1.Causes of death in non-insulin-dependent diabetes mellitus.
Tomio KAMETANI ; Yutaka IGARASHI ; Takayuki HORIGAMI ; Masanori KAWATO ; Tadayuki NAGAI ; Masayuki KATO
Journal of the Japanese Association of Rural Medicine 1990;39(2):107-110
We analyzed the causes of death in 74 non-insulin-dependent diabetes mellitus (NIDDM) patients who died in Koseiren Takaoka hospital between 1982 and 1988 and compared with 334 non-diabetic dead patients.
The first cause of death in NIDDM was malignant neoplsma (35.1% of NIDDM). The second was ischemic heart disease (17.6%). The third was infection (12.2%). The ratios of cerebral infarction and diabetic nephropathy were 9.5% each. The ratios of ischemic heart disease and cerebral infarction in diabetics were twice those in non-diabetics. The tratio of uremia in diabetics wassix-fold. In patients over 61 years old, the ratios of ischemic heart disease and diabetic nephropathy were large. Nevertheless, in patients under 60 years old, the proportion of cerebral infarction was higher. The proportions of cerebral infarction and ischemic heart disease were higher in the group of long diabetic duration than in group of short duration.
Compared with past Japanese reports, the proportions of malignant neoplasma and ischemic heart disease in diabetics increased and the proportions of diabetic nephropathy and coma decreased.
This study concluded that not only the control of diabetes mellitus but also the examination of malignant neoplasma was important in management of diabetes mellitus. The proportion of the causes of death in diabetics will change with changes of the circumstances and the progress of medical treatment.
2.A Case of Diabetes Mellitus with Normal Pressure Hydrocephalus.
Tomio KAMETANI ; Tatsushi MORITA ; Isao TANAKA ; Hideo KOSHIDA ; Yutaka IGARASHI ; Takayuki HORIGAMI ; Tadayuki NAGAI ; Masayoshi KATO
Journal of the Japanese Association of Rural Medicine 1994;43(1):41-44
The patient was a 56-year-old male. He had a history of alcoholism since 1975 and diabetes mellitus since 1978. He was treated with insulin therapy. But the control of diabetes mellitus was very poor and he had six hypoglycemic comas attacks. He had diabetic triopathy but no symptoms of gait disturbance, dementia and incontinence. Brain computerized tomography and magneting resonance imaging revealed severe communicating hydrocephalus with mild brain atrophy.111In-DPTA cisternography revealed retension of isotope in the ventricle after 48 hours. The pressure of cerebrospinal fluid was normal.
This case report is interesting as it suggests the relationship between normal pressure hydrocephalus and hypoglycemia.
3.Effective Treatment of Reactive Hypoglycemic Coma with Acarbose: A Case Report.
Tomio KAMETANI ; Masaharu NOMURA ; Tsukasa YAMAZAKI ; Tatsushi MORITA ; Isao TANAKA ; Hideo KOSHIDA ; Takayuki HORIGAMI ; Masayoshi KATO ; Kiyohide KITAGAWA
Journal of the Japanese Association of Rural Medicine 1995;44(4):609-612
We report a case of reactive hypoglycemic coma in a 77-year-old man. Seven months after partial gastrectomy for early gastric cancer, he presented with syncopal attacks and seizure. His plasma glucose and insulin levels at coma were 18 mg/dl and 27μU/ml. Insulinoma was neglected with computerized tomography, magnetic resonance imaging and angiography. Because dietary control was insufficient, oral diazoxide therapy was done. But diazoxide did not protectthe overresponse of the insulin and reactive hypoglycemia in 75 g GTT. Octreotide (100 micrograms IM) inhibited insulin release and prevented hypoglycemia. Acarbose delayed the response of insulin butdid not inhibited insulin release. However, acarbose also prevented reactive hypoglycemia. We concluded that acarbose is an effective therapy for reactive hypoglycemic coma.