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Download PDF. More article options. ePub DOI: / Calcificaciones pulmonares metastásicas en un hiperparatiroidismo terciario. del denominado hiperparatiroidismo refractario (secunda- rio y terciario sin respuesta al tratamiento con calcitriol). Material y métodos: Estudio retrospectivo con. of tertiary hyperparathyroidism. Sr. Director: El hiperparatiroidismo terciario ( HPTT) ocurre en un % de los pacientes trasplantados renales con función renal.

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Request PDF on ResearchGate | On Nov 1, , José Ruiz and others no han tenido impacto en la cirugía del hiperparatiroidismo terciario. Hiperparatiroidismo terciario - Download as PDF File .pdf), Text File .txt) or read online. Endocrinología. Objetivo. Dar a conocer nuestra experiencia en la cirugía del denominado hiperparatiroidismo refractario (secundario y terciario sin respuesta al tratamiento con.

Kurt A. Kennel and Bart L. Clarke Case Presentation A year-old female initially presented at age 13 with intermit- tent paresthesias and tetany associated with hypocalcemia 5. She had no features of Albrights hereditary osteodys- trophy or family history of hypocalcemia. She was treated with calcium and vitamin D supplementation and her symptoms resolved. Repeat bone biopsy showed healed osteitis fibrosa.

The cellular etiol- ogy of THP is unknown but is postulated to be a result of a monoclonal expansion of parathyroid cells [13]. It is believed that these cells have an altered set point of their calcium-sensing receptor CaSR so that PTH is secreted despite elevated iCa concentrations [14].

Patients with long-standing chronic stimulation of their para- thyroid glands often develop autonomy, such that they do not respond to calcium and calcitriol supplementation or phosphate restriction in their diet. In this situation, little can be done to stop overproduction of PTH short of parathyroidectomy, although certain interventions may be successful in temporarily reducing excess secretion of parathyroid hormone.

Spanish translation section - - BJS - Wiley Online Library

Phosphate binders such as calcium acetate, sevelamer, or lanthanum are usually used to control hyperphosphatemia in patients where dietary restriction of phosphorus to mg each day is not suf- ficient. Certain synthetic active vitamin D analogues such as parical- citol, doxercalciferol, and others have been shown to reduce PTH secretion by moderate amounts without simultaneously stimulat- ing absorption of calcium and phosphate by the intestine. These have a modulating effect on the amount of PTH release by autonomous glands by direct transcriptional inhibition of PTH synthesis in the parathyroid glands and tend to reduce circulating PTH concentrations [15, 16].

Higher doses of these agents may lead to an increase in serum calcium or phosphate by stimulating intestinal absorption and tend to increase FGF levels. Cinacalcet is a calcimimetic compound that effectively lowers PTH secretion by autonomous or semiautonomous parathyroid glands. This allosteric sensitizer of the calcium-sensing receptor 20 Tertiary Hyperparathyroidism causes parathyroid chief cells to sense higher levels of extracel- lular calcium than are actually present, leading to decreased production of PTH, which leads to decreased serum calcium [].

Cinacalcet is typically started at 30 mg once daily, with follow-up serum calcium measurement within 1 week. The most common side effect is nausea with vomiting, but taking cinacal- cet with meals minimizes these side effects.

Hypocalcemia may also occur, and cinacalcet should not be given if serum calcium is less than 8. Cinacalcet may be titrated upward to a maximum of 90 mg four times daily in the setting of parathyroid cancer, but is titrated to a maximum of 60 mg three times daily for THP.

Patients with THP are usually at least moderately responsive to cinacalcet. Hemodialysis or peritoneal dialysis will help control calcium and phosphorus abnormalities in end-stage chronic kidney dis- ease, but usually do not help reduce PTH secretion in most patients.

Renal transplantation corrects many abnormalities as long as the transplanted kidney continues to function well, and usually helps improve PTH secretion overall, but not in all cases. For patients who have persistent THP despite optimal medical management, or after beginning dialysis treatment, or undergo- ing renal transplantation, surgery is usually recommended as a last resort.

Because patients with THP typically have all four parathyroid glands oversecreting PTH, surgery usually removes three and one-half glands or all four glands with autotransplanta- tion of a part of one gland into the neck, chest, or forearm mus- cle.

Surgery to remove three and one-half glands leaves the remaining half-gland in place with intact blood supply. Autotransplantation of one-half gland usually leads to revascu- larization of the parathyroid tissue from surrounding muscle blood supply. In both cases, success of control of PTH oversecre- tion is high, and risk of hypoparathyroidism is low.

In some cases four-gland hyperplasia is associated with four mildly to moder- ately enlarged glands of the about same size, but in other cases, asymmetry is noted, with some glands larger than the others. In K. Clarke patients who develop recurrent THP later due to continued autonomy of the half-gland left in situ or autotransplanted, medi- cal therapy may be tried again, and if this fails, surgery may be recommended again.

Repeat surgery for THP is associated with a higher risk of hypoparathyroidism [20]. In the case presented, it is presumed that suboptimal calcium or calcitriol replacement led to chronic mild hypocalcemia, which led to chronic stimulation of her parathyroid glands.


At some point one or more of her parathyroid glands became autonomously secreting, and she developed THP with hypercal- cemia. Cessation of her paresthesias was a harbinger of develop- ment of THP. Parathyroid sestamibi scan and neck ultrasound each suggested two enlarged inferior parathyroid glands.


At surgery, both the right and left inferior parathyroid glands were visibly enlarged, whereas the superior glands were of normal size and appearance. Baseline intraoperative PTH was After the left inferior mg gland was removed, PTH decreased further to 6. Acharya, S.

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