Hyperparathyroidism. Sarah Rodriguez, MD Shawn Newlands, MD, PhD University of Texas Medical Branch Grand Rounds Presentation February 2006. PTH/Calcium Homeostasis.
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Sarah Rodriguez, MD
Shawn Newlands, MD, PhD
University of Texas Medical Branch
Grand Rounds Presentation
Low circulating serum calcium concentrations stimulate the parathyroid glands to secrete PTH, which mobilizes calcium from bones by osteoclastic stimulation. PTH also stimulates the kidneys to reabsorb calcium and to convert 25-hydroxyvitamin D3 (produced in the liver) to the active form, 1,25-dihydroxyvitamin D3, which stimulates GI calcium absorption. High serum calcium concentrations have a negative feedback effect on PTH secretion.
I.Parathyroid-related-Primary hyperparathyroidism-Lithium therapy-Familial hypocalciuric hypercalcemia
II. Malignancy-related-Solid tumor with metastases (breast)-Solid tumor with humoral mediation of hypercalcemia (lung, kidney)-Hematologic malignancies (multiple myeloma, lymphoma, leukemia)
III. Vitamin D-related-Vitamin D intoxication-↑ 1,25(OH)2D; sarcoidosis and other granulomatous diseases-Idiopathic hypercalcemia of infancy
IV. Associated with high bone turnover-Hyperthyroidism-Immobilization-Thiazides-Vitamin A intoxication
V. Associated with renal failure-Severe secondary hyperparathyroidism-Aluminum intoxication-Milk-alkali syndromeHypercalcemia
**Primary hyperparathyroidism and cancer account for 90% of cases of hypercalcemia
Incidence increases above age 40
Most patients with sporadic primary hyperparathyroidism are postmenopausal women with an average age of 55 years
>80% of cases are caused by a solitary parathyroid adenoma
Approximately 10% are caused by “double adenoma”Primary Hyperparathyroidism
CA/CRT ratio: (24 hr urine calciumXserum crt)/(24 hr urine crtXserum calcium)
creatinine clearance (mL/min) = ((urine creatinine in mg/dL) * (urine volume in mL)) / ((plasma creatinine in mg/dL) * (time period in minutes))
Scintigraphy Images 1000 women
Familial Syndromes 1000 women
MEN I 1000 women
STIGMATA OF MEN I 1000 women
MEN IIA (Sipple’s Syndrome) 1000 women
This benign condition can be easily mistaken for mild hyperparathyroidism. It is an autosomal dominant inherited disorder characterized by hypocalciuria (usually < 50 mg/24 h), variable hypermagnesemia, and normal or minimally elevated levels of PTH. These patients do not normalize their hypercalcemia after subtotal parathyroid removal and should not be subjected to surgery. The condition has an excellent prognosis and is easily diagnosed with family history and urinary calcium clearance determination.
Secondary HPT 1000 women
severe hypercalcemia, severe
bone disease, severe pruritis,
calciphylaxis, severe myopathy
Tertiary hyperparathyroidism develops in patients with long-standing secondary hyperparathyroidism, which stimulates the growth of an autonomous adenoma. A clue to the diagnosis of tertiary hyperparathyroidism is intractable hypercalcemia and/or an inability to control osteomalacia despite vitamin D therapy.
- calcium- phosphate product > 70
- severe bone disease and pain
- extensive soft tissue calcification with tumoral calcinosis
A. Order the mibi/schedule the surgery
B. Consider estrogen replacement in this perimenopausal woman
C. Take a careful family history
D. Look for stigmata of MEN I
A. Have primary team order a mibi before you see the patient
B. Suspect MEN IIA and have the primary team order ret-proto oncogene screening
C. Evaluate the pt in the dialysis unit with careful questioning as to symptoms of pruritis, skin calcifications or necrosis