-
Journal of Medical Case Reports Oct 2014In this report, we describe challenges we encountered in the clinical management of a patient with hypoparathyroidism who had previously undergone a bariatric procedure.
INTRODUCTION
In this report, we describe challenges we encountered in the clinical management of a patient with hypoparathyroidism who had previously undergone a bariatric procedure.
CASE PRESENTATION
We report the case of a 38-year-old Caucasian woman who had undergone a Roux-en-Y gastric bypass procedure for treatment of obesity. She also had a past history of right lobectomy to treat a benign thyroid nodule. Another thyroid nodule was diagnosed after her bariatric surgery, so a new thyroid surgery was performed. Permanent hypoparathyroidism occurred after the second thyroid surgery. A Roux-en-Y gastric bypass resulted in important weight loss, but the preferential site of calcium absorption was bypassed. The lack of endogenous parathyroid hormone secretion due to post-surgical hypoparathyroidism abolished the physiological mechanism that compensates the reduced calcium absorption, which was a challenge for us to overcome. In this report, we describe our clinical therapeutic choices to maintain normocalcemia and normophosphatemia in this patient. Higher doses of exogenous calcium citrate, calcitriol and cholecalciferol were used, but hypocalcemia was still present. To improve vitamin D absorption with resultant improvement of calcium homeostasis, we speculated that adding pancrelipase to meals would increase lipid absorption and possibly fat-soluble vitamins, including vitamin D. Only after the addition of pancrelipase did the patient improve without weight regain according to clinical and laboratory assessments.
CONCLUSION
The use of exogenous pancreatic enzymes improved calcium homeostasis in this bariatric patient. The role of these enzymes on vitamin D absorption and subsequent rise in calcium levels in hypoparathyroid patients who undergo bariatric procedures need further investigation.
Topics: Adult; Female; Gastric Bypass; Humans; Hypoparathyroidism; Obesity; Thyroid Nodule; Thyroidectomy
PubMed: 25348653
DOI: 10.1186/1752-1947-8-357 -
Journal of Cystic Fibrosis : Official... Jan 2015
Topics: Colonic Diseases; Cystic Fibrosis; Fibrosis; Humans; Pancreatic Extracts; Pancreatin; Pancrelipase; Polymethacrylic Acids; Risk Assessment; United Kingdom
PubMed: 25242743
DOI: 10.1016/j.jcf.2014.09.002 -
Endocrinology Sep 2014Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of glucose homeostasis and energy balance. However, the role of PTP1B in pancreatic endocrine...
Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of glucose homeostasis and energy balance. However, the role of PTP1B in pancreatic endocrine function remains largely unknown. To investigate the metabolic role of pancreatic PTP1B, we generated mice with pancreas PTP1B deletion (panc-PTP1B KO). Mice were fed regular chow or a high-fat diet, and metabolic parameters, insulin secretion and glucose tolerance were determined. On regular chow, panc-PTP1B KO and control mice exhibited comparable glucose tolerance whereas aged panc-PTP1B KO exhibited mild glucose intolerance. Furthermore, high-fat feeding promoted earlier impairment of glucose tolerance and attenuated glucose-stimulated insulin secretion in panc-PTP1B KO mice. The secretory defect in glucose-stimulated insulin secretion was recapitulated in primary islets ex vivo, suggesting that the effects were likely cell-autonomous. At the molecular level, PTP1B deficiency in vivo enhanced basal and glucose-stimulated tyrosyl phosphorylation of EphA5 in islets. Consistently, PTP1B overexpression in the glucose-responsive MIN6 β-cell line attenuated EphA5 tyrosyl phosphorylation, and substrate trapping identified EphA5 as a PTP1B substrate. In summary, these studies identify a novel role for PTP1B in pancreatic endocrine function.
Topics: Animals; Female; Gene Knockout Techniques; Glucose; Glucose Intolerance; Insulin; Insulin-Secreting Cells; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Pancrelipase; Protein Tyrosine Phosphatase, Non-Receptor Type 1
PubMed: 24956127
DOI: 10.1210/en.2013-2004