Effect of Calcitonin Replacement Therapy in Idiopathic Juvenile Osteoporosis

Jackson, Elizabeth; Strife, C. Frederic; Tsang, Reginald C.; Marder, Harold K.

doi:10.1001/archpedi.1988.02150110115034

Cited by 13 publications

(12 citation statements)

References 12 publications

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“…Calcitonin (CT) is a potent anti-reabsorptive hormone active at physiological concentration by inhibition of osteoclastic activity, at least in vitro [3]. CT deficiency has been related to some form of childhood [10,23] and adulthood [14,22] osteoporosis. Thus, even if a CT deficiency may be supposed in diabetic osteopenia, only few controversial data are available on CT levels in diabetic adults [7,20] or in experimental diabetic rats [8,19].…”

Section: Offprint Requests To: G Saggesementioning

confidence: 99%

Calcitonin secretion in children with insulin-dependent diabetes mellitus

et al. 1991

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To test the hypothesis that calcitonin (CT) deficiency may contribute to bone mineral loss in insulin-dependent diabetes mellitus (IDDM), we studied basal and calcium stimulated (2 mg/kg body wt. in 5 min) CT levels in 15 children with IDDM and osteopenia. Ten age-sex matched healthy children were studied as controls. Since extractable CT (exCT) allows more sensitive and specific measurement of CT monomer, we measured both total serum CT (tCT) and exCT. Diabetic children had slightly but significantly (P less than 0.05) higher basal levels of both tCT (24.5 +/- 7.1 ng/l) and exCT (5.6 +/- 1.6 ng/l) than controls (tCT: 18.7 +/- 5.4 ng/l; exCT: 4.3 +/- 1.2 ng/l). Calcium stimulation test pointed out significant increase (P less than 0.001) of tCT and exCT in both groups with peak values not significantly different in IDDM in respect to controls. However, diabetic children showed a reduced CT reserve evidenced by a lower peak/basal ratio (diabetics: tCT 1.68, exCT 1.84; controls: tCT 2.49, exCT 2.88) and by a more rapid decrease in CT levels. We conclude that CT deficiency is not a causative factor of diabetic osteopenia. The slightly higher basal CT values suggest that an increased bone reabsorption may be operative in IDDM and it stimulates CT secretion. This chronic "C" cell stimulation may induce the reduction in CT reserve observed employing the calcium infusion test.

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Section: Offprint Requests To: G Saggesementioning

confidence: 99%

Calcitonin secretion in children with insulin-dependent diabetes mellitus

et al. 1991

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“…Early hormonal replacement is the most effective method to prevent gonadal insufficiency‐induced bone loss, which is the most important prediction of osteoporosis in thalassemia. 1,2,22,31,32 In women, estrogen with progestational agents are usually prescribed. While the benefit of estrogen outweighs the risk in this population, concern for a possible increased risk of breast cancer requires detailed patient discussions.…”

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confidence: 99%

The Morbidity of Bone Disease in Thalassemia

Vichinsky¹

1998

Annals of the New York Academy of Sciences

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As thalassemia patients age, bone disease becomes a serious cause of morbidity. The frequency and type of bone disease is affected by the underlying type of thalassemia and its treatment. Problems include rickets, scoliosis, spinal deformities, nerve compression, fractures and severe osteoporosis. In early stages, patients may be asymptomatic but can present with back pain, a limp, dyspnea, neurological emergencies, or sudden fractures. The etiologies are often multifactorial, culminating with increased bone resorption and remodeling. They include hormonal deficiency, bone marrow expansion, nutritional deficiency, or desferal toxicity. Particular risk factors include older patients, low baseline hemoglobin, delayed puberty, hormonal failure, and high iron stores. Nutritional deficiencies may further compound the patient's risk for bone disease. Increasing evidence suggests that these complications and their associated long-term morbidity can be prevented if an annual screening is done, followed by long-term intervention. Patients treated with amino biphosphonates inhibit bone resorption and may demonstrate rapid healing. Intra-nasal calcitonin has also been successful in treating osteopenia. Early use of estrogen and testosterone appears to markedly lower the risk for selective patients. Both transfused and non-transfused patients should be educated about risk factors and early symptoms. All patients should be screened annually for bone disease. Once adolescence occurs, annual testing in selected cases should include bone density studies with X-ray absorptiometry.

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“…However, bone deformities resulting from fractures may be severe, persist into adulthood and cause neurological impairment. Therapeutic attempts with oral calcium, sodium fluoride, oestrogens [22], and parenteral calcitonin [11,12] failed to prevent their progression. In our patient, the appearance of massive neurological defects prohibited a conservative approach.…”

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confidence: 99%