We observed changes in fasting blood sugar and plasma lipids following reduction of oral hypoglycemic agents in 22 diabetics where control of blood sugar was good over a period of about 1 yr without episodes of hypoglycemia.
1. The “good control” group, based on the criteria of Marble of the Joslin Clinic prior to the reduction of oral hypoglycemic agents, comprised 18 patients with an average age of 62.3 yr and an average period of 8.8 yr from the onset of diabetes. The average observation periods before and after the reduction of oral hypoglycemic agents were 11.8 months and 2 yr, respectively. On average, the dose of oral agents was reduced by 65% of the initial dose. Subsequent to this reduction 14 cases (78%) remained as “good controls” and 4 cases (22%) became “fair controls”. the mean fasting blood glucose prior to the reduction of oral agents in the group remaining as “good controls” even after the reduction was significantly lower than that in the group becoming “fair controls” after the reduction (86.8±5.9 mg/dl versus 95.1±5.4 mg/dl, p<0.05).
No significant changes in body weight or level of plasma lipids were oberved during the study. The degree of diabetic complications, such as albuminuria, retinopathy and abnormality of electrocardiographs, also underwent no significant changes.
2. The “fair control” group based on the same criteria comprised 4 patients with an average age of 66 yr and an average period of 8.75 yr from the onset of diabetes. On average, the dose of hypoglycemic agents was reduced by 35 % of the initial dose. Subsequent to this reduction, 2 cases remained as “fair controls” and 2 cases became “poor controls.” No significant changes in level of plasma lipids or degree of diabetic complications were observed during the study.

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Environmental and genetic factors have been considered important in the pathogenesis of diabetes mellitus. However, in insulin dependent diabetics (IDD), recent investigations suggest that an autoimmune process may be responsible for its pathogenesis.
The clinical association between IDD and autoimmune diseases and a high rate of occurrence of organ-specific antibodies such as antithyroid antibodies in IDD have already been reported. Also, using an indirect immunofluorescence technique, circulating antibodies to pancreatic islet cells have recently been detected by many research groups in the United Kingdom.
However, islet-cell antibodies (I.C.Ab.) were first described by Bottazzo et al. and Mac-Cuish et al. in the sera of IDD with polyendocrine diseases.
Irvine et al. clarified that I.C.Ab. were most common in newly diagnosed IDD of recent onset and the prevalence of humoral I.C.Ab. was strongly dependent on the duration of the diabetes. Moreover, they have also shown that diabetics who did not require insulin for treatment but who were I.C.Ab.-positive showed a significant tendency to subsequently require insulin.
In collaboration with W. J. Irvine of the Royal Infirmary (Edinburgh), pancreatic islet-cell antibodies were detected by us in IDD. Fresh postmortem snap-frozen pancreatic tissue of blood group 0 and antihuman IgG-FITC (Wellcome) were used. Six out of 123 diabetics treated with insulin had I.C.Ab. in their sera.
The prevalence of I.C.Ab. in the control population was low, at 0.5%(p<0.005). The inverse relationship observed between the prevalence of these antibodies and duration of the diabetes was the same as that reported by Dr. Irvine. I.C.Ab. were present in 16% of IDD during the first year and in 8.3% between 1 and 3 yr after the disease onset.
The prevalence of I.C. Ab. fell to 0 % at more than 4 yr.

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Clinical observations were carried out on 552 patients with diabetes mellitus (DM) who had developed the diseaset below the age of 30 and had been followed up by members of the Kyushu Diabetes Research Group in 20 medical agencies covering the entire Kyushu area of southern Japan (population 13, 602, 000). Among the patients, 152 cases had an age of onset below 15 yr (group A), 235 between 15 and 25 yr (group B), and 165 between 25 and 30 yr (group C).
The incidence of females was significantly higher than that of males among patients who developed DM below the age of 25, whereas this was not the case among patients who developed DM between the ages of 25 and 30.
The incidence of insulin dependency was highest in group A patients and lowest in group C patients.
Among the patients who developed DM below the age of 25, the incidence of insulin dependency was significantly higher in those lacking a family history of DM than in those with a family history of DM. However, among group C patients, no significant difference in the incidence of insulin dependency between patients with and without a family history of DM was observed.
The above results suggest firstly that group C patients differ from group A or B patients in their clinical features, and secondly that a higher incidence of insulin dependency is associated with a younger age of onset and absence of a family history of DM.
No seasonal fluctuations in the onset of juvenile-onset diabetes were observed insofar as the present study was concerned.

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Quantitative bacterial culture on clean-catch urine was carried out in a group of 155 diabetic outpatients and in the same number of non-diabetic outpatients with the same distribution of age and sex, in order to investigate the prevalence of and contributing factors to bacteriuria in the diabetic patients.
Significant bacteriuria was detected at a rate of 5.8% and 2.8%, respectively, in the two groups. However, this difference was not statistically significant. Moreover, no significant differences were obtained when the data was analyzed according to sex and age group.
In the diabetic patients, factors such as history of previous catheterization, age, duration, regimen and control of diabetes, and diabetic retinopathy were not related to the incidence of bacteriuria. On the other hand, factors such as diabetic neuropathy, nephropathy, hypertension, and females, were found statistically to contribute to the development of bacteriuria.

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This report concerns 5 cases of diabetes mellitus complicated with sudden deafness. The relationship between the clinical features of diabetes mellitus and hearing impairment is discussed. Diabetic retinopathy and neurological abnormalities, as judged from ankle jerk and/or vibratory sensation in the lower limbs, were observed in all cases except one male adult onset-type diabetic patient. The deafness, affecting one ear, was accompanied by transitory tinnitus, which was also combined with attacks of vertigo in two cases. The results of an audiometric examination revealed unilateral perceptive hearing loss in all cases except one. The degree of deafness and shape of the hearing loss were within wide limits, varying from 22.5 dB to anakusis.
Although steroid hormone was administered orally in 4 patients for treatment of sudden deafness, hearing improvement was observed in only 2 patients who visited an otorhinolaryngologist within 2-7 days after the onset of their attack of deafness. On the other hand, no improvement was found in the other patients, including one case with good diabetic control and without diabetic complications, where the treatment was started more than a month after the onset of sudden deafness.
It is suggested that the precocity treatment is essential if good results are to be obtained regarding sudden deafness.

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To our Knowledge, only 2 cases of acute diabetes following an attack of infectious mononucleosis (IM) have previously been reported. The case described here thus represents the third such occurrence of acute diabetes, during the clinical course of Epstein-Barr (EB) virus infection.
A 7-yr-old boy was admitted due to severe diabetic symptoms. Fifty days prior to admission, he had experienced vomiting and diarrhea followed by a fever of up to 39°C for 3 weeks. One week after these symptoms had subsided, he experienced severe polydipsia, polyuria, polyphagia and lost 3 kg of body weight. On admission he displayed systemic lymphnode enlargement and hepatomegaly. His laboratory data revealed leukocytosis (9700/mm³) with 3 % atypical lymphocytes, hyperglycemia (plasma glucose 600 mg/dl) and ketonemia (β-hydroxybutyrate 4296 μM). Serological analysis showed the Paul-Bunnell heterophile antibody test to be positive (1: 224) on admission and negative one month later. The immunofluorescence test for antibody to EB viral capsid antigen was at a titer of 1: 160 on admission, rose to as high as 1: 640 after 3 weeks and persisted at the same level for a further 3 months. The titer of IgM antibody for EB virus was 1: 640 on hospitalization, decreased to 1: 40 one month later and remained at the same level for the next 3 months. The patient's histocompatibility antigen was a phenotype of HLA-AW 26, BW 40/AW 24, B 7. The antibody against a microsomal component of thyroid cells appeared at the 7th month of diabetes. After successful treatment of the acute diabetes with insulin for one month, an oral glucose (O.75 g/kg body weight) tolerance test was performed. This demonstrated an almost total absence of immunoreactive insulin response. Subsequently, the patient has remained insulin dependent for more than 1 yr. He had no family history of diabetes and had not been obese. A urinary glucose test performed 1 yr before his admission was found to be negative by inquiring about his physical record at primary school.
It is thus not likely that latent diabetes became overt due to the current infection. The time lag between the acute phase of IM and the onset of diabetes also opposes such occasional aggravation. In conclusion, therefore, the acute diabetes in the present case is considered to be newly induced by an irreversible injury of pancreatic B cells infected with EB virus.

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