and followed-upor =24 weeks after treatment was stopped were analysed for pre-treatment factors of importance for achieving a virological sustained response (SR). Furthermore, the predictive value for a virological SR of a positive or negative HCV RNA test at week 12 of treatment was evaluated. A low baseline viral load and genotype non-1b were pre-treatment factors indicating a favourable response. Thus, 44% (38/86) of patients with a low baseline viral load vs. only 16% (14/86) of those with a high viral load had a virological SR (p0.0001). Of patients with a negative qualitative HCV RNA test after 12 weeks of interferon treatment, 46% (44/95) had virological SR, whereas only 5.9% (4/68) of those with a positive test had (p0.0001). Prolonged (6 months) treatment with interferon-alpha tended to increase the chance of virological SR (p0.052).

Health care workers at risk for hepatitis B virus infection are recommended for vaccination. Low-dose intradermal (i.d.) administration of vaccine has been suggested as a less expensive alternative to intramuscular (i.m.) inoculation. To evaluate the i.d. vaccination route, health care workers were included in a prospective study. The subjects were vaccinated with 0.1 ml (= 2 microg) recombinant vaccine (Engerix B, SmithKline Beecham) i.d. at 0, 1 and 6 months. Two months after the third vaccination, measurement of the anti-HBs level was conducted. An anti-HBs level > or =10 IU/l was considered protective. Those with an anti-HBs level

The recipients of blood components, from the first 12 anti-hepatitis C virus (HCV) positive donors identified by blood donor screening, 1985-1991, were traced retrospectively and tested to assess the HCV transmission rate, HCV genotypes and disease severity. Three enzyme-linked immunosorbent assay (ELISA) positive but RIBA-indeterminate and HCV RNA-negative donors did not transmit HCV to their 9 traced recipients. Nine RIBA- and HCV RNA-positive donors had donated blood to 27 now living recipients of whom 16/27 (59%) were viraemic 1-5 years later. Nine recipients had resolved infection, as determined by PCR HCV RNA. Five of these were RIBA-2 positive but HCV RNA-negative and 4 recipients were RIBA-2-indeterminate and HCV RNA-negative. Two recipients negative in all tests had probably received blood before the donor became infected with HCV. The HCV genotype in each case was identical between the donor and the recipient. Of the viraemic recipients, 50% (8/16) were unsuitable for further investigation or therapy due to their high age and/or underlying severe disease. At most, only 30% (8/27) of the recipients were suitable for further investigation and/or treatment. Two of these were already diagnosed as being infected with HCV before being traced. It is concluded that the benefit of a general tracing of recipients of blood components from HCV-infected donors is doubtful since only a few of them are suitable candidates for treatment. Our results seem to indicate that it is more appropriate to recommend anti-HCV testing to those seeking medical care who have received transfusions or undergone major surgery before 1992, i.e. before anti-HCV-screening was initiated.

Clinical course, serological response and effect of antibiotic treatment were evaluated in 34 patients with uncomplicated enterocolitis and in 27 patients with reactive arthritis (ReA) due to Yersinia enterocolitica. Patients participating in this prospective multicentre trial were randomised to treatment or no treatment with antibiotics. Only 3 (11%) of the patients who later developed ReA asked for medical care because of intestinal symptoms and fever and they all developed arthritis within 2 days after admission to hospital, i.e. before an etiological diagnosis was obtained. Patients with ReA had a history of milder intestinal symptoms than patients with uncomplicated enterocolitis. The peak IgA titer to Y. enterocolitica, as measured by enzyme linked immunosorbent assay, was higher in ReA patients and it was not affected by the presence of HLA-B27 antigen. On the other hand, untreated patients with uncomplicated enterocolitis had the longest duration of IgG antibodies. The duration of IgG antibody response was shortened in uncomplicated enterocolitis patients treated with antibiotics, but not in ReA patients. Treatment did not influence intestinal or ReA symptoms. It is concluded, that patients with uncomplicated enterocolitis due to Y. enterocolitica differ in intestinal symptoms and serological response, compared with patients who develop ReA. These parameters could however not be used to predict the development of arthritis in individual patients.

Staphylococcus aureus septicaemia is still a serious disease with a high mortality. The absence of leukocytosis in serious bacterial infections is generally considered as an unfavourable prognostic sign. The leukocyte pattern in 75 patients with S. aureus septicaemia was reviewed retrospectively. In the 66 patients where leukocyte determinations were done within 2 days of positive blood culture, 21 presented without leukocytosis which contrasts to only 1/35 patients with Escherichia coli septicaemia studied as controls (p less than 0.001). During follow up of S. aureus septicaemia only 5 of the patients developed leukocytosis greater than 10 x 10(9)/l and 2 leukopenia. There was no significant difference in mortality in patients without initial leukocytosis (14%) compared to patients with initial leukocytosis (24%). Except for septic arthritis, which was associated significantly more often with leukocytosis, complications were found with about the same frequency in both groups. Thus absence of leukocytosis seems not be an unfavourable prognostic sign in S. aureus septicaemia.

Oral bile acid loading tests using 1 g of unconjugated chenodeoxycholic acid (CDA) were performed in subjects with Gilbert's syndrome before and after reduced caloric intake. The study was carried out to ascertain whether the hepatic handling of CDA was restricted in the same manner as recently described for ursodeoxycholic acid. In subjects with Gilbert's syndrome, the bile acid concentrations after the oral loading tests did not differ significantly from those found in reference groups. No differences were found in the serum bile acid values before and after caloric restriction, indicating that the bile acid handling was not influenced by the increased bilirubin levels obtained after fasting. Our results indicate that the hepatic handling of CDA is normal in Gilbert's syndrome.

Septicemia is a rare but serious complication of infection with Yersinia enterocolitica (Y.e.). Seven cases of Y.e. septicemia are presented. Five of the patients had no underlying disease predisposing to septicemia. Five patients displayed recurrent episodes of septicemia, despite treatment with recommended doses of antibiotics to which the isolates were sensitive in vitro. One patient developed endocarditis which required surgical replacement of the aortic valve. Other clinical manifestations were arthritis, diverticulitis and pulmonary abscesses. The outcome was fatal to 3 elderly patients. The serological response to Y.e. was followed by tube agglutination and a diffusion-in-gel enzyme-linked immunosorbent assay. One patient, with a benign course of illness, had transient elevated Y.e. antibody titres, while the 3 cases with a protracted disease showed sustained antibody responses for 6-18 months. Blood isolates of Y.e. had ordinary virulence characteristics identical to fecal isolates and produced extracellular beta-lactamase. All isolates were sensitive in vitro to trimethoprim-sulfamethoxazole, mecillinam, piperacillin, cefotaxime, ceftazidime, chloramphenicol and gentamicin. The lowest MIC values were recorded for mecillinam. Full synergistic activity was demonstrated when mecillinam was combined with trimethoprim-sulfamethoxazole, cefuroxime or rifampicin.

33 patients with biopsy-proven chronic non-A, non-B posttransfusion hepatitis (NANB PTH) were randomized 2:1 to treatment with interferon alpha-2b (Introna) or to controls. The treatment group received 3 MU interferon 3 times weekly subcutaneously for 36 weeks. 22/33 (67%) patients were reactive for antibodies against hepatitis C virus (anti-HCV). 11/19 (58%) treated patients versus none of the 12 controls had a complete response with normalization of serum alanine aminotransferase levels (p less than 0.001). Another 4/29 (21%) treated patients had a partial response which was also seen in 4/12 (33%) controls; 4 treated patients were nonresponders, all with chronic active hepatitis. Nonresponders had a significantly higher mean weight than responders (p less than 0.05) and tended to have a longer duration of their disease before therapy. During the 6-month follow-up period post treatment 4/11 (36%) complete responders had a sustained response and 7/11 (64%) relapsed. All who were retreated responded again. We conclude that a majority of patients with chronic NANB PTH will respond to 9 months interferon alpha-2b treatment, but that only 1 out of 3 will have a sustained response 6 months post treatment, and that the reactivity for anti-HCV was not correlated to the outcome of therapy.

Five children aged 1/2--10 years with benign meningococcemia are reported. The clinical picture was quite uniform: good general condition, spikes of fever, skin eruptions as maculopapules--sometimes haemorrhagic, appearing in association with febrile periods, and arthralgia (big joints). The diagnosis involves either isolation of meningococci (MC) from blood, demonstration of MC with immunofluorescence in skin eruptions, or a significant elevation of MC antibody titre in connection with typical clinical signs and symptoms. Important differential diagnoses are Henoch-Schönlein syndrome, disseminated gonococcal infection, septicemia of other origins, subacute bacterial endocarditis, viral infections, hypersensitivity reactions and subsepsis allergica. By co-agglutination technique, the causative agent of meningococcemia in 4 of the 5 children was shown to be MC group B. These have some features in common with gonococci, whereby an incorrect diagnosis might be suggested as demonstrated in one of our patients. The question is raised whether MC group B is the main causative agent in benign meningococcemia.

32 patients with biopsy-proven chronic non-A, non-B posttransfusion hepatitis and raised aminotransferase levels since more than 1 year were randomized 2:1 to treatment with interferon alpha-2b, Introna, or to controls. The interferon group received 3 MU interferon 3 times weekly subcutaneously. Interim results 12 weeks after randomization showed that 14/21 (67%) patients in the treatment group had normalized their serum alanine aminotransferase levels whereas none of 11 patients in the control group had (p less than 0.001). If interferon alpha-2b is only suppressive during ongoing therapy or curative will be shown later during continued follow-up.

A simplified enzymatic method for determination of serum 3 alpha-hydroxy bile acids (3 alpha-HBA) has been evaluated. Analytical precision was low in the normal range but satisfactory for elevated values. The fasting upper reference value was 8.0 mumol/l. In 12 healthy subjects serum 3 alpha-HBA levels were measured after oral loads (125, 250, 500, and 1000 mg) of unconjugated chenodeoxycholic acid (CDA). After the 125-mg CDA loading dose no significant increase in serum 3 alpha-HBA was observed, but with the 250 mg CDA loading dose serum 3 alpha-HBA levels were elevated at 30, 60, and 120 min. The loading doses of 500 mg and 1000 mg CDA produced significant increases in serum 3 alpha-HBA levels throughout the observation period (3 h). When sera with increased serum bile acids were analyzed by radioimmunoassay for CDA, the results correlated well with those obtained enzymatically. The usefulness of the simplified method is evident in this situation, and we also find it useful for serum bile acid determination after an oral bile acid loading test with CDA. The method is easy to perform and requires only standard laboratory equipment.

Three different bile acid provocation tests--an intravenous stimulation with cholecystokinin (CCK), a test meal, and an oral bile acid load of 500 mg chenodeoxycholic acid (CDA)--were compared in 12 healthy subjects. Blood samples were drawn every 30 min for 3 h, and serum bile acids (SBA) were measured by an enzymatic method (Enzabile). The CCK stimulation gave significant SBA elevations only at 30 min. After the test meal and the CDA loading tests SBA elevations were observed from 30 min and throughout the observation period. Maximal increases were obtained at 120 min after the test meal but already at 30 min after the CDA loading test. We conclude that among these three bile acid provocation tests the oral CDA loading test is to be preferred because it gives marked and rapid elevation of SBA in all subjects and is independent of bile acid pool size and normal function of the gallbladder.

A case of septicemia and meningitis caused by Fusobacterium aquatile is described. The insidious onset of the megningitis and occurrence of multiple cranial nerve affections were outstanding features. In spite of adequate antibiotic treatment the course was protracted, and the outcome was permanent damage to 3 of the affected cranial nerves.

Two cases of infection of the central nervous system (CNS) with Haemophilus parainfluenzae — a 12-month-old girl with meningitis and a 17-month-old girl with brain abscess—are reported. Both infants had long-standing upper respiratory infection before CNS disease. Both recovered after treatment.