Hidero Suzuki

Syndrome of Plasma Cell Dyscrasia, Polyneuropathy, and Endocrine Disturbances: Report of a Case

Abstract A case of a small amount of IgG λ M component, chronic progressive polyneuropathy, primary hypothyroidism, diabetes mellitus, elevated serum estrogen level, gynecomastia, impotence, genera...

Spontaneous production of bone-resorbing lymphokines by B cells in patients with systemic lupus erythematosus

The culture supernatant of B cells from patients with active systemic lupus erythematosus (SLE) who had never been treated with corticosteroids had bone-resorbing activity (BRA) which stimulated the45Ca release from prelabeled murine fetal bones. Then we studied the characteristics and the relationship of this BRA with several lymphokines previously reported. The BRA was eluted as three peaks at approximately 17,000, 35,000, and 80,000 daltons by Sephacryl S-200 column chromatography. Recombinant (r)IL 1α, rIL 1β, and rTNF possessed BRA, but rIL 4 and rIL 6 did not. Furthermore, the BRA from SLE B cells was absorbed with anti-IL 1α antibody but not with anti-IL 1β and anti-TNF antibody. Therefore, the fact that SLE B cells produce BRA which corresponds to IL 1α and IL 1α produced by B cells might be one of the causes of bone destruction in SLE patients.

Reduced function of HLA-DR-positive monocytes in patients with systemic lupus erythematosus (SLE)

Accessory function of monocytes for T-cell activation was studied in patients with systemic lupus erythematosus (SLE). Nylon column-purified T cells alone were not activated to proliferate by stimulation with concanavalin A (Con A), but the addition of dish-adherent monocytes restored the T-cell response in a dose-dependent manner (accessory function). This accessory function is mediated by HLA-DR-positive monocytes. This accessory function of monocytes was markedly impaired in SLE patients. The dysfunction of monocytes was marked in an active stage of SLE but not in an inactive stage of SLE. Furthermore, SLE T cells were not fully activated with Con A in the presence of normal monocytes, suggesting that both monocyte and T-cell functions were impaired in SLE patients. The dysfunction of SLE monocytes was due to neither the development of suppressor monocytes nor the overproduction of prostaglandins, because SLE monocytes did not suppress the accessory function of normal monocytes and indomethacin did not restore the dysfunction of SLE monocytes. The percentage of HLA-DR-positive cells in a monocyte population was markedly decreased in active SLE patients and moderately decreased in inactive SLE patients. Thus, the impairment of accessory function of monocytes in SLE patients seems to be derived from a decrease in HLA-DR-positive monocytes. These results suggest that the dysfunction of HLA-DR-positive monocytes plays an important role in the pathogenesis of SLE.

Inhibitory effect of anti-class II antibodies on human B-cell activation

The role of class II antigens for B-cell activation was analyzed using purified human B cells and anti-class II monoclonal antibodies. The stimulation of purified B cells with Staphylococcus aureus Cowan I induced proliferation and differentiation into immunoglobulin-producing cells in the presence of interleukin-1 and T-cell-derived factors (B-cell growth factor and B-cell differentiation factor). The addition of anti-class II monoclonal antibodies inhibited B-cell responses. However, anti-class I monoclonal antibody did not inhibit B-cell responses. When mitomycin C and cycloheximide-treated B cells were added to the induction culture of B cells as the stimulator, B-cell responses were enhanced in a dose-dependent manner. Furthermore, the stimulator B cells also partially restored the suppressed B-cell responses which were induced by the pretreatment of B cells with anti-class II antibody. This enhancing effect of stimulator B cells on B-cell responses was inhibited by the pretreatment of stimulator B cells with anti-class II antibody. The treatment of B cells with anti-class II antibody and complement depleted the activity of both responder B cells and stimulator B cells. These results suggest that cellular interaction among B cells exists in the B-cell activation induced with Staphylococcus aureus, Cowan I and anti-class II antibody inhibits B-cell activation by interfering in this cellular interaction.

Collagenase-like peptidase activity in fibrotic liver tissue

Abstract Activities of an enzyme capable of digesting carbobenzoxy-glycyl-prolyl-leucyl-glycyl-proline proved to be significantly elevated in fibrotic and cirrhotic human liver tissues, as well as in experimentally induced fibrotic rat liver tissues. Hydroxyproline content was also elevated.

Monocyte (macrophage)-specific antibodies in patients with systemic lupus erythematosus (SLE)

Antibodies reactive for monocytes (macrophages) were found in the sera of patients with systemic lupus erythematosus (SLE). These antibodies were preseent in both IgG and IgM fractions and worked under both warm (37°C) and cole (4°C) conditions. These antibodies were specific for monocytes, because cytotoxic antibodies for monocytes were absorbed with monocytes, but not with T cells, B cells, and granulocytes. Furthermore, their specificity is also different from anti-HLA-DR antibody. The presence of these antibodies correlated with the activity of disease. They were found in 12 of 14 active SLE and 7 of 16 inactive SLE patients. The treatment of normal monocytes with these SLE sera and complement resulted in the depletion of their accessory function for T-cell activation and their phagocytic activity. In the previous paper, we reported that the accessory function of monocytes for T-cell activation was impaired in SLE patients. These results suggest that monocyte-specific antibodies play an important role in the pathogenesis of SLE through disturbing the monocyte regulatory function for immune responses.

Alkaline Phosphatase Isoenzymes in Carcinoma Tissue of Gastro‐intestinal Tract

The enzymological and immunological properties of alkaline phosphatase (ALP) isoenzymes in carcinoma tissues of the gastro‐intestinal tract were compared with those of purified human intestinal, placental and hepatic ALPs to investigate the gene expression of gastro‐intestinal cancer cells. The results were as follows: ALP obtained from carcinoma tissues of 77 patients was separated into 6 bands (ALPa, ALPb, ALPc, ALPd, ALPe and ALPf) by polyacrylamide‐gel disc electrophoresis. It was concluded that ALPa was similar in its enzymological and immunological properties to hepatic‐type ALP, ALPb was similar to placental‐type ALP (Regan ALP or Nagao ALP), ALPc to intestinal‐type ALP (metaplasia ALP), ALPd to hepatoma‐type ALP (Warnocks variant ALP), ALPe to intestinal‐type ALP except for electrophoretic mobility, and ALPf was similar to hepatic‐type ALP except for neuraminidase sensitivity. ALPb appeared in 16 out of 55 cases (29%) of gastric carcinoma, and 2 out of 21 cases (10%) of colonic carcinoma. ALPd appeared in 4 out of 55 cases (7%). ALPe appeared in 2 out of 55 cases (4%) of gastric, and 3 out o 21 cases (14%) of colonic carcinoma. ALPf appeared in 1 out of 55 cases (2%) of gastric, and 1 out of 21 cases (5%) of colonic carcinoma. These ALP isoenzymes (ALPb, ALPd, ALPe and ALPf) probably originate from the cancer cells themselves and may represent an abnormal gene expression of cancer cells in the process of onco‐developmental differentiation.

Prognosis of liver cirrhosis

Clinical surveys on 224 patients with liver cirrhosis were made to assess the recent advance in the treatment for liver cirrhosis. These patients consisted of those received treatment in our Department in the years from 1938 to 1965.SummaryClinical surveys on 224 patients with liver cirrhosis were made to assess the recent advance in the treatment for liver cirrhosis. These patients consisted of those received treatment in our Department in the years from 1938 to 1965.Of the principal causes of death in cirrhotics studied, hepatic coma has recently decreased and bleeding from the alimentary tract has increased. Cachexia or infection as the cause of death has also decreased.Such an improvement is likely to be attributable to introducing a high protein, high caloric diet. Alternatively, the therapeutic use of potent diuretic drugs has brought success in the treatment of ascites and edema, however, there has been found no betterment in the survival rate of cirrhotics with ascites.Among the abnormal findings which were shown in cirrhotics, icterus index more than 30, bromsulphalein retention exceeding 30 percent in 45 min, albumin/globulin ratio less than 0.5, zinc sulfate test more than 30, and reduced albumin less than 1.5 g/dl were of much omnious significance. The majority of those died within a year. Prothrombin time, total protein values, and transaminase activities in sera were not to be related to the prognosis.Most of deaths without any marked abnormalities in laboratory findings died of massive hemorrhage from the alimentary tract.

A CASE REPORT ON AN AMYLOID GOITER WITH RECURRENT SYMPTOMS OF SUBACUTE THYROIDITIS

亜急性甲状腺炎を思わせる症状をくりかえした1例につき,甲状腺のOpen biopsyを行ない,組織所見においてamyloid沈着を証明したが,炎症性の組織変化は全く認められず,さらに各種臨床検査および肝生検をおこなつたところ, amyloidの沈着は甲状腺にのみ撰択的であつた.今日まで報告されているamyloid甲状腺腫で亜急性甲状腺炎を思わせる症状を呈した例はないので,このような症状との関連につき詳細な検討を試みた.

The effect of plasma exchange on the skin lesions in systemic lupus erythematosus.

The clinical effects and the changes of laboratory data after plasma exchange (PE) in 11 patients with systemic lupus erythematosus (SLE) refractory to the corticosteroid and other drug therapy were investigated.After several PEs, 8 out of 11 patients clinically improved especially in the skin lesions, namely butterfly-shaped skin rashes or skin ulcers and so on.And the decrease of the antibody to DNA and immune complex was significantly correlated with the degree of the clinical improvement.Furthermore, the intensity of anti-endothelial cell antibody demonstrated by the indirect immunofluorescent method, which was different from antibody to DNA or immune complex, was closely related to the skin lesions of SLE. But the change of the intensity of anti-endothelial cell antibody and the degree of the improvement of skin lesions are not necessarily correlated and this reason remains to be elucidated.