A case of Graves' disease developing with exacerbation of sarcoidosis.

A 53-year old female was referred to our hospital with bilateral abnormal shadow in the chest X-ray. Computed tomography revealed multifocal ill-defined densities and thickening of bronchial wall and pulmonary vessels by fine nodules combined with massive enlargement of bilateral mediastinal and hilar lymph nodes. Analyses of bronchoalveolar lavage fluid and transbronchial lung biopsy specimen showed the increase in CD4/CD8 ratio and the presence of non-caseating granulomas, respectively. In addition, serum angiotensin-converting enzyme was extremely high, leading to the diagnosis of sarcoidosis. Simultaneously, she complained of palpitation and sweating. Endocrinological examination showed comorbid hyperthyroidism without anti-TSH receptor antibody (TRAb). In the first 2-3 months, pulmonary shadow gradually disappeared without steroid administration. In parallel, serum thyroid hormone levels were gradually normalized in the beginning, but increased after 3 months with an appearance of TRAb. After initiation of treatment with antithyroid agent, hyperthyroidism was improved within 9 months, and changed into hypothyroidism thereafter. The clinical course of this rare case suggest that immunological storm by exacerbation of sarcoidosis may trigger the onset of autoimmune thyroid disease, in which hyperthyroidism with stimulating type of TRAb subsequently changed into hypothyroidism with blocking-type TRAb.

Rat-Bite Fever in Human with Streptobacillus notomytis Infection, Japan.

We report a case of rat-bite fever in a 94-year-old woman with Streptobacillus notomytis infection. We established an epidemiologic link between exposure to rats and human infection by performing nested PCRs that detected S. notomytis in the intraoral swab specimens obtained from rats captured in the patient's house.

Association between nighttime sleep duration, midday naps, and glycemic levels in Japanese patients with type 2 diabetes.

OBJECTIVES: To clarify the relationship between nighttime sleep duration, midday naps, and glycemic control in Japanese patients diagnosed with type 2 diabetes (n = 355) or impaired glucose tolerance (n = 43). METHODS: A total of 398 patients completed a self-administered questionnaire on sleep duration/quality and were divided into five groups according to their self-reported nighttime sleep duration: <5 h, 5-6 h, 6-7 h, 7-8 h, and >8 h. Each group was further divided into two subgroups each according to the presence or absence of midday naps. Poor glycemic control was defined as HbA1c ≥ 7.0%. RESULTS: Short nighttime sleep (<5 h), poor sleep induction, daytime sleepiness, and low sleep satisfaction were associated with high HbA1c levels. HbA1c was higher in the short nighttime sleep/no nap group than in non-nappers with different nighttime sleep duration, whereas the short nighttime sleep/nap group showed similar HbA1c levels to the other nap subgroups. In multivariate logistic regression models, after adjusting for a number of potential confounders, short (<5 h) nighttime sleep without nap was significantly associated with poor glycemic control compared with 6-7 h nighttime sleep without nap (OR [95% CI]: 7.14 [2.20-23.20]). However, taking naps reduced this risk for poor glycemic control in short sleepers. Other risk factors for poor glycemic control were low sleep satisfaction (1.73 [1.10-2.70]) and poor sleep induction (1.69 [1.14-2.50]). CONCLUSIONS: Poor sleep quality and quantity could aggravate glycemic control in type 2 diabetes. Midday naps could mitigate the deleterious effects of short nighttime sleep on glycemic control. CLINICAL TRIALS REGISTRATION: UMIN 000017887.

Evaluation of metabolic parameters and body composition in Japanese patients with type 2 diabetes mellitus who were administered tofogliflozin for 48 weeks.

Sodium glucose cotransporter 2 inhibitors are unique antihyperglycemic agents that cause osmotic diuresis and calorie loss to urine. We previously reported that administration of tofogliflozin, a sodium glucose cotransporter 2 inhibitor, for 8 weeks decreased fat-free mass without affecting fat mass. We thus investigated the impact of tofogliflozin on metabolic parameters and body composition for 48 weeks in Japanese patients with type 2 diabetes mellitus. This single-arm open-label study enrolled 20 patients. Patients received tofogliflozin 20 mg once daily for 48 weeks. At week 48, changes in metabolic parameters and body composition from baseline were evaluated. Two patients discontinued administration due to adverse events during the first 8 weeks; however, no other adverse events occurred after that period. Seventeen patients completed the 48 weeks of administration of tofogliflodin. Body weight and body mass index decreased during the treatment period. Hemoglobin A1c decreased from 7.8% to 7.1%. The degree of improvement in hemoglobin A1c was correlated with body mass index, fat mass, and plasma glucose level at baseline. As for body composition, fat mass decreased without any change in fat-free mass (including total body water, extracellular water, and intracellular water). Red blood cell count and hematocrit increased, while the estimated glomerular filtration rate decreased. ALT and γ-GTP decreased and the decrease in γ-GTP was correlated with the loss of fat mass. In conclusion, our study clearly suggests that the body weight reduction caused by tofogliflozin administration for 48 weeks was almost entirely due to fat mass dissipation.

Impact of the 8-week Administration of Tofogliflozin for Glycemic Control and Body Composition in Japanese Patients with Type 2 Diabetes Mellitus.

Objective The adverse effects of selective sodium-glucose co-transporter 2 (SGLT2) inhibitors generally appear within about two or three months after treatment initiation in Japan. Therefore, we investigated the impact of tofogliflozin, a class of SGLT2 inhibitors, on glycemic control and body composition during this period in Japanese patients with type 2 diabetes mellitus. Methods This single-arm open-label study enrolled 20 patients. Patients received tofogliflozin 20 mg once daily for 8 weeks. At week 8, changes from baseline in body weight, serum metabolic markers, and body composition were evaluated. Results A total of 17 patients completed the 8-week administration of tofogliflodin. No serious adverse events were noted. Hemoglobin A1c (HbA1c) decreased significantly, from 7.8% to 7.3% with 8-week administration of tofogliflozin. Both the body weight and body mass index (BMI) also decreased. In addition, a decreased renal function of the boundary zone and hemoconcentration were detected. As for body composition, the free fat mass, total body water, extracellular water and intracellular water were all decreased significantly. Interestingly, the amount of fat mass did not change. The degree of improvement in HbA1c was correlated with the baseline fat mass and BMI. Conclusion An eight-week administration of tofogliflozin improved glycemic control and reduced the body weight and free fat mass in type 2 diabetic patients without affecting the fat mass. In this period, the hematocrit level and renal function should be monitored to guard against hemoconcentration and renal impairment, respectively.

Concurrent Therapy with a Low-carbohydrate Diet and Miglitol Remarkably Improved the Postprandial Blood Glucose and Insulin Levels in a Patient with Reactive Hypoglycemia due to Late Dumping Syndrome.

Reactive hypoglycemia induced by late dumping syndrome is often observed after gastrectomy. However, no effective therapy has yet been fully established. We herein describe a case in which concurrent therapy with a low-carbohydrate diet using low-glycemic-index food and an alpha-glucosidase inhibitor, miglitol, very effectively ameliorated the postprandial fluctuations in the blood glucose and plasma insulin levels in a patient with reactive hypoglycemia due to late dumping syndrome following total gastrectomy. The administration of miglitol under a low-carbohydrate diet using low-glycemic-index food may therefore be an ideal treatment for reactive hypoglycemia due to late dumping syndrome.