Primary hyperparathyroidism with hungry bone syndrome - a case report

Primary hyperparathyroidism with severe bone disease as a result of excessive parathyroid hormone ( PTH ) release and severe hypercalcaemia can lead to 'hungry bone syndrome' (HBS) post operatively. This is due to sudden cessation of PTH and drop in serum calcium. We reported a case a young man with primary hyperparathyriodism due to a single parathyroid adenoma with severe bone disease and post operatively developed hungry bone syndrome

Absorption of calcium from milk and tempeh consumed by postmenopausal Malay women using the dual stable isotope technique

Assessment of calcium bioavailability from non-dairy foods containing moderate amounts of calcium is especially important in populations that have habitually low dairy consumption. Absorption of calcium from milk and tempeh (a traditional fermented soy product) was compared in a sample of Malay subjects. A randomized, crossover design was utilized to assess calcium absorption in 20 postmenopausal women from either a glass of milk (114 g) or from a meal of tempeh (206 g); each containing 130 mg calcium. At each study of Phase 1 (mid-July) and Phase 2 (mid-August), intravenous (42)Ca and oral (44)Ca were administered and calcium absorption was measured in 24-h urine collections post-dosing; with a 1-month washout period between phases. Absorption of calcium from tempeh did not differ significantly from milk (36.9 +/- 10.6% vs. 34.3 +/- 8.6%, respectively). Due to differences in the calcium content of tempeh, four servings of this product would be needed to get the same amount of absorbed calcium as that obtained from a 4-ounce glass of milk. Tempeh may provide readily available calcium for this population of women at risk for low bone mass

Estrogen receptors in nonfunctioning pituitary neuroendocrine tumors: review on expression and gonadotroph functions

Estrogen (17β-estradiol or E2) is a crucial regulator of the synthesis and secretion of pituitary reproductive hormones luteinizing hormone, follicle-stimulating hormone, and prolactin. In this review, we summarize the role of estrogen receptors in nonfunctioning pituitary neuroendocrine tumors (NF-Pitnets), focusing on immunoexpression and gonadotroph cell proliferation and apoptosis. Gonadotroph tumors are the most common subtype of NF-Pitnets. Two major estrogen receptor (ER) isoforms expressed in the pituitary are estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). Overall, estrogen actions are mostly exerted through the ERα isoform on the pituitary. The G protein–coupled estrogen receptor (GPER) located at the plasma membrane may contribute to nongenomic effects of estrogen. Nuclear immunoreactivity for ERα and ERβ was highest among gonadotroph and null cell tumors. Silent corticotroph tumors are the least immunoreactive for both receptors. A significantly elevated ERα expression was observed in macroadenomas compared with microadenomas. ERα and ERβ may act in opposite directions to regulate the Slug- E-cadherin pathway and to affect invasiveness of NF-Pitnets. In the cellular pathway, ERs regulate estrogen-induced proliferation and differentiation and impact several signaling pathways including the MAPK and PI3K/Akt pathway. Estrogen was the first-discovered inducer of pituitary tumor transforming gene 1 that was abundantly expressed in NF-Pitnets. ERα can be a potential biomarker for predicting tumor size and invasiveness as well as therapeutic target for NF-Pitnets. Selective estrogen receptor modulators or antiestrogen may represent as an alternative choice for the treatment of NF-Pitnets

Reduction of insulin requirement in type 1 diabetes induced by BCG vaccination: a case report

Introduction Bacillus Calmette-Guerin (BCG) vaccinations reverse disease by restoring insulin secretion in a rodent model of type 1 diabetes. It stimulates innate immunity by inducing the host to produce tumor necrosis factor (TNF), which, in turn, kills disease-causing autoimmune cells and restores pancreatic beta-cell function through regeneration. Case presentation This is a case of a 32-year-old lady with a history of gestational diabetes on metformin, who presented at 10 months postpartum with significant weight loss over 1 month period followed by severe diabetic ketoacidosis. Her family history was negative for diabetes and her BMI was normal (22.5 kg/m2). At diagnosis, her C-peptide was 81 pmol/L, markedly elevated anti-GAD Ab of > 2000 U/L and HbA1c of 16%. She attained partial remission after 1 month of insulin initiation. The basal boluses regime was resumed with total insulin dose of 36 to 40 units/day at 6 months following the remission period. Her continuous glucose monitoring readings however, showed episodes of mixed hypoglycemia (min 3.2 mmol/L) and hyperglycemia (max 10.6 mmol/L) while on the insulin regime. Methods and Results We administered experimental 0.1 ml intradermal injections containing BCG 3.2×106 colony-forming units/injection at 6 and 7 months after the onset of her type 1 diabetes followed by a planned yearly BCG vaccinations thereafter. We observed that her insulin requirement had slowly reduced after her third BCG vaccination. At 32 weeks post first BCG vaccination, she went through a month of Ramadan Fasting with ONLY a single prandial insulin at pre dinner (Break of Fast)(8 to16 units/day) without any episodes of ketoacidosis. Her SBGM ranged from 5-8 mmol/L with total caloric intake of 1200-1500 kcal/day throughout the fasting period. This was further supported by marked improvement of her HbA1c from 8.1% down to 6.5% and increased in C-peptide level from 81 to 112 pmol/L. Discussion This patient demonstrated significant improvement in glycemic control following BCG vaccination earlier than those reported in previous clinical trials, however, the sustainability of good glycaemic control in her is still long way from being adequately established. In a previous 8-year long randomized clinical trial of type 1 diabetic subjects receiving BCG vaccination, stable and long-term reductions in blood sugar and epigenetic changes of restored tolerance had been observed. The significant clinical effects took three years to occur and remained steady for at least five additional years without further clinical interventions.1 BCG appears to have the ability to switch the immune system of type 1 diabetes from high oxidative phosphorylation to augmented early aerobic glycolysis. This case demonstrated preliminary metabolic and clinical benefits of BCG vaccinations in type 1 diabetic patient as early as 32 weeks post vaccination. Nonetheless, further clinical trial is needed to assess its long term effects in subjects of all ages and durations of type 1 diabetes