Table 1 Laboratory findings in a patient with diabetic ketoacidosis Laboratory Findings Urine: Protein (-) Sugar (?? ) Aceton body (+) Urobilinogen (n
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2 Table 1 Laboratory findings in a patient with diabetic ketoacidosis Laboratory Findings Urine: Protein (-) Sugar (?? ) Aceton body (+) Urobilinogen (n) Sediments(WBC 1/4-5 Epithel 1/4-5 Cylinder> 10/1) CBC: WBC 16, 500/mm3 RBC 468 ~ 104/mm3 Hb 16 g/dl Ht 44. 9% Plat. 26 ~ 104/mm3 Retic. 12%. Differential (Baso 1% Stab 28% Seg 57% Lymph 12% Mono 2%) Biochemistry: Na 138 meq/l K 5.0 meq/l Cl 102 meq/l BUN mg/dl B.S. 1, 005 mg/dl TP 7.1 g/dl TTT 0.7 u ZTT 2. 4 u GOT 16 u GPT 14 u LDH 280 u Al-P 11.0 u Cholesterol 204 mg/dl Ĉ-lipoprotein 463 mg/dl Fe 131 ć/dl TIBC 328 ć/dl LAP 205 G-Ru Amylase 70 u Blood Gas Analysis: ph po mmhg pco mmhg HCO meq/l (12/25) Total CO2 9.1 mm/l BE meq/l O2Sat % Osmolarity: 388 mosm/l (12/25) Serological tests: ASLO 12 u CRP ( }) RA (-) STS (-) Parainfluenza Virus Antibdy (+) HB Antigen (-) CEA 0.52 ng/ml Coagulation tests: Thrombotest 100% P.T sec P.T.T sec Thromboplastin Generation time 80 sec Fibrinogen 252 mg/dl FDP 5 Đg/ml ESR: 6 mm/hr E.C.G.: Pulmonary P, Sinus Tachycardia Chest X-P: n.p. Clinical Course (1) Fig. 1 Clinical course in a patient with diabetic ketoacidosis The acute renal failure, which emerged soon after admission, was treated by hemodialysis (total 21 times) and thereafter ameliorated spontaneously.
3 高 ミオ グ ロ ビ ン血 症 と と もに急 性 腎 尿 細 管壊 死 を 併 発 した 糖 尿 病 性 昏 睡 の1例 Table 2 Changes of blood cells, coagulation radioimmunoassayed Clinical Course Fig. Some factors, in blood myogenic during enzymes, clinical electrolytes and course (2) 2 Renal epithelial regenerated. substances biopsy cells There shows of is renal no clear acute tubules lesion tubular necrosis degenerated of glomeruli. 413 (right and PAS ~ desquamated 200, and left also HE ~ some 100) newly
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5 5) Bradley, R.F.: Diabetic ketoacidosis and coma. In: Joslin's Diabetes Mellitus edited by Marble, A.A. White, P., Bradley, R.F., Krall, L.P. 11th ed. Philadelphia, Lea & Febiger (1973) p ) Pirovino, M., Neff, M.S., Sheron, E.: Myo- globulinuria and acute renal failure with acute polymyositis. New York State J. Med. 79: (1979) 1) Sänksen, P.H., Srivastava, M.C., Tompkins, C.V., Nabarro, J.D.N.: Growth hormone and cortisol responses to insulin infusion in patients with diabetes mellitus. Lancet II: (1972) 2) Page, M.M., Alberti, K.G.M.M., Greenwood, R., Gumaa, K.A., Hockday, T.D.R., Lowy, C., Nabarro, J.D.N., Pyke, D.A., SOnksen, P.H., Watkins, P. J., West, T.E.T.: Treatment of diabetic coma with continuous low dose infusion of insulin. Brit. Med. J. 2: (1974) 3) Semple, P.F., White, C., Manderson, W.G.: Continous intravenous infusion of small dose of insulin in treatment of diabetic ketoacidosis. Brit. Med. J. 2: (1974) 8) Fukuyama, Y., Ando, T., Yokota, T.: Acute diabetic ketoacidosis. Diabetes 23: (1974) fluminant myoglobinuric polymyositis with picorna virus-like crystals. J. Neurol. Neurosurger. and psychiatr. 40: (1977) 11) Velez-Garcia, E., Hardy, P., Dioso, M., Perkoff, G.T.: Cysteine-stimulated serum creatinephosphokinase: Clin. Med. 68: (1966) Unexpected results. J. Lab. 12) Knight, A.H., Williams, D.N., Spooner, R.I., Goldberg, D.M.: Serum enzyme changes in
6 Abstract A Case of Diabetic Ketoacidosis with Acute Renal Tubular Necrosis and Severe Hypermyoglobulinemia Takeharu Itatsu, Akira Ohta and Naruki Matsuda Department of Internal Medicine, Nagoya Second Red Cross Hospital, Nagoya, Japan A case of diabetic coma associated with acute renal tubular necrosis is reported. The patient was a 24-yr-old man. He had suffered from a common cold 2 weeks before admission. His complaints on admission were abdominal pain, thirst, polyuria and weightloss. Hyperglycemia (1, 005 mg/dl) and acetonuria with metabolic acidosis (ph 7. 1) indicated diabetic ketoacidosis. Continuous intravenous infusion of insulin (4 unit/hr) was begun immediately. However, he became oliguric and markedly edematous. Acute renal failure accompanied by severe hypermyoglobulinemia (23, 680 ng/ml) and a transient DIC (platelets 2. 3 x 104/mm3, serum FDP 40 mg/dl) probably resulted from acute renal tubular necrosis, which was demonstrated by renal biopsy and spontaneously relieved after the performance of the 21st hemodialysis. The severe hypermyoglobulinemia may have derived not only from the ketoacidosis itself and circulatory disturbance, but also from direct invasion of viruses into the muscle tissues. This may represent a major factor contributory to the acute renal tubular necrosis.
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