Find information on thousands of medical conditions and prescription drugs.

Hyperparathyroidism

In medicine (endocrinology), hyperparathyroidism is overactivity of the parathyroid glands and excess production of parathyroid hormone (PTH). Consequences are weakness of bone tissue (predisposing for fracture) and hypercalcemia (high calcium levels). more...

Home
Diseases
A
B
C
D
E
F
G
H
Hairy cell leukemia
Hallermann Streiff syndrome
Hallux valgus
Hantavirosis
Hantavirus pulmonary...
HARD syndrome
Harlequin type ichthyosis
Harpaxophobia
Hartnup disease
Hashimoto's thyroiditis
Hearing impairment
Hearing loss
Heart block
Heavy metal poisoning
Heliophobia
HELLP syndrome
Helminthiasis
Hemangioendothelioma
Hemangioma
Hemangiopericytoma
Hemifacial microsomia
Hemiplegia
Hemoglobinopathy
Hemoglobinuria
Hemolytic-uremic syndrome
Hemophilia A
Hemophobia
Hemorrhagic fever
Hemothorax
Hepatic encephalopathy
Hepatitis
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatoblastoma
Hepatocellular carcinoma
Hepatorenal syndrome
Hereditary amyloidosis
Hereditary angioedema
Hereditary ataxia
Hereditary ceroid...
Hereditary coproporphyria
Hereditary elliptocytosis
Hereditary fructose...
Hereditary hemochromatosis
Hereditary hemorrhagic...
Hereditary...
Hereditary spastic...
Hereditary spherocytosis
Hermansky-Pudlak syndrome
Hermaphroditism
Herpangina
Herpes zoster
Herpes zoster oticus
Herpetophobia
Heterophobia
Hiccups
Hidradenitis suppurativa
HIDS
Hip dysplasia
Hirschsprung's disease
Histoplasmosis
Hodgkin lymphoma
Hodgkin's disease
Hodophobia
Holocarboxylase...
Holoprosencephaly
Homocystinuria
Horner's syndrome
Horseshoe kidney
Howell-Evans syndrome
Human parvovirus B19...
Hunter syndrome
Huntington's disease
Hurler syndrome
Hutchinson Gilford...
Hutchinson-Gilford syndrome
Hydatidiform mole
Hydatidosis
Hydranencephaly
Hydrocephalus
Hydronephrosis
Hydrophobia
Hydrops fetalis
Hymenolepiasis
Hyperaldosteronism
Hyperammonemia
Hyperandrogenism
Hyperbilirubinemia
Hypercalcemia
Hypercholesterolemia
Hyperchylomicronemia
Hypereosinophilic syndrome
Hyperhidrosis
Hyperimmunoglobinemia D...
Hyperkalemia
Hyperkalemic periodic...
Hyperlipoproteinemia
Hyperlipoproteinemia type I
Hyperlipoproteinemia type II
Hyperlipoproteinemia type...
Hyperlipoproteinemia type IV
Hyperlipoproteinemia type V
Hyperlysinemia
Hyperparathyroidism
Hyperprolactinemia
Hyperreflexia
Hypertension
Hypertensive retinopathy
Hyperthermia
Hyperthyroidism
Hypertrophic cardiomyopathy
Hypoaldosteronism
Hypocalcemia
Hypochondrogenesis
Hypochondroplasia
Hypoglycemia
Hypogonadism
Hypokalemia
Hypokalemic periodic...
Hypoparathyroidism
Hypophosphatasia
Hypopituitarism
Hypoplastic left heart...
Hypoprothrombinemia
Hypothalamic dysfunction
Hypothermia
Hypothyroidism
Hypoxia
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Medicines

Etiology

  • Primary hyperparathyroidism is usually the result of a benign parathyroid tumor (adenoma) that loses its sensitivity to circulating calcium levels. Usually, only one of the four parathyroid glands is affected.
  • In chronic renal failure secondary hyperparathyroidism can result. Its result on bone metabolism is renal osteodystrophy.

Signs and symptoms

The rhyme "moans, groans, stones, and bones, with psychic overtones" has been used to describe the classic symptoms of hyperparathyroidism: abdominal pain, lethargy or dysphoria, kidney stones, osteoporosis (and resultant fractures), and depression.

Other symptoms include: headaches, sleep disorders, memory problems, gastroesophageal reflux, decreased sex drive, thinning hair, hypertension, and heart palpitations.

In short-lived hyperparathyroidism, hypercalcemia might be the only sign, sometimes producing such symptoms as nausea, vomiting, lethargy, depression, muscular weakness and an altered mental state.

Diagnosis

Diagnostic workup for hypercalcemia often includes testing the PTH levels. Ultrasound of the neck area may reveal enlarged glands. Occasionally, scintigraphy with MIBI is necessary to identify adenomas or hyperplastic parathyroids.

Treatment

The only definitive treatment is surgery. Surgical techniques for hyperparathyroidism now are much less invasive and much more effective than in the past. The procedure is called parathyroidectomy. Usually, the surgery will only involve one of the glands, and so a successful surgery will allow the parathyroids to go back to correctly regulating blood calcium levels.

If hypercalcemia is severe, bisphosphonates may be required to maintain bone. Hyperparathyroidism can be treated medically with cinacalcet (a calcium receptor blocker), which is very expensive.

Read more at Wikipedia.org


[List your site here Free!]


Vitamin D insufficiency as a cause of hyperparathyroidism
From American Family Physician, 1/1/05 by Robert C. Oh

TO THE EDITOR: I read with interest the article on hyperparathyroidism in the January 15, 2004, issue of American Family Physician. (1) However, I noticed that hypovitaminosis D (vitamin D insufficiency) was not mentioned in much detail. Although the concept is not new, I would like to point out that this is an under-recognized but increasingly important cause of secondary hyperparathyroidism, which is a condition that may be of significant relevance to family physicians and their patients.

Hypovitaminosis D increases the risk for fractures, bone pain, and the development of either osteomalacia or rickets. Risk factors include lack of sun exposure, inadequate dietary intake, and advanced age (caused by the skin's decreasing ability to synthesize vitamin D). Studies have shown a prevalence of 30 to 50 percent in elderly persons in community settings. (2) Even in the nonelderly, 57 percent of hospitalized patients in Boston had evidence of vitamin D deficiency. (3)

In a recent study conducted in Minnesota, (4) an alarming 93 percent of children and adults with chronic musculoskeletal pain were vitamin D deficient. Surprisingly, the most severely deficient persons were patients aged 10 to 29 years. Diagnosis of vitamin D deficiency is based on a low 25-hydroxyvitamin D3 level. Traditionally, levels less than 12 ng per mL (31 nmol per L) have been considered the lower limits of normal. However, levels of 25-hydroxyvitamin D3 less than 20 ng per mL (52 nmol per L)) triggers a compensatory increase in parathyroid hormone (PTH) and, hence, accelerates bone resorption. This suggests that vitamin D deficiency occurs before the lower limits of traditional population-based values for PTH. (5) Unlike primary hyperparathyroidism, PTH levels are usually less than 100 pg per mL (850 pmol per L) in secondary hyperparathyroidism caused by hypovitaminosis D. Overall, optimal bone health may occur with 25-hydroxyvitamin D3 levels greater than 30 to 50 ng per mL (78 to 130 nmol per L).

Treatment for hypovitaminosis D is supplementation with vitamin D and calcium. Two methods are suggested here. Replacement with 50,000 IU vitamin D once a week for eight weeks given with supplemental calcium will restore tissue stores quickly and may be more useful for patients with levels of 25-hydroxyvitamin D3 less than 20 ng per mL. Daily supplementation with 800 IU of vitamin D and calcium for those patients with levels between 20 and 30 ng per mL also is safe and effective. (6) Repeating levels of 25-hydroxyvitamin D3 and PTH after two to three months ensures adequate treatment and compliance.

Family physicians should consider screening for hypovitaminosis D in all patients who may be at risk, regardless of age. Elderly persons, and even children with dietary lack and limited sun exposure, are vulnerable to vitamin D deficiency. The American Academy of Pediatrics recently recognized the continuing reports of rickets and recommends 200 to 400 IU of daily vitamin D supplementation to all children. Older adults also may warrant vitamin D and calcium supplementation without screening. Understanding the risk factors, and recognizing subnormal 25-hydroxyvitamin D3 levels and mild hyperparathyroidism will allow the family physician to detect hypovitaminosis D. Early diagnosis and treatment is critical to prevent the more serious complications of rickets in children and osteomalacia in adults.

ROBERT C. OH, M.D.

Madigan Army Medical Center Department of Family Medicine Tacoma, WA

98431-1100

REFERENCES

(1.) Taniegra ED. Hyperparathyroidism. Am Fam Physician 2004;69:333-9.

(2.) Allain TJ, Dhesi J. Hypovitaminosis D in older adults. Gerontology 2003;49:273-8.

(3.) Thomas MK, Lloyd-Jones DM, Thadhani RI, Shaw AC, Deraska DJ, Kitch BT, et al. Hypovitaminosis D in medical inpatients. N Engl J Med 1998;338:777-83.

(4.) Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc 2003;78:1463-70.

(5.) Malabanan A, Veronikis IE, Holick MF. Redefining vitamin D insufficiency. Lancet 1998;351:805-6.

(6.) Lips P. Vitamin D deficiency and secondary hyperparathyroidism in the elderly: consequences for bone loss and fractures and therapeutic implications. Endocr Rev 2001;22:477-501.

The opinions and assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the U.S. Army medical department or the U.S. Army at large.

COPYRIGHT 2005 American Academy of Family Physicians
COPYRIGHT 2005 Gale Group

Return to Hyperparathyroidism
Home Contact Resources Exchange Links ebay