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The Sumida River, a typical urban river in Tokyo, has been recognized as a site for fostering Tokyo’s urbanlife that serves as a venue of leisure and relaxation for its residents. As the Teikyo University of Science(TUS) is located near the Sumida River, students spend a lot of time nearby. Clarifying the characteristics ofSumida River, and teaching it to students, are important not only for enhancing environmental awarenessamong students, but also local environment conservation. In this study, chemical oxygen demand (COD)and electric conductivity (EC) data, major sources of contamination, and the characteristics of the river wereanalyzed and interpreted as follows. 1) Although our COD and EC data showed that Sumida River wasaffected by tidal movement, the river water in our research area (from Otakebashi Bridge to Senju-OhashiBridge) might exhibit backward and forward movements, and it was slightly affected by sea water from theTokyo Bay. 2) Major chemical contaminant sources of investigated area were determined to be the Miyagiwastewater purification facility (WPF) and the Mikawajima WPF at the upstream and downstream sides ofthe TUS, respectively. 3) We presume a two-fraction zone in the Sumida River from our analytical resultsand public data, including a "high COD zone" with an upstream stagnant zone upper the Shirahige Bridge,and a "low COD zone" with a downstream flush zone under the Shirahige Bridge. Raising environmentalawareness concerning the urban river among its residents presumably might contribute to maintaining itsclean and safe environment. We came to conclusion that the importance of educating the citizens aboutkeeping urban rivers environmentally clean and safe for the future generations.

Idiopathic hypothalamitis is a rare condition that can cause anterior pituitary dysfunction and central diabetes insipidus (CDI), occasionally accompanied by a disturbance of autonomic regulation known as hypothalamic syndrome. This condition has been described as a subtype of autoimmune (lymphocytic) hypophysitis; however, some cases of isolated hypothalamic involvement with no inflammatory lesions in either the pituitary gland or infundibulum have been reported. The detailed epidemiology and pathophysiology of isolated hypothalamitis have not been clarified. We herein report a case of a solitary hypothalamic lesion in a young woman who showed spontaneous development of CDI and panhypopituitarism accompanied by hyperphagia. The hypothalamic lesion increased from 11 × 7 to 17 × 7 mm over 16 months based on the sagittal slices of magnetic resonance imaging examinations. The negative results for anti-pituitary antibodies and anti-Rabphilin-3A antibodies suggested that upward extension of lymphocytic adenohypophysitis or infundibulo-neurohypophysitis was unlikely. Infectious disease, granulomatosis, Langerhans cell histiocytosis, vasculitis, and systemic neoplastic diseases were excluded by the findings of a laboratory investigation, cerebrospinal fluid examination, and imaging studies. To make a definitive diagnosis, we performed a ventriculoscopic biopsy of the hypothalamic lesion. Histology revealed an infiltration of nonspecific lymphoplasmacytes with no evidence of neoplasm, which was consistent with a diagnosis of idiopathic hypothalamitis. Subsequently, the patient was treated with methylprednisolone pulse therapy followed by oral prednisolone. The hypothalamic lesion improved and remained undetectable after withdrawal of the prednisolone, suggesting that the glucocorticoid treatment was effective for isolated hypothalamitis while the patient remains dependent on the replacement of multiple hormones.

Amiodarone-induced thyrotoxicosis (AIT) is a complication of amiodarone therapy that can be difficult to diagnose and manage, especially in patients with dilated cardiomyopathy (DCM). We describe a 47-year-old female patient with DCM who experienced the sudden onset of type II AIT with symptoms mimicking low cardiac output syndrome, namely, general malaise and nausea. Early type II AIT was diagnosed, and effectively treated with prednisolone.

Objective: Hypothyroidism is not commonly considered a cause of hyperkalemia. We previously reported that hyperkalemia was observed mainly in elderly patients treated with renin-angiotensin-aldosterone system (RAS) inhibitors when levothyroxine treatment was withdrawn for the thyroidectomized patients with thyroid carcinoma to undergo radioactive iodine treatment. Here, we investigated whether acute hypothyroidism causes hyperkalemia in patients who were not treated with RAS inhibitors. We also investigated factors influencing potassium metabolism in hypothyroid patients. Methods: We conducted a single-center, prospective cohort study of 46 Japanese patients with thyroid carcinoma undergoing levothyroxine withdrawal prior to radioiodine therapy. All patients were normokalemic before levothyroxine withdrawal. Blood samples were analyzed 3 times: before, and at 3 and 4 weeks after levothyroxine withdrawal. We investigated factors that may be associated with the elevation of serum potassium levels from a euthyroid state to a hypothyroid state. Results: None of the patients developed symptomatic hyperkalemia. The mean serum potassium level was significantly higher at 4 weeks after levothyroxine withdrawal compared to baseline. The serum sodium levels, the estimated glomerular filtration rate (eGFR), and the plasma renin activity (PRA) decreased significantly as hypothyroidism advanced. In contrast, the plasma levels of adrenocorticotropic hormone, cortisol, aldosterone, and antidiuretic hormone were not changed, while serum thyroid hormone decreased. At 4 weeks after their levothyroxine withdrawal, the patients' serum potassium values were significantly correlated with the eGFR and the PRA. Conclusion: Acute hypothyroidism can cause a significant increase in the serum potassium level, which may be associated with a decreased eGFR and decreased circulating RAS. Abbreviations: ACTH = adrenocorticotropic hormone; ADH = antidiuretic hormone; ATPase = adenosine triphosphatase; eGFR = estimated glomerular filtration rate; HbA1c = glycated hemoglobin; K+ = potassium; Na+ = sodium; PRA = plasma renin activity; RAS = renin-angiotensin-aldosterone system; T4 = thyroxine; TSH = thyroid-stimulating hormone

A 44-year-old Japanese man was referred to our hospital for the evaluation of paroxysmal hypertension. (123)I-metaiodobenzylguanidine (MIBG) single-photon emission computed tomography (SPECT) revealed specific uptake in the left adrenal gland in addition to high levels of serum and urinary catecholamines although computed tomography and magnetic resonance imaging were not able to detect a definite adrenal mass. Left adrenalectomy was performed and he was diagnosed with adrenal medullary hyperplasia (AMH). A diagnosis of unilateral AMH is important because AMH resection can effectively treat hypertension.

Aims/Introduction The role of glucagon abnormality has recently been reported in type 2 diabetes; however, its role in gestational diabetes mellitus (GDM) is still unknown. The glucose intolerance in GDM is heterogeneous, and not all patients require insulin treatment during pregnancy. Here, we investigated whether glucagon abnormality is associated with the requirement for insulin treatment during pregnancy. Materials and Methods A total of 49 pregnant women diagnosed with GDM were enrolled. They underwent a 75‐g oral glucose tolerance test during mid‐gestation, and we measured their plasma glucagon levels (by a new sandwich enzyme‐linked immunosorbent assay) at fasting (0 min), and at 30, 60 and 120 min after glucose load in addition to the levels of plasma glucose and serum insulin. All participants underwent another oral glucose tolerance test at postpartum. Results Of the 49 patients, 15 required insulin treatment (Insulin group) and 34 were treated with diet therapy alone until delivery (Diet group). The early‐phase glucagon secretion after glucose load, as determined by the changes in glucagon from the baseline to 30 min, was paradoxically augmented during mid‐gestation in the Insulin group, but not in the Diet group. The impaired glucagon suppression during mid‐gestation in the Insulin group was not associated with insulin secretory/sensitivity indexes studied, and was ameliorated postpartum, although the plasma glucose levels remained higher in the Insulin group versus the Diet group. Conclusions Impaired early‐phase suppression of glucagon could be associated with the requirement for insulin treatment during pregnancy in patients with GDM., We evaluated the glucagon responses to oral glucose load in patients with gestational diabetes mellitus using a new sandwich enzyme‐linked immunosorbent assay. We investigated whether the glucagon abnormality is associated with the requirement for insulin treatment during pregnancy.

Objective: Patients with Graves disease (GD) tend to gain weight after treatment, but it remains unknown if weight gain is associated with an increase in the visceral and/or subcutaneous f...

Aims: To evaluate the glycaemic control of combination therapy with basal insulin and liraglutide, and to explore the factors predictive of efficacy in patients with type 2 diabetes when switched from longstanding basal-bolus insulin therapy. Methods: We studied 41 patients who switched from basal-bolus insulin therapy of more than 3 years to basal insulin/liraglutide combination therapy. Glycaemic control was evaluated at 6 months after switching therapy and used to subdivide the patients into good-responders (HbA1c, Diabetes Research and Clinical Practice, 144, pp.161-170; 2018

A 27-year-old woman with a history of gestational diabetes mellitus (GDM) developed type 1 diabetes mellitus (T1D) in the early postpartum period. Women with a history of GDM are at an increased risk of developing T1D, which is rarer than type 2 diabetes mellitus. A postpartum follow-up 75-g oral glucose tolerance test and the measurement of glutamic acid decarboxylase autoantibodies aided in the early detection of T1D in this patient. Careful attention should be paid to women with a history of GDM who exhibit clinical features suggestive of future development of T1D.

Cerebrotendinous xanthomatosis (CTX) is a rare, autosomal recessive, inborn disruption in bile acid synthesis characterized by severe systemic xanthomas, cataracts and neurological injuries occurring before adolescence without elevation of the serum cholesterol or triglyceride levels. CTX is caused by a deficiency of the mitochondrial enzyme sterol 27-hydroxylase, which is encoded by the CYP27A1 gene. We herein report a 50-year-old Japanese woman with late-onset CTX who had no relevant symptoms before the development of bilateral Achilles tendon xanthomas in middle age. A genetic analysis revealed a compound heterozygous mutation in the CYP27A1 gene with a previously known missense mutation (NM_000784.3:c.1421 G>A) and a novel frame shift mutation of NM_000784.3:c.1342_1343insCACC.

It has been reported that glucose responses during the oral glucose tolerance test differ between healthy women and men. However, it remains unknown what factors contribute to these differences between the sexes. The present study analyzed the insulin and glucagon responses during the oral glucose tolerance test in 25 female and 38 male healthy young adults aged 22–30 years. The plasma glucose levels at 120 min were significantly higher in women than men. Insulin secretion was significantly greater at 30, 90 and 120 min from baseline in women than men. Glucagon suppression was greater at 30 and 120 min from baseline in men than women when determined by a sandwich enzyme‐linked immunosorbent assay glucagon kit. These results suggest that the differences in glucose responses during the oral glucose tolerance test are mediated by the difference between the sexes in bi‐hormonal responses in healthy individuals.

Background: There have been great concerns about pediatric thyroid cancers after the accident at the Fukushima Daiichi Nuclear Power Plant in 2011. Case presentation: We report a case of a 7-year-old Japanese girl with sporadic papillary thyroid carcinoma (PTC) harboring an ETV6/NTRK3 rearrangement. The patient presented with tumors in both lobes and underwent thyroidectomy followed by radioactive iodine (RAI) ablation. Histopathology showed a classic type of PTC with cervical lymph node metastasis. Conclusions: Genetic evaluation showed ETV6/NTRK3 fusion but no BRAF mutations or RET/PTC rearrangements. RET/PTC rearrangement and BRAF mutations often contribute to the pathogenesis of PTC; however, rearrangements of NTRK genes are relatively rare in pediatric PTC. Although NTRK rearrangement has been shown to often present unique pathological types and infiltrative architectures in the western population, such findings were not observed in this patient. Thus, the present case of classic PTC with ETV6/NTRK3 rearrangement highlights the disparate collection of clinic-pathological features compared to the trend in the western population. We therefore emphasize the need to further accumulate clinical as well as genetic data in pediatric PTCs.

A 71-year-old man was admitted to our hospital with muscle pain on legs, anorexia, vomiting and fever after the discontinuation of oral betamethasone. Laboratory studies revealed elevated CRP, and ...

Aims Sodium-glucose cotransporter 2 inhibitors (SGLT2i) cause substantially less weight loss than would be expected based on their caloric deficits, probably due to enhanced appetite regulation known as “compensatory hyperphagia,” which occurs to offset the negative energy balance caused by increased glycosuria. We examined whether any specific nutrients contributed to the compensatory hyperphagia in diabetic patients taking SGLT2i. Methods Sixteen patients with type 2 diabetes were newly administered dapagliflozin 5 mg daily as the experimental SGLT2i group. Sixteen age-, sex- and BMI-matched type 2 diabetes patients not receiving dapagliflozin served as controls. A brief-type self-administered diet history questionnaire (BDHQ) was undertaken just before and 3 months after study initiation to evaluate changes of energy and nutrient intakes in each group. Results At 3 months, daily intakes of total calories and the proportions of the three major nutrients were not significantly increased in either group. However, daily sucrose intake was significantly increased after treatment versus the baseline value in the SGLT2i group (p =.003), but not in controls. The calculated intakes of all other nutrients were not significantly changed in either group. Conclusions Dapagliflozin treatment specifically increased sucrose intake, which might be an ideal target for nutritional approaches to attenuate compensatory hyperphagia., Diabetes Research and Clinical Practice, 135, pp.178-184; 2018

A 46-year-old woman with a history of Graves' disease presented with the chief complaints of appetite loss, weight loss, fatigue, nausea, and sweating. She was diagnosed with diabetic ketoacidosis (DKA), thyroid storm, and influenza A. She was treated with an intravenous insulin drip, intravenous fluid therapy, intravenous hydrocortisone, oral potassium iodine, and oral methimazole. As methimazole-induced neutropenia was suspected, the patient underwent thyroidectomy. It is important to maintain awareness that thyroid storm and DKA can coexist. Furthermore, even patients who have relatively preserved insulin secretion can develop DKA if thyroid storm and infection develop simultaneously.

Objective: Synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome is a rare, chronic, relapsing inflammatory osteoarticular disorder with dermatologic manifestations. SAPHO syndrome can be a rare cause of atypical symptoms including neurologic defects. We report a case with SAPHO syndrome with the endocrinologic defects most likely associated with SAPHO syndrome.Methods: Case report and review of the literature.Results: A 61-year-old Japanese female with SAPHO syndrome presented with polyuria and polydipsia. Pituitary magnetic resonance imaging (MRI) with gadolinium enhancement showed an enlarged infundibulum and pituitary with ring-enhancing masses located at the posterior pituitary and upper infundibulum. Extensive diagnostic workup excluded local and systemic infection, brain metastasis, and various secondary hypophysitis as the cause of the infundibular and pituitary lesions. There were spontaneous improvements in the MRI findings taken 4 months after her initial presentation. The patient underwent a biopsy of the anterior pituitary, which showed a sterile lymphocytic infiltration.Conclusion: There are rare cases of SAPHO syndrome patients in which transient neurologic symptoms associated with the self-limiting ring-enhancing lesions consisting of a sterile and nonspecific inflammation are described. Since cystic formation in the infundibulum caused by idiopathic lymphocytic hypophysitis has not been reported, to the best of our knowledge, we concluded that the endocrinologic defects in our patient were most likely associated with SAPHO syndrome. Thus, SAPHO syndrome should be considered as one of the causes not only for ring-enhancing lesions in the brain but also for secondary hypophysitis, especially in patients with dermatologic and osteoarticular manifestations.

A 72-year-old Japanese man developed progressive disturbance in ambulation with flexion contractures 5years before this admission. At 49 years of age, he was diagnosed with hypopituitarism after an operation for a Rathke's cleft. On admission, he could not fully extend his knees and hips because of painful muscle stiffness of the lower extremities. Initially, we suspected Stiff-person syndrome and initiated diazepam, which had no effect. Serum anti-glutamic acid decarboxylase antibody was negative. Next, we suspected flexion contractures associated with hypopituitarism. Endocrine evaluation revealed that ACTH, cortisol, and other hormone levels were lower than those reported in the previous evaluation. We treated the patient with hydrocortisone and his symptoms dramatically improved. It is rare for patients with hypopituitarism to have flexion contracture. This case suggests that we should consider hypopituitararism in the setting of flexion contractures. (Received October 18, 2018; Accepted March 26, 2019; Published June 1, 2019).

Objective: Exenatide once weekly (ExeOW) is one of the long-acting glucagon-like peptide 1 receptor agonists. Embedding exenatide in poly(D,L-lactide-co-glycolide) microspheres enables the once-weekly subcutaneous injection of exenatide as a treatment for diabetes. We report a case of a patient with type 2 diabetes and hypothyroidism who developed long-standing subcutaneous nodules after treatment by ExeOW injection.Methods: Case report and review of the literature. A 57-year-old Japanese man with type 2 diabetes treated with ExeOW and primary hypothyroidism.Results: We observed multiple subcutaneous nodules remaining at the ExeOW injection site for >10 weeks. As the patient's thyroid hormone levels normalized, these nodules decreased and disappeared, and his hemoglobin A1c levels improved.Conclusion: The patient's clinical course suggests that the hydrolysis of ExeOW at the site of injection may be inhibited by concomitant hypothyroidism, in which glycosaminoglycans including hyaluronic acid are known to accumulate (including in the skin). This case may indicate that hypothyroidism prolongs the existence of subcutaneous nodules from ExeOW treatment.Abbreviations: ExeOW = exenatide once weekly GLP-1 = glucagon-like peptide 1 HbA1c = hemoglobin A1c NGSP = National Glycohemoglobin Standardization Program PLG = poly(D,L-lactide-co-glycolide)

Biased agonism is a paradigm that may explain the selective activation of a signaling pathway via a GPCR that activates multiple signals. The autoantibody-induced inactivation of the calcium-sensing receptor (CaSR) causes acquired hypocalciuric hypercalcemia (AHH). Here, we describe an instructive case of AHH in which severe hypercalcemia was accompanied by an increased CaSR antibody titer. These autoantibodies operated as biased allosteric modulators of CaSR by targeting its Venus flytrap domain near the Ca(2+)-binding site. A positive allosteric modulator of CaSR, cinacalcet, which targets its transmembrane domain, overcame this autoantibody effect and successfully corrected the hypercalcemia in this patient. Hence, this is the first study to our knowledge that identifies the interaction site of a disease-causing GPCR autoantibody working as its biased allosteric modulator and demonstrates that cinacalcet can correct the AHH autoantibody effects both in vitro and in our AHH patient. Our observations provide potentially new insights into how biased agonism works and how to design a biased allosteric modulator of a GPCR. Our observations also indicate that the diagnosis of AHH is important because the severity of hypercalcemia may become fatal if the autoantibody titer increases. Calcimimetics may serve as good treatment options for some patients with severe AHH.

Background Patients with central diabetes insipidus (CDI) are known to lose weight because their polydipsia interferes with their nutritional intake. We retrospectively examined weight changes in CDI patients when they switched from nasal to oral desmopressin. Methods Twenty-three patients with CDI were included. Weight change was defined as an increase or decrease of more than 3 kg or 3% body weight. As factors contributing to the weight change, we studied the patients' clinical characteristics and quality of life (QOL) scores as determined by our original questionnaire. Results Five patients showed a weight loss of 5.9 kg (2.4-9.0 kg), and two patients showed weight gain, while 16 out of 23 patients were weight neutral. When the patients with weight gain and weight neutral were analyzed together, the mean weight change was +0.3 kg (-0.5 to +1.1 kg). All the patients who lost weight had a Body Mass Index ≥22 kg/m2 (38% vs. 0%, P=0.027) and higher frequencies of abnormally high serum levels of AST (40% vs. 0%, P=0.005). The sum of the QOL scores was similar between the two groups, but higher in patients who lost weight after switching to oral desmopressin (43.3±2.7) than in those who did not (38.2±5.0, P=0.01). Conclusions Switching the treatment from nasal to oral desmopressin may cause weight loss in patients with CDI who seemed to have polydipsia-associated weight gain.

Central diabetes insipidus (CDI) is characterized by polyuria and polydipsia due to a deficiency of vasopressin. Currently, the treatment goal for CDI is improvement of quality of life (QOL) by desmopressin (DDAVP) without developing hyponatremia. However, there is no reliable measure for QOL in CDI patients. We evaluate our original questionnaire for QOL, consisting of 12 questions focusing on polyuria, polydipsia, and DDAVP treatment, in CDI patients who underwent a switch from nasal spray to oral disintegrating tablets of DDAVP. Twenty-five CDI patients under nasal DDAVP treatment, six with newly developed CDI, and 18 healthy individuals without known polyuric/polydipsic disorders as control subjects were enrolled. QOL scores were determined by our questionnaire at the enrollment and 3 months after the start of oral DDAVP treatment and were examined by the Wilcoxon signed-rank test. Eleven questions detected improvement in QOL. The sum of the QOL scores of the eleven questions increased from 29.2 ± 5.6 under nasal to 36.8 ± 4.5 under oral DDAVP (p < 0.001). There were no clinically relevant changes in serum levels of Na. After eliminating two questions about DDAVP treatment, the sum of QOL scores was 15.3 ± 6.5 in untreated CDI patients, 24.4 ± 5.2 in those with nasal treatment, 28.9 ± 4.9 in those with oral DDAVP, and 29.5 ± 3.6 in healthy controls. The difference among groups was significant (p < 0.05 in Steel-Dwass test) except between patients treated with oral DDAVP and healthy controls. Our questionnaire can be used to accurately assess QOL in CDI patients.

Context The risk of thyroid cancer increases and persists for decades among individuals exposed to ionizing radiation in childhood, although the long-term effects of childhood exposure to medium to low doses of radiation on thyroid dysfunction and autoimmune thyroid diseases have remained unclear. Objective To evaluate radiation dose responses for the prevalence of thyroid dysfunction and autoimmune thyroid disease among atomic bomb survivors exposed in childhood. Design, setting, and participants Hiroshima and Nagasaki atomic bomb survivors who were younger than 10 years old at exposure underwent thyroid examinations at the Radiation Effects Research Foundation between 2007 and 2011, which was 62 to 66 years after the bombing. Data from 2668 participants (mean age, 68.2 years; 1455 women) with known atomic bomb thyroid radiation doses (mean dose, 0.182 Gy; dose range, 0 to 4.040 Gy) were analyzed. Main outcome and measures Dose-response relationships between atomic bomb radiation dose and the prevalence of hypothyroidism, hyperthyroidism (Graves' disease), and positive for antithyroid antibodies. Results Prevalences were determined for hypothyroidism (129 cases, 7.8%), hyperthyroidism (32 cases of Graves' disease, 1.2%), and positive for antithyroid antibodies (573 cases, 21.5%). None of these was associated with thyroid radiation dose. Neither thyroid antibody-positive nor -negative hypothyroidism was associated with thyroid radiation dose. Additional analyses using alternative definitions of hypothyroidism and hyperthyroidism found that radiation dose responses were not significant. Conclusions Radiation effects on thyroid dysfunction and autoimmune thyroid diseases were not observed among atomic bomb survivors exposed in childhood, at 62 to 66 years earlier. The cross-sectional design and survival bias were limitations of this study.

Recent genome-wide association studies have identified Tribbles homolog 1 (TRIB1) as one of the candidate genes associated with lipid profiles. TRIB1 is known to interact with MAP kinases, thereby regulating their activities. The single nucleotide polymorphism rs2954029 of TRIB1 is located within an intron and is associated with lipid profiles. The aim of the present study is to investigate the TRIB1 rs2954029 (A>T polymorphism) with conventional predictors of coronary artery diseases such as carotid intima-media thickness (CIMT) and cardio-ankle vascular index (CAVI), and with lipid profiles in general population. This study enrolled 2,581 Japanese adults, 942 men and 1,639 women with a median age of 68 years (range 29 to 94 years), who participated in a screening program for the general population living in Goto City, Nagasaki Prefecture, Japan from 2008 to 2010. For the determination of TRIB1 rs2954029 genotypes, the polymerase chain reaction method was used. The differences in each parameter among the TRIB1 rs2954029 genotypes were evaluated using analysis of covariance. Genotype frequencies of TRIB1 rs2954029 in all participants were 25.5% for AA, 50.4% for AT, and 24.0% for TT. In women, the AA genotype showed significantly higher log triglyceride (TG) concentrations than the AT genotype (P = 0.004) and the AT + TT genotypes (P = 0.004). On the other hand, there were no associations with CIMT and CAVI among the TRIB1 rs2954029 genotypes. In conclusion, the TRIB1 rs2954029 is associated with serum TG concentrations in Japanese community-dwelling women., The Tohoku Journal of Experimental Medicine, 233(2), pp.149-153; 2014

Background: The glucokinase regulator gene (GCKR) rs780094 has been shown to be strongly associated with some metabolic traits and atherosclerotic parameters, while the association between GCKR rs780094 and carotid intima-media thickness (CIMT) has not been fully investigated in the general population. The associations between the GCKR rs780094 genotype and metabolic traits including CIMT were examined in a Japanese community-dwelling population. Methods: A total of 2491 Japanese adults (907 men and 1584 women) who participated in a medical screening program for the general population from 29 to 94 years of age during 2008 to 2010 were enrolled. GCKR rs780094 was genotyped by the TaqMan polymerase chain reaction method, and associations with metabolic markers including CIMT were evaluated. Results: GCKR rs780094 AA genotype was significantly associated with higher TG (p < 0.001 vs. GG), lower HDL-C (p = 0.021 vs. GG), and lower HbA1c (p = 0.023 vs. GG). The AA genotype showed significantly thinner CIMT (p = 0.001 vs. GX). These associations were seen only in men. Conclusions: GCKR rs780094 was associated with TG, HDL-C, and HbA1c levels, as well as with CIMT in Japanese community-dwelling men, but not women., Clinical Chemistry and Laboratory Medicine, 52(2), pp.289-295; 2014

Hypothalamic hyperphagia and obesity are characterized by a lack of satiety and an abnormally high appetite that is difficult to control. We herein report the cases of two patients with hypothalamic hyperphagia and obesity with MRI-detectable hypothalamic lesions. These patients suffered from diabetes mellitus associated with an abnormal eating behavior and weight gain. Liraglutide was successfully used to treat their diabetes mellitus and suppress their abnormal appetites. Glucagon-like peptide-1 analogues, including liraglutide, are promising treatment options in patients with hypothalamic hyperphagia and obesity, as these agents enhance the hypothalamic input of the satiety signal, which is lacking in such patients., Internal Medicine, 53(16), pp.1791-1795; 2014

Thyroid storm is a rare and life-threatening complication of thyrotoxicosis that requires prompt treatment. Thyroid storm is also known to be associated with precipitating events. The simultaneous treatment of thyroid storm and its precipitant, when they are recognized, in a patient is recommended; otherwise such disorders, including thyroid storm, can exacerbate each other. Here we report the case of a thyroid storm patient (a 55-year-old Japanese male) complicated with a perforated duodenal ulcer. The patient was successfully treated with intensive treatment for thyroid storm and a prompt operation. Although it is believed that peptic ulcer rarely coexists with hyperthyroidism, among patients with thyroid storm, perforation of a peptic ulcer has been reported as one of the causes of fatal outcome. We determined that surgical intervention was required in this patient, reported despite ongoing severe thyrotoxicosis, and reported herein a successful outcome.

To retrospectively analyze the individual risk factors for radioactive iodine (RAI)-associated nausea and vomiting, and to examine the anti-emetic effect of ramosetron (5-hydroxytryptamine-3 receptor antagonist) in RAI therapy. Patients with differentiated thyroid carcinoma who underwent first-time RAI therapy at Nagasaki University Hospital between January 2009 and 2013 were included (N = 81). As a routine treatment, all patients were administered 30 mg of domperidone per day. Patients who underwent RAI therapy between April 2011 and January 2013 were also administered 0.1 mg of ramosetron per day in addition to domperidone. Nausea and vomiting were evaluated based on Common Terminology Criteria for Adverse Events version 4.0. RAI-associated nausea and vomiting of any grade were seen in 37.0 and 6.2 % of patients in total, respectively. Moderate to severe nausea (grade 2–3) was seen in 22.2 % of patients and associated with the dose of RAI per body weight (odds ratio = 1.046, p = 0.013), but not with the use of ramosetron, in multivariate logistic regression analysis. We have identified the dose of RAI per body weight to be an individual risk factor associated with moderate to severe RAI-associated nausea. This study failed to show that the combined use of ramosetron and domperidone reduced the frequency of RAI-associated nausea and vomiting.

Background and purpose: The differences in the characteristics of thymus histology, coexisting autoimmune diseases and related autoantibodies between anti-muscle-specific receptor tyrosine kinase (MuSK)-antibody (Ab)-positive myasthenia gravis (MG) patients, and anti-acetylcholine receptor (AChR)-Ab-positive MG patients are not clearly defined. Methods: The types of thymus histology, coexisting autoimmune diseases and associated Abs in 83 MuSK-Ab-positive patients nationwide were investigated and were compared with those in AChR-Ab-positive patients followed at our institute (n = 83). As for the autoantibodies associated with thymoma, titin Abs were measured. Results: Thymoma was not present in any of the MuSK-Ab-positive patients but presented in 21 patients (25.3%) amongst the AChR-Ab-positive patients. Titin Abs were absent in MuSK-Ab-positive patients but positive in 25 (30.1%) of the AChR-Ab-positive patients. Concomitant autoimmune diseases were present in eight MuSK-Ab-positive patients (9.6%) amongst whom Hashimoto's thyroiditis and rheumatoid arthritis predominated, whereas 22 AChR-Ab-positive patients (26.5%) had one or more concomitant autoimmune diseases of which Graves' disease predominated. Conclusions: Differences in frequency of thymoma and thymic hyperplasia, coexisting autoimmune diseases and autoantibody positivity between MuSK-Ab-positive and AChR-Ab-positive MG were indicated, suggesting that, in contrast with AChR-Ab-positive MG, thymus does not seem to be involved in the pathogenic mechanisms of MuSK-Ab-positive MG., European Journal of Neurology, 20(9), pp.1272-1276; 2013