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An Overview Of The Main Parathyroid Disorders: Hyperparathyroidism And Hypoparathyroidism

Updated on February 11, 2014

Hyperparathyroidism

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Secondary And Tertiary Hyperparathyroidism

Previous hubs on this series have been on primary hyperparathyroidism, so more emphasis will be on secondary and tertiary hyperparathyroidism and a little on hypoparathyroidism.

Secondary and Tertiary Hyperparathyroidism

These are seen in conditions where there is resistance to the action of PTH. Increased levels of PTH are seen in the presence of persistent hypocalcemia. Increased secretion of PTH is the result of chronic stimulation by hypocalcemia. Secondary hyperparathyroidism is seen in rickets, osteomalacia, malabsorption syndrome, chronic renal failure and skeletal fluorosis. Removal of the primary cause early in the disease may correct the parathyroid dysfunction also but this is not invariable so. Though in the initial stages, the parathyroids are stimulated by hypocalcemia, later on, the glands become autonomous because of the development of adenomas. This condition is known as tertiary hyperparathyroidism.

Biochemical profile includes normal or low (never high) serum calcium with normal or elevated serum phosphate. Bone changes are the result of excessive parathyroid activity and calcium deficiency. Serum alkaline phosphatase is high.

Therapy is intended to abolish hypocalcemia which is the chronic stimulus for stimulation of parathyroid. Surgical removal of the adenoma is indicated in tertiary hyperparathyroidism.

Pseudohyperparathyroidism: This refers to the condition in which PTH like substances (peptides or prostaglandins) are secreted by other tumours like carcinomas of the breast, kidneys, lungs and uterine cervix, lymphomas and also leukemias. Often this leads to severe and fulminant hypercalcemia.

A Doctor And A Patient

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Hypoparathyroidism

Definition: Deficiency in the secretion of parathyroid hormone (PTH) leads to hypoparathyroidism. This is characterized by hypocalcemia, hyperphosphatemia and low levels of circulating PTH. The hyperphosphatemia leads to calcification of the basal ganglia in 50% of cases.

Etiology:

  1. Accidental surgical removal of parathyroids or interference with their blood supply during surgery in the neck.
  2. Idiopathic atrophy of the parathyroids.
  3. Destruction of the parathyroid by carcinomatous secondaries, infarction, radioiodine therapy or irradiation of the neck.
  4. Neonatal hypoparathyroidism may occur as a transient phenomenon in premature infants and infants of mothers with hyperparathyroidism or diabetes mellitus.

The term “Pseudohypoparathyroidism” refers to the condition in which the target tissues become resistant to the action of PTH. As a result, there is overactivity and hyperplasia of the parathyroids with excessive secretion of PTH. In spite of the raised blood levels of PTH, the clinical and biochemical features are those of hypoparathyroidism. Vitamin D deficiency, hypomagnesia, chronic renal failure, and other renal tubular defects give rise to pseudohypoparathyroidism. In most cases, it is an inherited disorder.

Depending upon the lesion, postoperative hypoparathyroidism may be transient or permanent. Idiopathic hypoparathyroidism may run in families. It may be associated with other congenital abnormalities involving mal-development of the third and fourth pharyngeal puches such as Di George syndrome. Other immune-mediated endocrinopathies such as Addison’s disease, hypothyroidism and hypofunction of ovaries, and pernicious anemia may coexist. Antibodies against parathyroids and other organs specific antibodies may be present.

Reynaud's Syndrome

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A Child Patient With Hypoparathyroidism

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Clinical Manifestations

Clinical features depend upon the onset, duration and the severity of hypocalcemia. Prominent features are tetany, dental abnormalities, subcapsular cataracts, myocardial dysfunction and neurological abnormalities. Tetany is due to hypocalcemia. It manifests as muscle cramps, paraesthesia of the hands, feet and mouth, spasmophilia (carpopedal spasm, bronchospasm and laryngospams) and severe neuromuscular irritability. Physical exertion, emotional stress, hyperventilation, vomiting and ischemia to the limb may precipitate tetany. Latent tetany can be identified by eliciting the Chvostek’s sign. Trousseau’s sign and also be electromyography. Hyperexcitability of the facial muscles, demonstrable as contraction of the facial muscles on tapping the facial nerve is the Chvostek’s sign.

Troussea’s sign is elicited by making the forearm ischemic by applying a sphygmomanometer cuff to the arm and keeping the pressure above systolic blood pressure for five minutes. The hand goes into painful carpopedal spasm and assumes the “accoucheur’s hand position”. Laryngeal spasm gives rise to inspiratory dypsnea or stridor (laryngismus stridulus). Common neurological manifestations include convulsions which are unresponsive to conventional anticonvulsant therapy, paraesthesia and psychiatric behavious. Other manifestation such as papilledema and extrapyramidal disturbances like chorea, parkinsonism and athetosis may develop.

The skin is dry and scaly. The hair is brittle and coarse. Deformity and moniliasis of the nails are common. The enamel of the teeth is pitted, dental roots are short and blunt, and early loss of teeth is common. Subcapsular posterior or anterior zonular cataracts develop. Cardiac adnormalities may occur. The electrocardiogram shows prolonged QT interval. The acute manifestations of hypoparathyroidism are corrected dramatically by the intravenous administration of calcium.

© 2014 Funom Theophilus Makama

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