Cardiovascular disease is increased in individuals with type 1 or type 2 diabetes mellitus (DM). Left ventricular hypertrophy (LVH), which is an ominous prognostic sign and an independent risk factor for cardiac events, is often present in type 2 DM patients. The aim of our cross-sectional study was to evaluate the prevalence of LVH, and risk factors for its development, in normotensive type 2 diabetic patients without antihypertensive medication. The objectives of the study were to find out the prevalence of high left ventricular mass (LVM) in normotensive type 2 diabetic patients and compare it with nondiabetics and to uncover the risk factors for the development of high LVM in normotensive type 2 diabetic patients. A total of 130 age- and sex-matched subjects were selected (65 cases, diabetic normotensive, and 65 controls, nondiabetic normotensive) and baseline data were collected. LVM and left ventricular mass index (LVMI) were calculated using echocardigraphic parameters and body surface area. LVMI was significantly higher in patients with type 2 DM compared with age-, sex-matched healthy population (104.9 ± 21 vs. 78.5 ± 22.7 g/m2, respectively; P < 0.05). BMI, HbA1c, and duration of diabetes were significantly associated with LVH whereas sexes, age, PPBS, were not.

Varicella zoster infection is known to cause neurological involvement. The infection is usually self-limiting and resolves without sequelae. We present a series of three cases with neurological presentations following chicken pox infection. The first case is a case of meningitis, cerebellitis and polyradiculopathy, the second is a florid case of acute infective demyelinating polyradiculoneuropathy (Guillian-Barré syndrome) in a middle-aged female and the third case is a young man in whom we diagnosed acute transverse myelitis. All these cases presented with distinct neurological diagnoses and the etiology was established on the basis of history and serological tests confirmatory for chicken pox. The cases responded differently to treatment and the patients were left with minimum disability.

Many pathologies can cause gonadotropin-independent precocious puberty (GIPP) in prepubertal boys. Leydig cell tumor is one rare cause of this presentation. Here we present a six-year-old boy with features of isosexual precocious puberty, high testosterone levels, low gonadotropin levels, and bone age advancement. Testicular USG revealed a left-sided testicular tumor. The left testis was removed surgically, and the Leydig cell tumor was confirmed on histopathology. Post orchiectomy, the boy had elevated testosterone levels with raised luteinizing hormone (LH) levels. A diagnosis of gonadotropin-dependent precocious puberty (GDPP) was made. He has been initiated on monthly gonadotropin-releasing hormone (GnRH) agonist therapy.

Hypoparathyroidism is a common encounter in endocrinology practice. A thorough search for the etiology is generally futile and most cases are labeled as idiopathic. Familial idiopathic hypoparathyroidism is a large chunk of these idiopathic cases. Here we present two cases who presented with features of hypocalcemia and were eventually diagnosed with hypoparathyroidism. Our first case is that of a middle-aged woman who presented with spontaneous tetany and perioral numbness. She had very low serum calcium values, low serum magnesium, hypokalemia, hypercalciuria and undetectable parathormone levels. She was initially managed with parenteral calcium, magnesium and oral potassium chloride which was shifted to oral replacements once stabilized. Focused exome sequencing for causes of hypoparathyroidism and hypocalcemia revealed a frameshift mutation in GCM2 (NM_004752.4) on chromosome 6, c737dupA variant (p. Asp246Glufs*25) located at Exon 5. The second case presented is that of a one-month-old infant presenting with hypocalcemic seizures, severe hypocalcemia, hyperphosphatemia, and low parathormone levels. The infant was stabilized with parenteral calcium and trial of subcutaneous teriparatide for further improvement. Oral calcium and calcitriol were instituted once stabilized and teriparatide was tapered off. Focused exome sequencing revealed a homozygous mutation involving GCM2 (ENST0000379491.5) on chromosome 6, variant CM2 chr6:10876558_10877139insT located on Exon1-2. Both of these mutations are novel and underscore the profound effect of GCM2 on parathyroid gland development in infants and maintenance in adults.

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