[A case of primary effusion lymphoma effectively treated by oral corticosteroid therapy].

Primary effusion lymphoma is a rare type of lymphoma which is confined to those body cavities associated with human herpes virus 8 infection in its development. We describe a 93-year-old man with primary effusion lymphoma in the pleura, but who was negative for herpes virus 8 infection. Chest computed tomography revealed bilateral pleural effusion, but did not show any evidence of a tumor mass or lymph node enlargement. Cytological analysis of his pleural effusion revealed atypical lymphoid cells with immunophenotypes which were positive for CD10, CD19 and CD20. Clonal rearrangement of the immunoglobulin-heavy chain gene was detected by Southern blot analysis, and a diagnosis of primary effusion lymphoma was made. Although dyspnea and severe hypoxia developed, accompanied with increased pleural effusion, chemotherapy was not indicated because of his age. We thus tried oral corticosteroid therapy for palliation which resulted in a dramatic, long-term decrease of his pleural effusion. We present a rare case of primary effusion lymphoma effectively controlled by corticosteroid therapy.

[Clinical evaluation of performance of a new diagnostic method for deep mycosis by measuring beta-glucan concentration in the blood].

beta-Glucan Test MARUHA for high sensitive diagnosis of deep mycosis which was developed recently detects (1-->3)-beta-D-glucan, a component of the cell wall. The performance of beta-Glucan Test MARUHA is evaluated in this report. Although existing methods to detect (1-->3)-beta-D-glucan have trouble with sulfa drugs, hemolysis, and immunoglobulin G (IgG), these problems were overcome by the beta-Glucan Test MARUHA: No effect was observed for beta-Glucan Test MARUHA at lower than 200 micrograms/ml, 500 mg/dl, and 6,000 mg/dl of sulfa drugs, hemoglobin, and IgG, respectively. The effect of drugs administrated on the measurement value of beta-glucan Test MARUHA was checked at several concentrations. However, almost no effect of drugs, such as, 5 kinds of antifungals, 8 kinds of antibiotics, a kind of antibacterial, 2 kinds of infusions, and a kind of contrast media was observed at the practical concentrations.

[Comparison of four diagnostic methods using clinical blood by measuring (1-->3)-beta-D-glucan].

Using Amebocyte lysate of horseshoe crab to measure (1-->3)-beta-D-glucan specifically, a component of the cell wall, several kinds of diagnostic methods for deep mycosis are in practical use in Japan. However, the most important problem is that the judgment of positive or negative is method dependent. To elucidate the cause of the problem, each measurement value of the identical sample by four methods, beta-Glucan Test Maruha (MARUHA), beta-Glucan Test Wako (WAKO). FUNGITEC G Test (FUNGITEC-G) and FUNGITEC G Test MK (FUNGITEC-MK) was compared with the clinical data using 119 cases and 289 tests. Each case was divided into three groups; proven fungal infection, probable fungal infection and non-fungal infection. The negative cases for all the methods tested in the groups of proven fungal infection and probable fungal infection were allergic bronchopulmonary aspergillosis and cryptococcosis, and that for all the methods tested except FUNGITEC-MK method in the group was pulmonary aspergilloma. It seems that these cases cannot be detected correctly by only measuring (1-->3)-beta-D-glucan. On the other hand, the ratio of false positive, positive for non-fungal infection group was high in the case of FUNGITEC-MK. About 23% against the total case was positive for FUNGITEC-MK method, but negative for MARUHA, WAKO, and FUNGITEC-G methods. Although the difference of the sensitivity among four methods was not observed, the specificity, the diagnostic efficiency, and the positive predictive value of FUNGITEC-MK method were remarkably lower than those of the other methods due to false positive measurement. In conclusion, MARUHA, WAKO and FUNGITEC-G except FUNGITEC-MK is not method dependent. It is suggested that FUNGITEC-MK detects non-specific reaction resulted in false positive.

A case of Wegener's granulomatosis complicated with seropneumothorax.

Abstract We report the case of a 52-year-old man with Wegener's granulomatosis complicated with seropneumothorax. Pneumothorax or seropneumothorax has previously been reported as a rare complication of Wegener's granulomatosis. The patient was successfully treated with prednisolone and cyclophosphamide, and seropneumothorax was resolved without tube drainage. This case suggests that the pathogenesis of seropneumothorax may be associated with the disease activity of Wegener's granulomatosis because it developed spontaneously before treatment with immunosuppressive agents and without being complicated by infection.

Effects of azithromycin on shiga toxin production by Escherichia coli and subsequent host inflammatory response.

Shiga toxin (Stx)-producing Escherichia coli (STEC) colonizes the human intestinal mucosa, produces Stx from phage, and causes the development of hemolytic-uremic syndrome via Stx-induced inflammatory cytokine production. Azithromycin exhibited strong in vitro activity against STEC without inducing Stx-converting phage, in marked contrast to norfloxacin. Azithromycin decreased the tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production from Stx-treated human peripheral mononuclear cells or monocytes to a greater extent than did clarithromycin. In Stx-injected mice, azithromycin significantly suppressed Stx-induced TNF-alpha, IL-1beta, and IL-6 levels in serum and improved the outcome as assessed by survival rate. In the STEC oral infection experiment using immature mice immediately after weaning (weaned immature-mouse model), all mice died within 7 days postinfection. Azithromycin administration gave the mice 100% protection from killing, while ciprofloxacin administration gave them 67% protection. The data suggest that azithromycin (at least at higher concentrations) has a strong effect on Stx production by STEC and on the Stx-induced inflammatory host response and prevents death in mice. Azithromycin may have a beneficial effect on STEC-associated disease.