A Pregnant Woman with Excess Vasopressinase-Induced Diabetes Insipidus Complicated by Central Diabetes Insipidus like Lymphocytic Infundibulo-Neurohypophysitis.

Background: Gestational diabetes insipidus (DI) is a very rare complication of pregnancy. We present a case of gestational DI combining two different types of DI. Case Presentation. A 39-year-old pregnant woman suddenly presented with thirst, polydipsia, and polyuria after 31 gestation weeks (GWs). Based on laboratory findings of hypotonic urine (78 mOsm/kgH2O) with higher plasma osmolality (298 mOsm/kgH2O) and higher serum sodium levels (149 mEq/L), gestational DI was suspected, and the clinical course was monitored without therapy until the results of a measurement of plasma arginine vasopressin (AVP) levels were available. However, she subsequently developed acute prerenal failure and underwent an emergency cesarean section at 34 GWs. Her resected placenta weighed 920 g, nearly twice the normal weight. Immediately following delivery, intranasal 1-desamino-8-D-arginine vasopressin was administered, and her symptoms promptly disappeared. Afterward, her predelivery plasma AVP level was found to have been inappropriately low (0.7 pg/mL) given her serum sodium level. The patient's serum vasopressinase level just before delivery was 2,855 ng/mL, more than 1,000 times the upper limit of the normal range, suggesting excess vasopressinase-induced DI. The presence of anti-rabphilin-3A antibodies in the patient's blood, a hypertonic saline infusion test result, and loss of the high-intensity signal of the posterior pituitary on fat-suppressed T1-weighted magnetic resonance images without thickening of the stalk and enlargement of the neurohypophysis suggested concurrent central DI-like lymphocytic infundibulo-neurohypophysitis (LINH). Conclusion: In addition to the degradation of AVP by excess placental vasopressinase due to the enlarged placenta, an insufficient compensatory increase in AVP secretion from the posterior pituitary gland due to LINH-like pathogenesis might have led to DI symptoms.

HLA typing of patients who developed subacute thyroiditis and Graves' disease after SARS-CoV-2 vaccination: a case report.

BACKGROUND: Cases of subacute thyroiditis (SAT) after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination have been reported. A human leukocyte antigen (HLA) allele, HLA-B*35, appears to be involved in the pathogenesis of SAT. CASE PRESENTATION: We conducted HLA typing of one patient with SAT and another with both SAT and Graves' disease (GD), which developed after SARS-CoV-2 vaccination. Patient 1, a 58-year-old Japanese man, was inoculated with a SARS-CoV-2 vaccine (BNT162b2; Pfizer, New York, NY, USA). He developed fever (38 °C), cervical pain, palpitations, and fatigue on day 10 after vaccination. Blood chemistry tests revealed thyrotoxicosis and elevated serum C-reactive protein (CRP) and slightly increased serum antithyroid-stimulating antibody (TSAb) levels. Thyroid ultrasonography revealed the characteristic findings of SAT. Patient 2, a 36-year-old Japanese woman, was inoculated twice with a SARS-CoV-2 vaccine (mRNA-1273; Moderna, Cambridge, MA, USA). She developed fever (37.8 °C) and thyroid gland pain on day 3 after the second vaccination. Blood chemistry tests revealed thyrotoxicosis and elevated serum CRP, TSAb, and antithyroid-stimulating hormone receptor antibody levels. Fever and thyroid gland pain persisted. Thyroid ultrasonography revealed the characteristic findings of SAT (i.e., slight swelling and a focal hypoechoic area with decreased blood flow). Prednisolone treatment was effective for SAT. However, thyrotoxicosis causing palpitations relapsed thereafter, for which thyroid scintigraphy with 99mtechnetium pertechnetate was conducted, and the patient was diagnosed with GD. Thiamazole treatment was then initiated, which led to improvement in symptoms. CONCLUSION: HLA typing revealed that both patients had the HLA-B*35:01, -C*04:01, and -DPB1*05:01 alleles. Only patient 2 had the HLA-DRB1*11:01 and HLA-DQB1*03:01 alleles. The HLA-B*35:01 and HLA-C*04:01 alleles appeared to be involved in the pathogenesis of SAT after SARS-CoV-2 vaccination, and the HLA-DRB1*11:01 and HLA-DQB1*03:01 alleles were speculated to be involved in the postvaccination pathogenesis of GD.

Examination of Malignant Findings of Thyroid Nodules Using Thyroid Ultrasonography.

BACKGROUND: It is important to distinguish benign thyroid nodules from malignant thyroid nodules. Hence, this study aimed to determine the characteristics of patients with thyroid cancer using thyroid ultrasonography. METHODS: We retrospectively examined the ultrasonographic findings of 327 patients with 457 thyroid nodules (age: 59.9 ± 14.3 years; sex, n (%): female 242 (74.0%)) at a single center from 2014 to 2016. Ultrasonography was used to determine the nodule size, shape, border, internal echogenicity, presence of coarse calcifications and microcalcifications within the nodule, internal blood flow and whether the nodule was solid or contained cystic structures. Thyroid fine needle aspiration cytology (FNAC) was performed in all patients. The ultrasonographic findings were compared between patients with benign nodules and those with papillary thyroid carcinoma (PTC). Furthermore, in the analysis of anti-thyroglobulin (Tg) antibody-negative patients with single nodules, values of serum Tg/nodule volume were calculated and compared between patients with benign nodules and those with PTC. RESULTS: There were 298 (65.2%) benign nodules, 33 (7.2%) PTCs and 126 (27.6%) others (104 follicular neoplasms, 19 masses of undetermined significance and three other malignant tumors). The nodules diagnosed as PTC had significantly lower internal echogenicity (P < 0.01), more microcalcifications (P < 0.01) and comprised more nodules rich in blood flow (P < 0.05) than benign nodules. Solid nodules were found significantly more in the PTC group (P < 0.01). The serum Tg/nodule volume ratio was significantly higher in the PTC group (P < 0.05). CONCLUSIONS: Findings suggestive of PTC were found from images obtained using thyroid ultrasonography. In the diagnosis of PTC, the frequency of FNAC examinations should be reduced as this method is costly and invasive.

Simultaneous development of Graves' disease and type 1 diabetes during anti-programmed cell death-1 therapy: A case report.

We present the first case of simultaneous development of Graves' disease and type 1 diabetes during anti-programmed cell death 1 therapy. A 48-year-old man with parotid gland adenocarcinoma and lung metastasis had received five courses of nivolumab. Fourteen days after administration of the sixth course, his casual plasma glucose and hemoglobin A1c levels were 379 mg/dL and 7.2%, respectively. Furthermore, thyrotoxicosis was detected with a blood test. Serum total ketone body and thyroid-stimulating hormone receptor antibody levels increased, and serum C-peptide level decreased to 0.01 ng/mL thereafter. Thus, we concluded that he simultaneously developed anti-programmed cell death 1 therapy-associated type 1 diabetes and Graves' disease. Among Japanese patients with autoimmune polyglandular syndrome type III, the frequency of human leukocyte antigen-DRB1*04:05 is higher in those with both type 1 diabetes and Graves' disease. Our case had human leukocyte antigen-DRB1*04:05, which might be associated with the simultaneous development of the two diseases.

Administration of thiamazole for Graves' disease might trigger the onset of type 1 diabetes.

Thiamazole might trigger the onset of type 1 diabetes.

Intrinsic insulin secretion capacity might be preserved by discontinuing anti-programmed cell death protein 1 antibody treatment in 'anti-programmed cell death protein 1 antibody-induced' fulminant type 1 diabetes.

Intrinsic insulin secretion capacity may be preserved by discontinuing anti-PD-1 antibody treatment in 'anti-PD-1 antibody-induced'fulminant type 1 diabetes.

H2O2 activates ryanodine receptor but has little effect on recovery of releasable Ca2+ content after fatigue.

We studied whether hydrogen peroxide (H(2)O(2)) at

[Impact of intravenous thrombolysis prior to percutaneous coronary intervention in reperfusion therapy for acute myocardial infarction].

OBJECTIVES: To elucidate the effectiveness and safety of intravenous thrombolysis (IVT) with mutant tissue plasminogen activator prior to percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. METHODS: Ninety consecutive patients were recruited with the following criteria: acute myocardial infarction with ST segment elevation or bundle branch block on electrocardiography, admission within 6 hr from onset, age of < or = 80 years and without previous PCI or coronary bypass graft surgery. They were divided into two groups. Group IV consisted of 53 patients treated with IVT prior to PCI and Group D consisted of the other 37 patients with direct PCI. Mutant tissue plasminogen activator, monteplase, was administered with a dose of 27,500 U/kg in Group IV (maximum injection dose, 160 x 10(4) U). The clinical features and in-hospital outcome were compared between the two groups. RESULTS: Patients in Group IV acquired earlier reperfusion estimated by electrocardiography recovery at 60 min after admission and higher Thrombolysis in Myocardial Infaction (TIMI) flow grade on the first coronary angiogram (TIMI 2 or 3 flow rate; Group IV vs Group D = 75% vs 35%, p < 0.0001). The duration from onset to TIMI 3 flow grade was not significantly different between Group IV and Group D (230 vs 260 min, p = 0.15). The incident of ST segment re-elevation with chest pain at recanalization was lower in Group IV than in Group D (23% vs 46%, p < 0.05). The duration from TIMI 3 recognition to peak creatine kinase level was longer in Group IV (466 vs 359 min, p = 0.039). Subacute thrombotic occlusion occurred in two patients in Group IV and three in Group D (NS). One patient in each group died from pump failure (NS). No severe bleeding complication was found in any patient. CONCLUSIONS: IVT prior to PCI was considered to be a safe, effective and useful therapy in patients with acute myocardial infarction. Different patterns of reperfusion might occur, because of the low frequency of ST re-elevation and elongation of duration from reperfusion to peak creatine kinase level in patients treated with IVT prior to PCI.