Hypercalciuria is a common side effect during total parenteral nutrition (TPN). We report a patient with long-term TPN, who demonstrated hypercalciuria, hypercalcemia and growth retardation. The patient is a six-year-old Japanese girl with Hirschsprung disease (jejunal agangliosis). Jejunostomy was performed at one-month old and since then her nutrition has depended mostly on TPN. When she was 3 years old, continuous TPN was switched to cyclic TPN (on TPN for 11 hrs and off TPN for 13 hrs). The urinary calcium level has been elevated (Ca/Cre ratio, 1.0) since 3 months of age, whereas serum calcium levels stayed within normal range for a while. The serum calcium levels started to elevate to 12 to approximately 13 mg/dl when she was 3 years and 8 months old. She showed growth retardation (height SD score was -4.2SD when she was 5 years and 8 months old) and deteriorated renal tubular function with renal glycosuria, elevated beta 2-microglobulin (beta2-MG) and N-acetyl-beta-D-glucosaminidase. She was referred to our division for the investigation and treatment of growth disturbance and Ca metabolism. Her bone age was delayed (BA/CA 0.62) and serum IGF-I level was decreased but her GH response to provocation test was normal. Bilateral nephrocalcinosis was revealed by renal echogram and CT scan. By reducing calcium content in TPN solution, the serum and urinary calcium levels could be maintained within normal range and her renal function and growth velocity was improved.
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http://dx.doi.org/10.1507/endocrj.47.supplmarch_s137 | DOI Listing |
Ann Endocrinol (Paris)
January 2025
Department of Endocrinology, Diabetes and Metabolic Diseases, Angers University Hospital, Reference Center for Rare Thyroid and Hormone Receptor Diseases, 49933 Angers cedex 09, France; Univ Angers, Inserm, CNRS, MITOVASC, Equipe CarMe, SFR ICAT, F-49000 Angers, France. Electronic address:
Primary hyperparathyroidism is treated surgically. Postoperatively, close monitoring of blood calcium levels is necessary to detect any hypocalcemia. Postoperative PTH assays can be performed within 24 hours to identify patients who will not develop permanent hypoparathyroidism.
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January 2025
Endocrinology Department, Huriez Hospital, Lille University Hospital, France. Electronic address:
Syndromic primary hyperparathyroidism has several features in common: younger age at diagnosis when compared with sporadic primary hyperparathyroidism, often synchronous or metachronous multi-glandular involvement, higher possibility of recurrence, association with other endocrine or extra-endocrine disorders, and suggestive family background with autosomal dominant inheritance. Hyperparathyroidism in multiple endocrine neoplasia type 1 is the most common syndromic hyperparathyroidism. It is often asymptomatic in adolescents and young adults, but may be responsible for recurrent lithiasis and/or bone loss.
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January 2025
Université Paris-Saclay, Inserm, Endocrine Physiology and Physiopathology, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Service d'Endocrinologie et des Maladies de la Reproduction and Centre de Référence des Maladies Rares de l'Hypophyse HYPO, F-94270 Le Kremlin-Bicêtre, France. Electronic address:
Primary hyperparathyroidism is rare in children. A germline mutation is identified in half of all children with primary hyperparathyroidism (70% of newborns and infants, and 40% of children and adolescents). The clinical manifestations of primary hyperparathyroidism in children are highly variable (often absent in newborns, rather severe and symptomatic in children and adolescents) and depend on the genetic cause, as well as the severity, rapidity of onset and duration of hypercalcemia.
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January 2025
Service d'Endocrinologie, Diabétologie, Métabolisme, Nutrition; Hôpital Huriez, CHU Lille; Inserm U1190, Institut Génomique Européen pour le Diabète, Université de Lille, F-59000 Lille, France. Electronic address:
The differential diagnosis of primary hyperparathyroidism can be considered clinically, biologically and radiologically. Clinically, primary hyperparathyroidism should be suspected in case of diffuse pain, renal lithiasis, osteoporosis, repeated fracture, cognitive or psychiatric disorder, or disturbance of consciousness. Nevertheless, the differential diagnosis of primary hyperparathyroidism is mainly biological, particularly in atypical forms, which must be differentiated from hypercalcemia with hypocalciuria or non- elevated PTH on the one hand, and from normo-calcemia with elevated PTH, hypophosphatemia or hypercalciuria on the other.
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January 2025
University of Brest, CHU Brest, UMR1304 GETBO, 29200 Brest, France; Endocrinology and Diabetology Department, CHU Brest, 29200 Brest, France.
Primary hyperparathyroidism is now predominantly an asymptomatic pathology, as blood calcium assay has become systematic. Diagnosis therefore requires screening for target organ damage when this is not already indicative of primary hyperparathyroidism.Classical clinical manifestations include bone, kidney and muscle signs, and are characterized by reversibility after parathyroid surgery.
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