DISEASES OF THE PARATHYROIDS

Dr Balram Das

 HYPOPARATHYROIDISM &
PSEUDOHYPOPARATHYROIDISM

 Acquired hypoparathyroidism is most commonly caused by anterior neck surgery. After total thyroidectomy, it occurs in
25% of patients transiently and 4% of patients permanently. The risk of permanent postoperative hypo- parathyroidism can be
reduced during thyroid surgery by taking parathyroid glands with suspected vascular damage and autotransplanting them into
the sternocleidomastoid muscle.
 Transient hypothyroidism may occur after surgical removal of a single parathyroid adenoma for primary
hyperparathyroidism due to suppression of the remaining normal parathyroids and accelerated remineralization of the skeleton
(“hungry bone syndrome”). Hypoparathyroid- ism may also occur after the resection of multiple parathy- roid adenomas. It
may be considered permanent if it persists more than 12 months following surgery.
 Autoimmune hypoparathyroidism may be isolated or combined with other endocrine deficiencies. Autoimmune
polyendocrine syndrome type I (APS-I) is also known as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy
(APECED). Hypoparathyroidism can also occur in SLE caused by antiparathyroid antibodies
HYPOPARATHYROIDISM & PSEUDOHYPOPARATHYROIDISM

 Magnesium deficiency causes functional hypopara- thyroidism. Although mild

hypomagnesemia stimulates PTH secretion, more profound hypomagnesemia (below 1.2
mg/dL) inhibits PTH secretion. Hypomagnesemia also causes resistance to PTH in bone
and renal tubules. Correction of hypomagnesemia results in rapid disappearance of the
condition. Hypermagnesemia also suppresses PTH secretion due to stimulation of the
glands calcium-sensing receptor (CaSR).
 Congenital hypoparathyroidism causes hypocalcemia beginning in infancy. However, it
may not be diagnosed for many years. Since hypoparathyroidism can be familial, genetic
screening for autoimmune regulator (AIRE) gene variants is recommended for any patient
with idiopathic hypoparathyroidism who has other manifestations of auto- immune
polyendocrinopathy-candidiasis-ectodermal dys- trophy syndrome (APECED).
 Clinical Findings

 Neuromuscular irritability :
 Chvostek sign (facial muscle contraction on tapping the facial nerve in front of the
tragus) is present in 70% of patients with hypocalcemia and in about 15% of individu- als
who are normocalcemic .
 Trousseau sign (flexion of the wrist and metacarpal-phalangeal joints with adduction of
the fingers after application of a sphygmomanometer cuff inflated to over systolic blood
pressure for 3 minutes) is present in over 90% of patients with hypocalcemia but in only
about 1% of normocalcemic individuals.
 Cardiovascular manifestations of acute hypocalcemia include arrhythmias (7%), such as
bradycardia, ventricular arrhythmias, and reduced EF.
 Clinical Findings

 CNS manifestations include seizures (11%) as well as depression (12%), psychiatric

changes, irritability, fatigue, cognitive impairment, and extrapyra- midal symptoms.
Ophthalmic manifestations include cat- aracts (17%); severe hypocalcemia may cause
papilledema. Renal manifestations of chronic hypoparathyroidism occur due to
hypercalciuria and include nephrolithiasis or nephrocalcinosis (15%), and renal
insufficiency (12%). Dermatologic manifestations include dry, rough skin; dry hair; scalp
and eyebrow hair loss; and brittle fingernails with transverse grooves. Chronic
hypocalcemia with hyperphosphatemia can cause calcifications in soft tissues, such as
joints, skin, and arteries.
Laboratory Findings

 Serum calcium is low. Because serum calcium is largely bound to albumin, the serum
ionized calcium should be determined in patients with hypoalbuminemia
 “Corrected” serum Ca2+ = Serum Ca2+ mg/dL + (0.8 × [4.0 − Albumin g/dL])
 Serum magnesium levels should always be measured AFTER 2 WEEKS
 The kidneys should ideally be imaged by non-contrast CT to determine the presence of
nephrolithiasis or nephrocalcinosis. CT scanning of the brain may reveal calcifications of
the basal ganglia and other areas in over 50% of patients with chronic hypocalcemia. The
bones may appear denser than normal and bone mineral density (BMD) is usually
increased, particularly in the lumbar spine. Cutaneous calcification may occur.
 Slit-lamp examination may show early posterior lenticular cataract formation. The ECG
may show heart block, a pro- longed QTc interval, and ST-T changes suggestive of an MI.
Complications

 Acute tetany with stridor, especially if associated with vocal cord palsy, may lead to
respiratory obstruction requiring tracheostomy. Seizures are common in untreated
patients. Hypocalcemia can also cause HF and dysrhythmias. Ossi- fication of the
paravertebral ligaments may occur with nerve root compression; surgical decompression
may be required. Overtreatment with vitamin D and calcium may produce
nephrocalcinosis and impairment of kidney func- tion. There may be associated
autoimmunity causing celiac disease, pernicious anemia, or Addison disease.
B. Emergency Treatment for Acute Hypocalcemia
(Hypoparathyroid Tetany)

 Airway.
 Intravenous calcium gluconate
 Oral calcium
 Vitamin D preparations
 Magnesium
Vitamin D preparations used in the treatment of
hypoparathyroidism.
 Recombinant human parathyroid hormone (rhPTH
 It must be given by subcutaneous injection every 1–2 days
 Transplantation of cryopreserved parathyroid tissue, removed
during prior surgery, restores normocalcemia in about 23% of
cases.
 PTH and PTH analogues as well as thiazide diuretics are
generally avoided during pregnancy.