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We herein report the case of a 41-year-old Japanese female office worker who developed symptomatic hypocalcemia with severe vitamin D deficiency following treatment for Graves’ disease with methimazole. The patient’s hypocalcemia was mainly caused by vitamin D deficiency due to unbalanced diets and inadequate exposure to sunlight in addition to the resolution of hyperthyroidism. Vitamin D deficiency is increasing worldwide, and it has been more recently shown to relate to the pathogenesis of Graves’ disease. However, vitamin D deficiency as a cause of hypocalcemia has received little attention. Taken together, this case suggests that we should take more care in calcium kinetics and vitamin D status during treatment for Graves’ disease with antithyroid drugs.

Although chronic pain due to diabetic neuropathy, defined as painful diabetic neuropathy (PDN), is a debilitating and distressing complication of diabetes, epidemiological data on PDN has been scarce, especially in Asia. We evaluated the prevalence of Japanese PDN and its impact on their quality of life (QOL) and metnal state. In addition, we examined to which extent physicians are aware of patients’ PDN. A total of 298 patients with diabetes were found to be eligible for the study. We revealed that substantial percentage (22.1%) of Japanese diabetic patients had PDN and that PDN had negative effect on patients’ QOL and mental state. However, physicians were aware of PDN in only 36.4% of patients with the condition. To the best of our knowledge, this is the first report showing the extent of physicians’ awareness of patients’ PDN. In conclusion, physicians treating diabetes need to be more aware of patients’ PDN in everyday clinical practice to prevent the progression of PDN and improve the patients’ QOL and mental state.

We report a case of 42-year-old male patient with hypogonadotropic hypogonadism. He suffered from general fatigue and erectile dysfunction after the treatment with transdermal fentanyl for chronic pain by traffic injury. Endocrine examinations and hormone stimulating tests showed that he had hypogonadotropic hypogonadism. Brain magnetic resonance imaging (MRI) showed no abnormal findings, and he had no past history of accounting for acquired hypogonadotropic hypogonadism. Therefore, his hypogonadism was diagnosed to be caused by opioid treatment. Although opioid-induced endocrine dysfunctions are not widely recognized, this case suggests that we should consider the possibility of endocrine dysfunctions in patients with opioid treatment.