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Secondary hyperparathyroidism refers to the excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) and associated hypertrophy of the glands. This disorder is especially seen in patients with chronic renal failure. It is often--although not consistently--abbreviated as SHPT in medical literature.
Signs and Symptoms
Bone and joint pain are common, as are limb deformities. The elevated PTH has also pleiotropic effects on blood, immune system and neurological system.
The PTH is elevated due to decreased levels of calcium or 1,25-dihydroxy-vitamin D3. It is usually seen in cases of chronic renal disease or defective calcium receptors on the surface of parathyroid glands.
Chronic renal failure is the most common cause of secondary hyperparathyroidism. Failing kidneys do not convert enough vitamin D to its active form, and they do not adequately excrete phosphorus. When this happens, insoluble calcium phosphate forms in the body and removes calcium from the circulation. Both processes leads to hypocalcemia and hence secondary hyperparathyroidism. Secondary hyperparathyroidism can also result from malabsorption (chronic pancreatitis, small bowel disease) in that the fat soluble vitamin D can not get reabsorbed. This leads to hypocalcemia and a subsequent increase in parathyroid hormone secretion in an attempt to increase the serum calcium levels.
If the underlying cause of the hypocalcemia can be addressed, the hyperparathyroidism will resolve. In patients with chronic renal failure, older treatments consists of dietary restriction of phosphorus, supplements with the active form of vitamin D (Paricalcitol), and phosphate binders. In recent years, a newer class of medications, calcimimetics cinacalcet, have achieved amazing response rates and has reduced the number of patients who eventually require surgery. Some of these patients may also see resolution of their sHPT following kidney transplantation.
If left untreated, the disease will progress to tertiary hyperparathyroidism, where correction of the underlying cause will not stop excess PTH secretion, i.e. parathyroid gland hypertrophy becomes irreversible.
v • d • eEndocrine pathology: endocrine diseases (E00-35, 240-259)
Hypothyroidism (Iodine deficiency, Cretinism, Congenital hypothyroidism, Goitre, Myxedema) - Hyperthyroidism (Graves disease, Toxic multinodular goitre, Teratoma with thyroid tissue or Struma ovarii) - Thyroiditis (De Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel's thyroiditis) - Euthyroid sick syndrome - Thyroid hormone resistance
Diabetes mellitus (type 1, type 2, coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy, MODY) - Hypoglycemia - Hyperinsulinism - Zollinger-Ellison syndrome - insulin receptor (Rabson-Mendenhall syndrome)
Hyperpituitarism (Acromegaly, Hyperprolactinaemia, SIADH) - Hypopituitarism (Simmonds' disease/Sheehan's syndrome, Kallmann syndrome, Growth hormone deficiency, Diabetes insipidus) - Adiposogenital dystrophy - Empty sella syndrome - Pituitary apoplexy - Adrenocorticotropic hormone deficiency
Cushing's syndrome (Nelson's syndrome, Pseudo-Cushing's syndrome) - CAH (Lipoid, 3β, 11β, 17α, 21α) - Hyperaldosteronism (Conn syndrome, Bartter syndrome) - Adrenal insufficiency (Addison's disease) - Hypoaldosteronism
ovarian dysfunction (Polycystic ovary syndrome, Premature ovarian failure) - testicular dysfunction (5-alpha-reductase deficiency) - testosterone biosynthesis (17-beta-hydroxysteroid dehydrogenase deficiency) - general (Hypogonadism, Delayed puberty, Precocious puberty)
Androgen insensitivity syndrome - Autoimmune polyendocrine syndrome - Carcinoid syndrome - Gigantism - Short stature (Laron syndrome, Psychogenic dwarfism) - Multiple endocrine neoplasia (1, 2) - Progeria - Woodhouse-Sakati syndrome
CRESCENTcme.org - The Critical RolE of Serum Calcium: An Educational Network for Secondary HyperparaThyroidism
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Categories: Parathyroid disorders
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