i) Hyperparathyroidism: Hyperparathyroidism is a disorder characterized by increased secretion of parathyroid hormone (PTH) from the parathyroid glands.
| Type | Characteristics |
| Primary | Increased PTH secretion by the parathyroid gland due to adenoma or parathyroid hypertrophy; lithium adverse effect; most common in postmenopausal women; familial cases present at younger ages; seen in MEN I and II |
| Secondary | Rise in PTH secondary to any cause of hypocalcemia such as Vit D deficiency, low calcium intake, malabsorption, chronic renal failure |
| Tertiary | Due to prolonged hypocalcemia especially in chronic renal failure, resulting in an autonomous and/or hypertrophied parathyroid gland that secretes excess PTH; persistence of secondary hyperparathyroidism even after renal transplant; change in set point of calcium sensing mechanisms |
Most cases of hyperparathyroidism are asymptomatic. When symptoms occur, they are mainly due to hypercalcemia or to the underlying condition (such as renal failure). Clinical features include constipation, bone pains, renal stones, abdominal pain, polyuria, pancreatitis, peptic ulcers, fractures, diastolic hypertension, chondrocalcinosis, psychosis, confusion, and anxiety. Some cases may show valvular calcifications, left ventricular hypertrophy, and depression.
Osteitis fibrosa cystica is a bone disorder seen in hyperparathyroidism. It is characterized by bone pain, subperiosteal bone resorption, osteolysis, a “salt and pepper” appearance of the skull, bone cysts, and “brown tumors” of the bones. Brown tumors are not neoplasms; they are hemorrhagic areas with reparative granulation tissue that appears brown from hemosiderin. These bone lesions are due to increased osteolytic activity caused by stimulation of osteoclasts by excess PTH. Serum alkaline phosphatase levels will be elevated.
Hypercalcemia may rarely cause calciphylaxis, which presents with skin necrosis, purple discoloration of the skin, ulceration, and crusting, especially in areas with high fat content like the abdomen and inner thigh. It is seen in secondary hyperparathyroidism due to activation of clotting factors and thrombosis of small blood vessels, leading to ischemic skin necrosis.
Condition: Primary hyperparathyroidism
Condition: Secondary hyperparathyroidism
Condition: Tertiary hyperparathyroidism
All symptomatic and severe cases of primary hyperparathyroidism are treated with parathyroidectomy. Technetium 99m sestamibi scan, with or without PET scan, is a highly sensitive and specific test for localizing abnormal parathyroid glands.
After parathyroidectomy, patients with large adenomas may develop “hungry bone syndrome,” which is associated with hypocalcemia, hypophosphatemia, and low urinary calcium excretion.
Secondary and tertiary hyperparathyroidism are managed with calcium and Vit D supplementation. Severe bone disease is treated with parathyroidectomy.
Hypercalcemia is treated with intravenous saline, loop diuretics like furosemide, calcitonin, and bisphosphonates. Cinacalcet sensitizes the calcium sensing receptor and decreases PTH levels.