[A case of elderly patient with pulmonary tuberculosis considered to be caused by exogenous reinfection].

A 84-year-old woman presented with chronic febrile illness and anorexia from June 1998. She was diagnosed as pulmonary tuberculosis and was admitted to our hospital in August 1998. Her sputum smear was Gaffky 2, and the type of chest radiograph was b III 3. By family contact examination in August 1998, chest radiological examinations of her husband, a 86-year-old man, showed consolidation in middle lobe, right pleural effusion and two calcified mediastinal lymphnodes. He was diagnosed as pulmonary tuberculosis complicated with pleurisy. He had poor controlled diabetes mellitus. Tubercle bacilli isolated from their sputa showed the same pattern in restriction fragment length polymorphism analysis. Pulmonary tuberculosis of the husband was considered to be caused by exogenous reinfection.

[Serum soluble interleukin-2 receptor in patients with pulmonary mycobacterial diseases].

Serum soluble interleukin-2 receptor (sIL-2R) levels were measured in patients with untreated pulmonary tuberculosis (24 cases), patients with multidrug-resistant intractable pulmonary tuberculosis (7 cases) and patients with pulmonary non-tuberculous mycobacteriosis (27 cases). Serum sIL-2R levels were elevated in patients with pulmonary mycobacterial diseases and were elevated in untreated pulmonary tuberculosis patients than in other patients. In patients with new tuberculosis, serum sIL-2R levels were higher in patients with extensive lesions. Serum sIL-2R level showed significant positive correlation with serum C-reactive protein level and erythrocyte sedimentation rate, and significant negative correlation with serum albumin level. In patients with intractable tuberculosis and patients with non-tuberculous mycobacteriosis, serum sIL-2R levels were lower than in patients with new tuberculosis. Even in patients with extensive lesions, serum sIL-2R levels were not elevated. Lower levels of serum sIL-2R, marker of immunocompetent cell activity, suggested that immunocompetent cell activity was suppressed in intractable tuberculosis and in non-tuberculous mycobacteriosis.

Crescentic glomerulonephritis developing 3 months after autologous peripheral blood stem cell transplantation for non-Hodgkin's lymphoma.

A 64-year-old woman underwent an ileocecal resection for ileus. The specimen revealed a diffuse large B cell lymphoma. The diagnosis was stage IIA non-Hodgkin's lymphoma. She received chemotherapy with the CHOP-etoposide regimen, resulting in partial remission. High-dose etoposide was used for PBSC mobilization before auto-PBSCT. Conditioning was ranimustine, carboplatin, etoposide and cyclophosphamide. Her renal function deteriorated gradually, starting 3 months post-PBSCT. Eight months post-transplant, serum creatine concentration was 7.1 mg/dl, and BUN was 59.2 mg/dl. Her hemoglobin concentration decreased to 5.3 g/dl, with no evidence of hemolysis. Renal biopsy revealed fibrous crescent formations in glomeruli, and mononuclear cell infiltration in interstitial spaces. Renal injury in this patient differs from BMT nephropathy, which is similar to hemolytic uremic syndrome, and represents another type of late renal injury after PBSCT.

[A case of catamenial hemoptysis (pulmonary endometriosis) cured by VATS lobectomy].

We report here a case in which for hemoptysis during menstruation (catamenial hemoptysis) right middle lobectomy was performed thoracoscopically under a preoperative diagnosis of pulmonary endometriosis with a successful outcome. The patient was a 27-year-old housewife who from the age of 24 years experienced hemoptysis during menstruation, and was diagnosed as having pulmonary endometriosis on the basis of detailed examinations including bronchoscopy and chest CT. From the age of 26 years hormone therapy was administered, but the hemoptysis recurred with the menstruation following its cessation. After admission to this department bronchoscopy performed at the time of menstruation revealed bleeding from right B4 while chest CT showed an abnormal shadow in right S4 b. Right middle lobectomy was then performed thoracoscopically under a diagnosis of right middle lobe endometriosis. In the resected specimen findings of pulmonary hemosiderosis, granulomatous phlebitis and micrometastases from a thyroid cancer were noted. The postoperative course was favorable with no further episodes of hemoptysis occurring. In this case histological proof of endometriosis could not be obtained, but the diagnosis of pulmonary endometriosis was strongly suggested by the clinical course and objective findings such as pulmonary hemosiderosis.

[Interferon production in peripheral blood cells of patients with pulmonary mycobacterial disease].

Production of interferon (IFN)-alpha and IFN-gamma were examined in 31 patients with acute tuberculosis, 12 patients with atypical mycobacterial disease. IFN production was examined in cultures of unseparated fresh whole blood. Production of IFN-alpha was induced by hemagglutinating virus of Japan and production of IFN-gamma was induced by PHA. Patients with mycobacterial disease produced significantly less IFN-alpha than healthy subjects. In patients with acute tuberculosis, effective chemotherapy for 2 months restored IFN-alpha production. Patients produced less IFN-gamma than healthy subjects, but the difference was not significant. Patients with high serum CRP levels tended to produce little IFN-alpha. These results suggest that measurement of IFN production is useful for immunological evaluation of patients with mycobacterial disease.

[The role of sulfatides in autoimmunity in children with various glomerular disease].

Previous studies have suggested that autoimmunity to a number of kidney antigens may exist in glomerular disease. Our own work suggested that sulfatide which is one of the major acidic glycolipids of human kidney may be antigenic. Glycolipids were isolated from lipid extract of human kidney using thin-layer chromatography (TLC). As the major acidic glycolipids, sulfatide, CDH-sulfate, GM3, GD3 were identified. Acidic fraction of lipid extract were chromatographed and then tested for antigen by immunostaining. Sera from patients with IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) contained antibody to the sulfatide of human kidney as determined by the direct binding of antibody to TLC. In addition, we measured the presence of sulfatide antibodies by enzyme linked immunosorbent assay (ELISA) in sera of patients with various glomerular disease: IgAN, HSPN, mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis (MPGN), focal and segmental glomeruosclerosis (FSGS), membranous nephropathy (MN), minimal change nephrotic syndrome (MCNS), acute post streptococcal glomerulonephritis (PSAGN), and lupus nephritis (LN). IgM class sulfatide antibody were demonstrated in many cases of them. The incidence of IgA class sulfatide antibody in HSPN and IgAN was significantly high, and also the high incidence of IgG class sulfatide antibody occurred in IgAN. On the other hand, we evaluated cellular hypersensitivity to sulfatide in IgAN, HSPN, and FSGS using an active E-rosette assay. Positive results occurred in IgAN and HSPN. It was suggested that delayed hypersensitivity to sulfatide may generate an autoimmune inflammatory process. It has been reported that laminin binds specifically to sulfatide. Autoimmunity to sulfatide may disturb the laminin binding and consequently interfere with renal function. These results suggested sulfatide antigen may play important role in occurrence and aggravation of glomerular disease.