Background: Patients with short bowel syndrome (SBS) have a high prevalence of metabolic bone disease due to nutrient malabsorption and potential effects of parenteral nutrition (PN). Human growth hormone (hGH) has been shown in some studies to have anabolic effects on bone, but hGH effects on bone in patients with SBS are unknown.
Methods: Adults with PN-dependent SBS underwent a 7-day period of baseline studies while receiving usual oral diet and PN and then began receiving modified diets designed to improve nutrient absorption and daily oral calcium/vitamin D supplements (1500 mg elemental calcium and 600 IU vitamin D, respectively). Subjects were randomized to receive in a double-blind manner either subcutaneous (sc) saline placebo as the control or hGH (0.1 mg/kg/d for 3 weeks, then 0.1 mg/kg 3 days a week for 8 subsequent weeks). Open-label hGH was given from week 13 to week 24 in subjects who required PN after completion of the 12-week double-blind phase. Markers of bone turnover (serum osteocalcin and urinary N-telopeptide [NTX]), vitamin D nutriture (serum calcium, 25-hydroxyvitamin D [25-OH D] and parathyroid hormone [PTH] concentrations), and intestinal calcium absorption were measured at baseline and at weeks 4 and 12. Dual x-ray absorptiometry (DXA) of the hip and spine was performed to determine bone mineral density (BMD) at baseline and weeks 12 and 24.
Results: The majority of subjects in each group exhibited evidence of vitamin D deficiency at baseline (25-OH D levels<30 ng/mL; 78% and 79% of control and hGH-treated subjects, respectively). Subjects treated with hGH demonstrated a significant increase from baseline in serum osteocalcin levels at 12 weeks (+62%; p<.05). The levels of NTX were increased over time in the hGH-treated group; however, this did not reach statistical significance. Both NTX and osteocalcin remained unchanged in control subjects. BMD of the spine and total hip was unchanged in subjects treated with placebo or hGH at 24 weeks. However, femoral neck BMD was slightly but significantly decreased in the placebo group at this time point but remained unchanged from baseline in the hGH-treated subjects.
Conclusions: hGH therapy significantly increased markers of bone turnover during the initial 3 months of therapy and stabilized femoral neck bone mass over a 6-month period in patients with severe SBS undergoing intestinal rehabilitation.
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http://dx.doi.org/10.1177/0148607106030006480 | DOI Listing |
Front Biosci (Schol Ed)
December 2024
Institute for Health and Sport, Victoria University, Melbourne, VIC 3030, Australia.
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December 2024
Department of Reproductive Medicine, Dongying People's Hospital, 257091 Dongying, Shandong, China.
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Front Endocrinol (Lausanne)
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Recordati Rare Diseases, Central and Eastern Europe, Warsaw, Poland.
Pasireotide is an effective treatment for both Cushing's disease (CD) and acromegaly due to its ability to suppress adrenocorticotropic hormone and growth hormone, and to normalize insulin-like growth factor-1 levels, resulting in tumor shrinkage. However, it may also cause hyperglycemia as a side effect in some patients. The aim of this study was to review previous recommendations regarding the management of pasireotide-induced hyperglycemia in patients with CD and acromegaly and to propose efficient monitoring and treatment algorithms based on recent evidence and current guidelines for type 2 diabetes treatment.
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Department C, National Institute of Nutrition of Tunis, Tunis, TUN.
Type 1 diabetes mellitus (T1DM) is a common autoimmune pathology requiring lifelong insulin therapy. We report the case of a 12-year-old girl with T1DM admitted to Department C of the National Institute of Nutrition of Tunis for diabetic ketosis. She had suffered from T1DM for five years, with poor glycemic control (hemoglobin A1C = 10%) and poor therapeutic adherence.
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Department of Chemical Pathology & Metabolic Diseases, University Hospitals of Leicester NHS Trust, Groby Road, Leicester LE39QP, United Kingdom.
Tumour-induced osteomalacia (TIO), also known as oncogenic osteomalacia, is a rare paraneoplastic syndrome mediated by the overproduction of phosphaturic hormone fibroblast growth factor 23. TIO is most commonly caused by mesenchymal tumours (PMTs), which are typically small, slow-growing and often undetectable on physical examination and conventional imaging techniques. Patients with TIO typically undergo a protracted period of diagnostic workup and medical treatment due to presentation with nonspecific symptoms and difficulty in localising the culprit tumour.
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