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in the interesting paper “Is it my calcium, Doctor?” (1), the authors
concluded that “Amy’s hypercalcaemia” is due to a “primary
hyperparathyroidism” and they don’t cite celiac disease (CD) as a specific
cause of hyperparathyroidism (HPT), although they first wrote that “she
had a previous history of celiac disease for which she was on a gluten
free diet” (GFD).
CD is frequently associated...
CD is frequently associated with abnormal bone metabolism involving
both mineralization, leading to osteomalacia, and bone mass reduction,
resulting in osteoporosis. Recent studies describe an elevated prevalence
of secondary HPT not only among adults (27%), but also among children
(53%) with CD (2).
The pathogenesis of bone metabolism in CD is not completely
understood, but at least two mechanisms must be considered, one relating
to malabsorption and the other to presence of systemic or local
In undiagnosed celiac subjects, malabsorption of calcium and/or
vitamin D leads to a secondary HPT. Although prompt introduction of a
strict GFD in paediatric patients can bring to normalized bone metabolism,
including parathyroid hormone (PTH) levels, in adolescents and in adults
with protracted exposure to gluten before CD diagnosis, GFD may not bring
rapid improvement in bone metabolism abnormalities (3). Long-term exposure
to gluten (for late diagnosis or bad compliance to GFD) and abnormal bone
metabolism produce chronic stimulation of the parathyroid, which in turn
causes parathyroid hyperplasia not responsive to GFD1.
The association between asymptomatic CD and normocalcemic or mildly
hypercalcemic HPT, like as in Amy’s case, is reported in literature (4):
some patients developed a parathyroid adenoma with hypercalcemic HPT which
improved after surgery, but in longstanding undiagnosed CD patients a
tertiary HPT characterised by autonomous hypersecretion of PTH causing
hypercalcemia may arise (4,5).
In conclusion we believe that CD must be considered also in “Amy’s
case” as possible cause of secondary HPT and that the compliance to GFD
should be evaluated.
1. Stanley S, Shaw NJ. Is it my calcium, Doctor? Arch Dis Ed Pract
2. Zanchi C, Di Leo G, Ronfani L et al. Bone metabolism in celiac
disease. J Pediatr. 2008;153(2):262-5.
3. Kalayci AG, Kansu A, Girgin N, et al. Bone mineral density and
importance of a gluten free diet in patients with celiac disease in
childhood. Pediatrics 2001;108;89-91
4. Maida MJ, Praveen E, Crimmins SR. Coeliac disease and primary
hyperparathyroidism: an association? Postgrad Med J 2006;82:833-5
5. Alzahrani AS, Al Sheef M. Severe primary hyperparathyroidism
masked by asymptomatic celiac disease. Endocr Pract 2008;14(3):347-5
Chiara Zanchi*, Federico Marchetti, Alessandro Ventura
Department of Paediatrics, Institute of Child Health, IRCCS Burlo
Garofolo, University of Trieste, Itaky
Via dell’Istria 65/1
PHONE: +39 040 3785312
FAX: +39 040 3785458
* Corresponding Author
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in the interesting paper “Is it my calcium, Doctor?” (1), the authors concluded that “Amy’s hypercalcaemia” is due to a “primary hyperparathyroidism” and they don’t cite celiac disease (CD) as a specific cause of hyperparathyroidism (HPT), although they first wrote that “she had a previous history of celiac disease for which she was on a gluten free diet” (GFD).
CD is frequently associated...