1. Hypoparathyroidism can be caused by neck surgery removing the parathyroid glands, autoimmune disorders, or genetic defects. 2. Symptoms include neuromuscular irritability, seizures, depression, and kidney problems due to low calcium levels. 3. Laboratory tests show low serum calcium levels and increased phosphate levels. Imaging can detect calcium deposits in tissues. 4. Treatment involves calcium and vitamin D supplementation, with recombinant PTH for severe cases. Emergency treatment focuses on stabilizing calcium levels and the airway.

1. DISEASES OF THE PARATHYROIDS
Dr Balram
Das

2. 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

3. 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).

4. 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.

5. 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.

6. 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

7. Imaging & Other Examinations
 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.

8. 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.

9. B. Emergency Treatment for Acute Hypocalcemia
(Hypoparathyroid Tetany)
 Airway.
 Intravenous calcium gluconate
 Oral calcium
 Vitamin D preparations
 Magnesium

10. Vitamin D preparations used in the treatment of
hypoparathyroidism.

11.  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.