A thyroid nodule is a discrete radiologically distinct lesion in the gland parenchyma. These are a common finding in the general population, majority being diagnosed incidentally during neck imaging. The major clinical relevance lies in the fact that 4-6.5% of nodules can be malignant. A thorough clinical evaluation and examination should be followed by serum TSH assessment and ultrasonography for assessment of size, number, imaging characteristics suggestive of malignancy, cervical lymphadenopathy. FNA should be done based on clinical and sonographic characteristics. Further choice of management modality and extent of surgery should be based on cytopathological findings supplemented by molecular testing if available.
SARS-CoV-2 pandemic has claimed millions of lives since its first identification in December 2019. Patients with diabetes are at a high risk of adverse outcomes after COVID-19 infection, whereas infection itself can be associated with severe hyperglycemia, including hyperglycemic emergencies. While the accelerated vaccine development and rollout have considerably decreased morbidity and mortality with reasonable safety, there are emerging reports of worsening of hyperglycemia in response to vaccination, with possible shared pathophysiology with COVID-19 infection-related hyperglycemia. We hereby report two young patients with type 1 diabetes (T1DM) who presented with severe diabetic ketoacidosis (DKA) after receiving second doses of COVISHIELD (ChAdOx1 nCoV-19) and COVAXIN (BBV152- inactivated whole virion) vaccines. Though a causal link cannot be established, post-vaccination immune response can potentially explain this transient worsening of hyperglycemia and hyperglycemic emergencies. We, hence report diabetic ketoacidosis (DKA) following COVID-19 vaccination in T1DM. We suggest that people with diabetes, particularly patients with T1DM with inadequate glycemic control should ideally be closely monitored for hyperglycemia and ketonemia for at least 2 weeks after receiving vaccination for COVID 19.
Graves’ disease (GD) is an autoimmune disease caused by autoantibodies against thyroid stimulating hormone receptor (TSH-R), resulting in stimulation of thyroid gland and overproduction of thyroid hormones resulting in clinical manifestations. It is uncommon in children and is 6 times more prevalent in females. The symptomatology, clinical and biochemical severity are a function of age of onset of disease. Prepubertal children tend to present with weight loss and bowel frequency, associated with accelerated growth and bone maturation. Older children are more likely to present with the classical symptoms of thyrotoxicosis like palpitations, tremors and heat intolerance. Prepubertal children tend to have a more severe disease, longer duration of complaints and higher thyroid hormone levels at presentation than the pubertal and postpubertal children. The non-specificity of some of the symptoms in pediatric age group can lead to children being initially seen by other specialities before being referred to endocrinology. Management issues are decided based on patient’s priorities and shared decision making between patient and treating physician. Radioactive Iodine Ablation is preferred when there is relatively higher value placed on Definitive control of hyperthyroidism, Avoidance of surgery, and potential side effects of ATDs. Similarly Antithyroid drugs are chosen when a relatively higher value is placed on possibility of remission and avoidance of lifelong thyroid hormone treatment, Avoidance of surgery, Avoidance of exposure to radioactivity. Surgery is preferred when access to a high-volume thyroid surgeon is available and a relatively higher value is on prompt and definitive control of hyperthyroidism, avoidance of exposure to radioactivity and avoidance of potential side effects of ATDs. Continental differences with regards to management do exist; radio-iodine ablation being preferred in North America while Anti-thyroid drug treatment remains the initial standard care in Europe.
Background: 17-HSD-3 deficiency is autosomal recessive, rare cause of 46XY, DSD. The diagnosis is often missed in early childhood due to subtle features, and the usual presentation is at puberty with primary amenorrhea and features of virilisation. Herein we describe 34-year 46XY female who was never diagnosed and found to have compound heterozygous mutations in exon 1 and exon 9 in HSD17B3 gene by genetic testing. Case Detail: Patient was first-born to a non-consanguineously married couple, term delivery with typical female external genitalia, and reared as female. There was history of right-sided inguinal hernia repair at 3 years of age. Breast development started at 15 years of age, along with deepening of voice and appearance of facial and body hair at 16-17 years. Initial evaluation by a Gynaecologist at 26 years of age for primary amenorrhea revealed a blind vagina, clitoromegaly, bilateral palpable gonads in inguinal region with 46XY karyotype. MRI revealed testes in inguinal canals and absence of Mullerian structures. No endocrine evaluation was done at this stage, and she underwent bilateral orchidectomy followed by estrogen supplementation. The patient first consulted us 8-years later, at 34 years of age. Since she had undergone bilateral orchidectomy, interpretation of hormonal evaluation including hCG-stimulation, was not feasible. Genetic sequencing revealed compound heterozygous mutations for c.128_131 del at exon 1 and c.644A>T novel mutation at exon 9 in HSD17B3 gene. The patient wanted to continue with the assigned female sex, and was continued on estrogen therapy along with genetic counselling. Discussion: Mutation in HSD17B3 is rare cause of 46XYDSD. Usually reared as female, these patients come to medical attention because of inguinal hernia or labioscrotal swelling in childhood or primary amenorrhea along with variable degree of virilization in pubertal age group. Without specific endocrine evaluation, it may be overlooked as androgen insensitivity and 5-alpha-reductase deficiency due to clinical similarities. Basal and stimulated hormonal evaluation of hormonal precursors and metabolites can provide valuable information about the level of defect. Confirmatory molecular mutation analysis is often required, particularly in the setting of gonadectomy, as was the case in our patient. A total of 70 different mutation in the HSD17B3 gene has been reported to date The p.Phe43CysfsTer9 mutation at exon 1 identified in our patient has previously been reported, but p.Glu215Val mutation at exon 9 has not been previously reported and is a novel mutation.
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