High viral eradication with a daily 12-week natural interferon-beta treatment regimen in chronic hepatitis C patients with low viral load. IFN-beta Research Group.

Virological sustained response (SR) is achieved in 31-49% of patients with chronic hepatitis C with combination therapy using interferon (IFN)-alpha and ribavirin for 24-48 weeks. However, as a period of 24-48 weeks is a burden for patients, we investigated the effect of daily intravenous administration of natural IFN-beta for 12 weeks in this study. In all, 112 patients were enrolled and received a daily administration of 6 MU of natural IFN-beta intravenously for 12 weeks. Serum HCV-RNA before treatment was assessed by the competitive reverse-transcription polymerase chain reaction assay. The patients were divided into two groups according to pretreatment viral load: the low viral load group (N = 25, <6.3 x 10(5) copies/ml), and the high viral load group (N = 87, > or =6.3 x 10(5) copies/ml) who were additionally administered IFN-beta thrice weekly for subsequent 14 weeks at the patients' request. Virological SR was obtained in 37% (41/112) of all the patients; 88% of those with a low viral load, and 22% of patients with a high viral load. Virological SR was attained in 21% of patients with HCV subtype 1, and in 67% of those with subtype 2a. In patients with HCV subtype 1b, virological SR was obtained in patients with the mutant-type (> or =4 amino acid mutations in the NSSA2209-48) having a low viral load (4/4), but not in those having a high viral load (0/3). The results suggest that a daily intravenous administration of natural IFN-beta for 12 weeks showed high therapeutic efficacy in patients with a low viral load despite the shorter treatment period and that the therapeutic efficacy depends on viral load rather than on the number of NS5A2209-48 amino acid mutations.

Prognostic factors in head and neck non-Hodgkin's lymphoma with special reference to serum lactic dehydrogenase and serum copper.

An analysis of prognostic variables was performed in a retrospective study of 121 patients with Ann Arbor stage I-II head and neck non-Hodgkin's lymphoma admitted from 1973 to 1988. The overall actuarial 5-year survival rate was 58.8% and the minimum follow-up 15 months. Nine clinical and laboratory parameters were studied, including serum lactic dehydrogenase (LDH) and serum copper (SCL), and subjected to univariate and multivariate analyses. In univariate analysis, histology and LDH were found to be significant prognostic variables. Evaluation by Cox's multivariate proportional hazard model revealed histology, SCL and sex to be of prognostic significance.

Multiple primary cancer risk in patients with squamous cell carcinoma of the oral cavity.

During 6375 patient-years of observation, 136 new cancers developed in 117 of 1429 patients with squamous cell carcinoma of the oral cavity. The risk of multiple cancers was excessive in the upper digestive or respiratory tract in patients with squamous cell carcinoma of the oral cavity, accounting for 87 (64%) of the 136 later cancers. In addition, multiplicity of cancers was site-specific, being common in the oral cavity-esophagus-lung axis and uncommon in sites such as the maxillary sinus and epipharynx. In addition, the observed-to-expected ratio was different in each site of the oral cavity-esophagus-lung axis, i.e., 57.5 for the oral cavity and pharynx, 12.0 for the esophagus, 7.3 for the larynx, and 2.0 for lung cancers.

Evidence for the failure of IgA specific T helper activity in a patient with immunodeficiency with hyper IgM.

A 28-year-old man with immunodeficiency with hyper IgM was studied. His serum immunoglobulins were characterized by the absence of IgA and low level of IgG associated with high level of IgM. The in vitro pokeweed mitogen (PWM)-induced immunoglobulin synthesis by his peripheral blood lymphocytes was depressed completely for IgA and moderately for IgG although normal numbers and proportions of IgA- and IgG-bearing lymphocytes (on the surface) were demonstrated in the peripheral blood. His T cells could not help IgA production by either normal or his own B cells, whereas they were more efficient helpers for IgM production by his own B cells than were normal T cells. In addition, his B cells produced no IgA and less IgG than normal B cells when co-cultured with normal T cells. This suggests that the failure of IgA specific T helper activity and the maturation arrest of B cells at the stage of the switchover from IgM- to IgG- and/or IgA-producing cells may be the major cause for the hypogammaglobulinaemia in this patient. It is uncertain whether the maturation arrest of B cells is secondary to the T cell defect in helper function for IgA production.