ismarehyperplastic.Asinprimaryhyperplasia,thedegreeof glandularenlargementisnotnecessarilysymmetric.Onmicroscopicexamination,thehyperplasticglandscontainanincreasednumberofchiefcells,orcellswithmoreabundant,clearcytoplasm(water-clearcells),inadiffuseormultinodulardistribution.Fatcellsaredecreasedinnumber.Bonechangessimilartothoseseeninprimaryhyperparathyroidismalsomaybepresent.Metastaticcalcificationmaybeseeninmanytissues.
The clinical manifestations of secondary hyperparathyroidism usually are dominated by those related to chronic renal failure. Bone abnormalities (renal osteodystrophy) and other changes associated with PTH excess are, in general, less severe than those seen in primary hyperparathyroidism. Serum calcium remains near normal because the compensatory increase in PTH levels sustains serum calcium. The metastatic calcification of blood vessels (secondary to hyperphosphatemia) occasionally may result in significant ischemic damage to skin and other organs—a process referred to as calciphylaxis. In a minority of patients, parathyroid activity may become autonomous and excessive, with resultant hypercalcemia—a process sometimes termed tertiary hyperparathyroidism. Parathyroidectomy may be necessary to control the hyperparathyroidism in such patients.
Primaryhyperparathyroidismisthemostcommoncauseofasymptomatichypercalcemia.
Inamajorityofcases,primaryhyperparathyroidismiscausedbyasporadicparathyroidadenomaand,lesscommonly,byparathyroidhyperplasia.
Parathyroidadenomasaresolitary,whilehyperplasiatypicallyisamultiglandularprocess.
Skeletalmanifestationsofhyperparathyroidismincludeboneresorption,osteitis fibrosa cystica, andbrown tumors. Renalchangesincludenephrolithiasis(stones)andnephrocalcinosis.
Mostcasesofhyperparathyroidismareclinicallysilentbecauseofearlydetectionofhypercalcemiaduringroutinebloodtesting.
Secondaryhyperparathyroidismiscausedbyhypercalcemiamostoftensecondarytorenalfailure,andtheparathyroidglandsarehyperplastic.
Malignanciesarethemostimportantcauseofsymptomatichypercalcemia,whichresultsfromosteolyticmetastasesorreleaseofPTH-relatedproteinfromnonparathyroidtumors.
Hypoparathyroidism is far less common than hyperparathyroidism. The major causes of hypoparathyroidism include the following: • Surgical ablation: The most common cause is inadvertent removal of parathyroids during thyroidectomy or other surgical neck dissections.
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Congenital absence: This occurs in conjunction with thymic aplasia (Di George syndrome) and cardiac defects, secondary to deletions on chromosome 22q11.2 (Chapter 7).
Autoimmune hypoparathyroidism: This is a hereditary polyglandular deficiency syndrome arising from auto-antibodies to multiple endocrine organs (parathyroid, thyroid, adrenals, and pancreas). This condition is caused by mutations in the autoimmune regulator (AIRE) gene and is discussed more extensively later, in the context of autoimmune adrenalitis.
The major clinical manifestations of hypoparathyroidism are secondary to hypocalcemia. Acute cases (as may occur after surgical ablation) manifest as increased neuromuscular irritability (tingling, muscle spasms, facial grimacing, and sustained carpopedal spasm or tetany), cardiac arrhythmias, and, on occasion, increased intracranial pressure and seizures. Manifestations of chronic hypoparathyroidism include cataracts, calcification of the cerebral basal ganglia, and dental abnormalities.