Tetsushi Sakurai

Monocyte-mediated suppression of T lymphocyte blastogenesis and its reversal by deoxyguanosine. Defects in patients with systemic lupus erythematosus

We investigated monocyte-mediated suppression of T lymphocyte blastogenesis in normals and patients with systemic lupus erythematosus (SLE). When monocytes from normals were cocultured with autologous T lymphocytes with a ratio of 1:1 and stimulated with phytohemagglutinin (PHA), 3H-thymidine incorporation by T lymphocytes was suppressed. This monocyte-mediated suppression was reversed by purine nucleoside phosphorylase substrate, deoxyguanosine. In SLE patients, both monocyte-mediated suppression and its reversal by deoxyguanosine were defective. The defective function was observed both in patients with active and inactive diseases. The defective function was studied sequentially before and after change in the clinical status of patients. The defects remained unaffected regardless of the disease activity. The defects in monocyte-mediated suppression and its reversal by deoxyguanosine in SLE patients as demonstrated in our study suggest the presence of intrinsic monocyte dysfunction in SLE.

A case of giant cell arteritis simulating aortitis syndrome : A case report.

73才の女性で,巨細胞動脈炎に甲状腺機能亢進症と糖尿病を合併した症例を経験した.大動脈弓部動脈群を侵す巨細胞動脈炎と大動脈炎症候群との鑑別には,発病年令,頭痛,側頭動脈の圧痛,肺・腎血管病変の有無, polymyalgia rheumaticaの合併の有無,抗大動脈抗体の存在およびその抗体価, HLAなどが参考になると考えられる.診断上,生検は必須であるが,病変が分節的に側頭動脈以外の小動脈にも及ぶことがある.甲状腺機能亢進症を合併していたが,両者の合併の背景には自己免疫学的な機序の関与が示唆された.

A CASE OF OSLER'S DISEASE WITH GASTRODUODENAL ULCERS

症例は65才,主婦.鼻出血,心窩部痛を主訴に入院した.父に鼻出血,娘に鼻出血および毛細血管拡張病変を認めた. 14才頃より鼻出血が時々あり, 57才頃より毛細血管拡張と口腔内出血が著しくなつた.入院時,皮膚,口腔・鼻腔粘膜の著しい毛細血管拡張,眼瞼結膜に強度の貧血を認めた.肺には異常血管雑音を聴取せず,肝は約4cm触知したが,脾腫は認めなかつた.検査所見では便潜血陽性,ヘモグロビン6.5g/dl,血清鉄, UIBCは鉄欠乏型であつた.肝機能障害を認め,超音波検査は肝硬変に一致した.凝固系検査は正常であつた.胃・十二指腸造影検査,内視鏡検査にて胃および十二指腸潰瘍を認め,潰瘍底部とその周辺部に毛細血管拡張病変を認めたこと,胃液検査にて胃酸が分泌過多であつたことから,本症における消化性潰瘍の発生機序について考察を加えた.

Fibrinogen/fibrin degradation products in serum of patients with idiopathic thrombocytopenic purpura: elevated levels during severe thrombocytopenic phase of the disease.

Sera from 23 patients with idiopathic thrombocytopenic purpura (ITP), 14 patients with aplastic anemia with severe thrombocytopenia and healthy control subjects were tested for the presence of fibrinogen/fibrin degradation products (FDP), using the tanned red cell hemagglutination inhibition immunoaassay. The concentrations of circulating FDP of ITP patients (mean 12.01 mug/ml) were significantly higher than those of the patients with aplastic anemia (mean 4.01 mug/ml, p less than 0.05) or normal controls (mean 3.10 mug/ml, p less than 0.001). The patients with untreated ITP with very low platelet counts had higher levels of FDP than those of the treated group (p less than 0.01). Serum FDP and a battery of other coagulation-fibrinolysis tests were serially carried out over a period of 10 weeks in two patients with ITP. The initially high FDP promptly decreased as circulating platelets increased in response to steroid in both patients, while plasma fibrinogen, euglobulin lysis time, prothrombin time and partial thromboplastin time remained essentially normal during the course of observation. The exact source of the increased serum FDP in ITP was not established, but a few possible mechanisms responsible for this abnormality were discussed.