Japan. SinarySerum interleukin 6 (IL-6) levels were measured in 75 patients with lung cancer and in 20 patients with benign lung diseases. IL-6 was detectable in 29 patients with lung cancer (39%), but was not detectable in any of the patients with benign lung diseases. Serum C-reactive protein levels and plasma fibrinogen levels were significantly higher and serum albumin concentration was significantly lower in lung cancer patients with detectable serum IL-6 levels than in those without detectable serum IL-6 levels and in patients with benign lung diseases. On the other hand, no significant difference was observed in blood platelet counts in these three groups. Moreover, serum IL-6 levels were not significantly different in lung cancer patients with or without clinically demonstrated distant metastasis. These results suggest that IL-6 may be a mediator of various reactions including an inflammatory response in lung cancer patients.Keywords interleukin 6; lung cancer; C-reactive protein; fibrinogen; cachexia; inflammatory response Interleukin 6 (IL-6) is known as a multifunctional cytokine which plays a central role in the host defence mechanism by regulating immune responses, haematopoiesis and acutephase reactions (Kishimoto, 1989). Recently, much attention has been focused on its role in the pathogenesis and progression of various malignancies. It has been reported that IL-6 is an autocrine growth factor for renal cell carcinoma cells (Miki et al., 1989;Koo et al., 1992) and that IL-6 is produced by other non-haematopoietic tumour cells, including bladder carcinoma (Rawle et al., 1989), ovarian carcinoma (Watson et al., 1990) and glioblastoma (Meir et al., 1990). In animal systems, IL-6 appears to have an important role in mediating cancer cachexia (Strassmann et al., 1992). Moreover, elevation of the serum IL-6 level is an adverse prognositic factor in patients with metastatic renal cell carcinoma (Blay et al., 1992). However, there is still little information about the role of IL-6 in vivo in patients with various malignancies.In patients with lung cancer, we have already reported that malignant pleural effusions contain IL-6 (Yanagawa et al., 1992), and we (Mizuno et al., 1994) and others (Matsuguchi et al., 1991) have reported that several lung cancer cell lines constitutively produce IL-6 in vitro. To clarify further the role of IL-6, we examined serum levels of IL-6 in patients with lung cancer. The relationship between serum IL-6 levels and the characteristics of the patients was also analysed. Enzyme immunoassay of IL-6 Serum levels of IL-6 were assayed essentially as described previously (Yanagawa et al., 1992). In brief, microtitre plates (Nunc, Naperville, IL, USA) were coated with anti-IL-6 monoclonal antibody in 100 per well phosphate-buffered saline (PBS). After overnight incubation at 4°C, the wells were blocked with 0.1% bovine serum albumin (BSA) in PBS and washed three times. Volumes of 200 MI of test samples were added to the duplicate wells. The plates were incubated at 37C for 24 h. Aft...

Immunoglobulin G (IgG) antibodies against purified cord factor (trehalose-6,6'-dimycolate) prepared from Mycobacterium tuberculosis H37Rv were determined by enzyme-linked immunosorbent assay (ELISA), and its diagnostic usefulness was evaluated. Serum specimens from 65 patients with active pulmonary tuberculosis, 58 patients with inactive pulmonary tuberculosis, 36 patients with diseases other than tuberculosis, and 66 healthy adults were examined. Patients with active pulmonary tuberculosis showed significantly higher titers of IgG antibodies against cord factor than did other groups (p < 0.001). The antibody titer greater than 0.29 in absorption difference (492 to 630 nm) of 160-times diluted serum was set as positive in ELISA. For patients with active and untreated pulmonary tuberculosis, the ELISA had a sensitivity of 81% and a specificity of 96%. From these results, it was concluded that the detection of IgG antibodies against cord factor is useful for serodiagnosis of active pulmonary tuberculosis. It was also indicated that the anticord factor antibody titers decline to the normal level as a result of antituberculosis chemotherapy.

18 beta-Glycyrrhetinic acid (GA) has been thought to be one of the major metabolites that causes licorice-induced pseudoaldosteronism. However, we found no difference in the blood level of GA between the patients with and without pseudoaldosteronism. We measured the blood concentration of 3 beta-D-(monoglucuronyl)18 beta-glycyrrhetinic acid (3MGA), another metabolite of 3 beta-D-diglucuronyl-18 beta-glycyrrhetinic acid (glycyrrhizin), by high performance liquid chromatography and found an increased concentration of 3MGA in 10 patients with licorice-induced pseudoaldosteronism, but not in 11 patients without pseudoaldosteronism. To investigate whether 3MGA can inhibit 11 beta-hydroxysteroid dehydrogenase, we incubated rat renal microsome with or without 3MGA and measured the conversion rate of [3H]cortisol to [3H]cortisone. 3MGA was found to be a potent inhibitor of 11 beta-hydroxysteroid dehydrogenase, allowing cortisol to exert its full mineralocorticoid effects. These results suggest that licorice-induced pseudoaldosteronism is due to an increased concentration of 3MGA, but not GA, in the circulating blood of these patients.

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