Causes of Hyperparathyroidism and Hypoparathyroidism

Hyperparathyroidism

Hyperparathyroidism may be primary or secondary.

1. Primary hyperparathyroidism

a. Sporadic

Causes

· Solitary adenoma (commonest)

· Cheif cell hyperplasia

· Carcinoma

 

b. Familial

· MEN = multuple endocrine neoplasia type-I Werlmer’s syndrome

· Autosomal dominant = as with inactivating germ line mutation of MEN-1 TSG on Ch-II

Clinical

• Hyper PTH > 80%
• Benign pituitary adenomas (functioing/non functioning)
• Parcreatoco-duodenal neuroendocine tumors (Beingn / malignant)(gastrinoma, insulinoma, insulinoma, glucagonoma, vipoma & other peptide hormones

MEN-2

· Occur in MEN-2A & renal in MEN-2B

Familial isolated hyper PTH

· Increased risk of PT carcinoma

2. Secondary hyper PTH

Due to chronic renal failure,

D Decreased calcitriol leads to decreased calcium & PO4 retention causing proliferation of PT cells and increase in gland parendepmal mass

3. Tertiary hyper PTH

Renal osteodystrophy, following renal transplantation, development of autonomous hyper function of PT tissue & increased calcemia

4. Parathyroid Ca

5. Persistant / recurrent hyper PTH

Ca occuring more than 1 yr after creative parathyroidectomy

Causes

· Missed pathology at 1^st surgical procedure

· Graft dependent recuence

· Parathyromatosis disseminated nodules of PT tissue within soft tissue of neck & suspicious mediastenemia caused by abnormal PT tissue at initial surgery. (reoperative PT surgery,risk of recurrent laugeal nerve injury & postopCa)

Causes of hypoparathyroidism

1. Primary hypoparathyroidism

PTH deficiency

Causes

1. Surgical damage to glands (common)

• During thyroidectomy
• Radical neck dissection
• Resection of PT gland in PT hyperplasia

2. Radiation therapy to neck

3. Damage from

• Infection
• Metastatic tumor
• Infiltration by granuloma (TB, sarcoidosis)
• Heavy metals (Wilsons, hemocheomatosis, transfusion hemosiderosis)

4. Hormone – Resistant (inherited) (Pseudohypoparathyroidism = PHP)

End organ resistance to PTH, plasma levels of which are hight in response to hypocalcemia

PHP = type (1a & 1b)

· Inability of PTH to generate an increase in urinary (AMP, PHP = type-II)

PHP type-II

· Inability of PTH to generate an increase in phosphaturic response

Idopathic

Dysembryogenesis (Di-George’s syndrome)

Appears as familial disorder, may have autoimmune basis presents at puberty where it is associated with mucoutaneous candidiasis due to immune def & other endocrine disorders.

Magnesium Deficiency

· Serum magnesium < 0.4 mmol/L)

· Suppresion of PTH secretion becoming unresponsive to calcium therapy unless patient becomes magnesium-replete.