Anne Klibanski — Page 4

PubMedDate not supplied

Hypercalcemia and local production of parathyroid hormone-related protein by a perisellar rhabdomyosarcoma after remote pituitary irradiation.

OBJECTIVE: To describe a case of metastatic rhabdomyosarcoma originating from the sphenoid sinus in a patient previously treated with conventional irradiation for a prolactinoma, presenting as hypercalcemia in the setting of a normal level of serum parathyroid hormone-related protein (PTHrP). METHODS: We report the case of a patient who underwent remote pituitary irradiation for a prolactinoma and then presented decades later with hypercalcemia of unknown cause. His clinical course, the initial biochemical and radiologic investigations, and the results of examination of pathology specimens are reviewed. RESULTS: The patient was found to have a mass in the sphenoid sinus. The pathologic features were consistent with alveolar rhabdomyosarcoma. Although he had a normal serum PTHrP level, staining of his tumor with an antibody against PTHrP revealed local production of PTHrP at the tumor margins. His bone marrow biopsy specimen showed 100% involvement with rhabdomyosarcoma. CONCLUSION: PTHrP staining of pathology specimens might explain hypercalcemia of undetermined cause in patients with a known malignant lesion, in whom elevated serum PTHrP levels cannot be demonstrated.

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PubMedDate not supplied

Cardiovascular risk in patients with growth hormone deficiency: effects of growth hormone substitution.

OBJECTIVE: To review the literature on the increased cardiovascular risk in patients with growth hormone (GH) deficiency and the positive effects of GH replacement. METHODS: We analyze the factors that contribute to cardiovascular risk in GH deficiency, including body composition and lipid profile, and summarize GH treatment strategies and results described in the literature. RESULTS: The prominent clinical finding in patients with GH deficiency is the increased abdominal fat, even in patients with normal weight. Cardiac ejection volume tends to be decreased, and arterial distensibility is diminished. The lipid status is also worsened, accompanied by increased inflammatory markers, such as highly sensitive C-reactive protein. Typically, GH treatment reduces visceral fat and increases muscle mass, changes that diminish cardiovascular risk. Because of direct effects as well as increased hemodynamic performance and increased blood volume, cardiac performance is improved. With GH therapy, total cholesterol and low-density lipoprotein levels decrease by 10% to 20%, and inflammatory markers such as C-reactive protein decline. Carbohydrate metabolism during moderate to long-term treatment is minimally affected, although obese patients with GH deficiency on rare occasion may have hyperglycemia or even diabetes. CONCLUSION: The relevance of the beneficial effects of GH on the cardiovascular system is strongly suggested but not fully proved. The results in a large cohort of GH-treated patients (the KIMS or Pharmacia and Upjohn International Metabolic Surveillance database) demonstrated no difference in cardiovascular risk in comparison with that in a control population after a mean of 3 years of treatment.

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