Search

Abstract Adverse reactions, including the onset of diabetes, after coronavirus disease 2019 (COVID‐19) vaccination have been reported. Herein, we report a case of a man who developed anti‐glutamic acid decarboxylase (GAD) antibody‐positive fulminant type 1 diabetes 15 weeks after COVID‐19 vaccination, atypical of the previously reported anti‐GAD antibody‐negative cases.

IntroductionWe report a case series of severe ketoacidosis after COVID-19 vaccination in a type 1 diabetes patients treated with insulin and an SGLT-2 inhibitor.Case ReportWe present two cases of type 1 diabetes mellitus. One patient was treated with insulin therapy and an SGLT-2 inhibitor, and the other patient was treated with insulin therapy alone. Both patients became ill after coronavirus disease-2019 vaccination, making it difficult to continue their diet or insulin injections. On admission, they developed severe diabetic ketoacidosis. This is the first report of ketoacidosis after coronavirus disease-2019 vaccination.ConclusionThe vaccine should be carefully administered to type 1 diabetes patients receiving intensive insulin therapy and a sodium-glucose transporter due to the high risk ketoacidosis. It is important to instruct patients to drink sufficient fluids and to continue insulin injections when they become sick.

We report on the case of a patient with dysgerminoma, a rare germ cell tumor, which showed hypercalcemia with an elevation of 1α,25-dihydroxycholecalciferol (calcitriol). A 27-year-old nulliparous woman presented with hypercalcemia during the examination of a right ovarian tumor with an elevation of calcitriol, lactate dehydrogenase, and alkaline phosphatase. Fractional excretion of calcium was elevated, and intact parathyroid hormone was suppressed. After undergoing right salpingo-oophorectomy, the patient’s serum calcium and calcitriol returned to the normal range within a week. A literature search was conducted on the topic by reviewing databases for dysgerminoma showing hypercalcemia. We identified 14 patients from the literature and performed a pooled analysis, including the results of our case. However, most cases lack data that can help investigate the potential association between parathyroid hormone, parathyroid hormone-related protein, calcitriol, and phosphorus in hypercalcemia. Thus, more case reports that include additional information are required to fully elucidate the mechanism of hypercalcemia associated with dysgerminoma.

Congenital hypothyroidism (CH) is the most prevalent congenital endocrine disorder and causes mental retardation. A male Japanese patient with first cousin marriage parents was diagnosed as CH at 10 months. He was born before introduction of mass screening for CH. With continuous thyroid hormone replacement therapy, normal thyroid hormone status was maintained until adulthood. Genetic screening of next-generation sequencing was performed at the age of 52 years, and we identified a new homozygous thyroid peroxidase (TPO) gene mutation (GRCh38.p13, chromosome 2 at position 1493997, c.1964 G>T, p.Cys655Phe). TPO is an important enzyme to produce thyroid hormone. As demonstrated by a homology analysis of TPO proteins among different species, cysteine 655 residue is highly conserved, suggesting an important role in maintaining TPO function and structure. An in silico study with three-dimensional structure of the novel mutation was performed and suggested that the mutation abolished disulfide bond between cysteines at positions 598 and 655. An in vitro functional analysis using HEK293 cells revealed that TPO activity of the mutant was significantly impaired compared with that of the wild type. Furthermore, study of immunohistochemistry showed that localization of TPO in cells did not differ between the wild type and the mutant. In conclusion, this single disulfide bond loss mutation of a new TPO homozygous mutation, p.Cys655Phe, reduced TPO activity and caused congenital hypothyroidism without affecting subcellular localization of TPO proteins.