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PubMed1995

A history of the parathyroid glands.

Diseases of the parathyroid glands have always existed, affecting occasional individuals in every period and culture of the past. The significant changes in body build associated with their dysfunction must have attracted in the popular mind bewildering connotations that can be gleaned from their mythology. Although their associated clinical features were described in the medical literature, the presence of the parathyroid glands and their function went long unrecognized. In the relatively slow evolution of endocrinology, compared with that of other medical disciplines, the parathyroid glands and their diseases were one of the last to be defined. It was only in the latter part of the nineteenth century that the glands were identified in humans by Ivar Sandström (1852-1889). Their subsequent experimental extirpation by Eugene Gley (1857-1930), as well as others, led to the differentiation of the neuromuscular symptoms that theretofore had been attributed to removal of the thyroid glands. That these symptoms were the result of the hypocalcemia that ensues parathyroidectomy was suggested in 1908 by W. G. MacCallum (1874-1944) and Carl Voegtlin (1879-1960). The possibility that parathyroid pathology may be associated with skeletal abnormalities was made in 1914 by Jacob Erdheim (18874-1937), and in the following year documented by Z. Schlagenhaufer from the observation that in patients with osteitis fibrosa cystica, only one parathyroid gland is enlarged. This was to set the stage for parathyroidectomy beginning in 1925, for the alleviation of bone disease of hyperparathyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Synchronous thyroid pathology in patients presenting with primary hyperparathyroidism.

BACKGROUND: Thyroid and parathyroid pathology may coexist; classically, this is described in multiple endocrine neoplasia. Other nonsyndromic scenarios result in pathologies of these endocrine organs coexisting. This can create a challenge in the clinical decision making and management of these patients. It is optimal to deal with both problems in one operative procedure, if surgery is required. METHODS: A retrospective review of cases of synchronous thyroid and parathyroid pathology that were managed surgically over a 3-year period by a single endocrine surgeon at a single university medical center. RESULTS: Seventeen cases of synchronous thyroid and parathyroid disease were discovered. All required surgical management of thyroid and parathyroid conditions. Reasons included removal of thyroid goiter for access to an adenoma, worrisome thyroid lesions coexistent with a parathyroid adenoma, and an intrathyroid parathyroid adenoma. Cases of incidental discovery of a second endocrine condition while the first was evaluated will be reported. CONCLUSIONS: A head and neck endocrine surgeon needs to be aware of the possible coexistence of thyroid and parathyroid pathologies so that, when encountered, they can be safely and efficiently managed in a single procedure.

Adenoma↗
PubMed1975

Hyperparathyroidism: evaluation of four decades of parathyroid surgery.

A review of 98 patients with hyperparathyroidism operated on at the University of Iowa during a 45-year period reveals a very great increase in the frequency of the clinical diagnosis. More patients are being operated on each year and more glands are being removed or biopsied. The proportion of patients in whom light microscopic examination of the parathyroid reveals hyperplasia remains less than 25%. Better methods are needed for identification of hyperplasia. Clinically, a few patients in whom the diagnosis of adenoma is made appear later to have more diffuse parathyroid disease. At present, however, when an adenoma is found, the decision to perform subtotal removal of apparently normal parathyroid tissue is made only reluctantly. The conclusion drawn from this review is that patients with hyperparathyroidism must be studied more intensively and followed for many years, whether or not an operation is performed. Although the diagnosis of hyperparathyroidism is now made readily and operative treatment seems to be more effective, much has yet to be learned about hyperparathyroidism.

Adenoma↗
PubMed2003

Minimally invasive parathyroidectomy for recurrent or persistent hyperparathyroidism using carbon track localization.

BACKGROUND: The present study documents the use of carbon tracking to localize parathyroid adenomas in three patients with persistent or recurrent parathyroid disease. METHODS: Three patients requiring second or third operations for hyperparathyroidism were operated upon after the parathyroid lesion had been localized preoperatively using a suspension of carbon particles in water. The enlarged parathyroid glands were identified by using one or more of the following: computed axial tomography, magnetic resonance imaging, ultrasound or Sestamibi nuclear scan. The lesion was then localized with ultrasound or computed axial tomography and a carbon track was inserted from the lesion to the skin, leaving a small skin tattoo as a marker for the surgeon. Each patient underwent a minimally invasive parathyroid operation. RESULTS: For each of the three patients the recurrent or persistent parathyroid adenoma was successfully identified and removed via a small incision. CONCLUSION: Minimally invasive techniques for primary hyperparathyroidism are changing our approach to parathyroid surgery. However, a minimally invasive technique is less applicable when the disease is persistent or recurrent. Although, when the recurrent or persistent parathyroid adenoma can be identified, localization and carbon tracking have proved useful in allowing the surgeon to remove the lesion via a minimally invasive technique.

Adolescent↗
PubMed1982

Quantitative bone histology in children with chronic renal failure.

Quantitative bone histology (on undecalcified sections following double tetracycline labeling), radiographs, and biochemistry were studied in 47 children, ages 1 to 17 years, with glomerular filtration rates (GFR) below 80 ml/min/1.73m2. The earliest histologic change was an increased osteoid surface accompanied by increased osteoblast and tetracycline surfaces. However, significant bone disease (increased osteoclastic surface, fibrosis, increased osteoid area, increased mineralization lag time, and reduced tetracycline uptake at osteoid surfaces) occurred only at GFR below 30 ml/min/1.73m2. Radiographs and alkaline phosphatase were normal in 25% of children with significant bone disease; parathyroid hormone was increased in 48% of children without bone disease. Thus, these noninvasive investigations were poor predictors of disease presence. GFR was the most sensitive indicator because bone disease occurred only at GFR below 30 ml/min/1.73m2 and was present in all children with GFR below 20 ml/min/1.73m2. It was concluded that bone histology is required for early detection of bone disease and is an essential tool in experimental studies of renal osteodystrophy. However, because the level of GFR will indicate the presence or absence of bone disease in most children, bone biopsy can be avoided generally in clinical practice.

Adolescent↗
PubMed1982

Idiopathic hypoparathyroidism and autoimmunity.

Only a small number of cases of idiopathic hypoparathyroidism linked to the presence of specific antibodies have been described until now. Serum antiparathyroid antibodies have been frequently discovered in the absence of overt parathyroid disease. This suggests either that this kind of antibody is only a marker of genetic predisposition to immunological disease or more probably that subclinical hypoparathyroidism does exist though we lack the sensitive laboratory tests to prove it.

Autoantibodies↗
PubMed1992

Recurrent laryngeal nerve palsy after thyroid and parathyroid surgery. Experience from Lund University.

All cases undergoing neck operation for thyroid or parathyroid disease at Lund University Hospital, Lund, over a 7 year period were examined with indirect laryngoscopy pre- and postoperatively for the determination of the true incidence of operatively induced palsy of the recurrent laryngeal nerves. A total of 1.048 patients were operated; 810 females and 238 males. At 439 operations, bilateral neck exploration was performed; hence, 1.487 nerves were at risk for complications. It was found that immediate postoperative recurrent laryngeal nerve palsy was induced in 72 patients (= 4.8% of nerves at risk). In 44 of these patients, the palsy was temporary and disappeared within 6 months. Therefore, a total of 28 patients developed permanent nerve palsy postoperatively. In 5 of these operations, the nerve was intentionally divided, yielding a true incidence of permanent accidental postoperative nerve palsy of 1.6% of nerves at risk.

Adolescent↗
PubMed1994

Familial benign hypercalcemia--from clinical description to molecular genetics.

Familial benign hypercalcemia (or familial hypocalciuric hypercalcemia), a syndrome of lifelong hypercalcemia inherited as an autosomal dominant trait, is distinct from the multiple endocrine neoplasia syndromes and other forms of inherited parathyroid disease. Familial benign hypercalcemia results from the inappropriate secretion of parathyroid hormone despite hypercalcemia, enhanced renal tubular reabsorption of calcium (independent of parathyroid hormone), and apparent tissue resistance to adverse effects of hypercalcemia. Heterozygosity for the familial hypercalcemia trait is benign, although homozygosity for the trait may lead to severe neonatal primary hyperparathyroidism. Genetic linkage studies show that most persons affected with familial hypercalcemia have a mutation on the long arm of chromosome 3 (3cen-q21), although one phenotypically indistinguishable family appears to have a mutation on the short arm of chromosome 19 (19p), and another family has neither 3q nor 19p mutations. One group has recently shown mutations in a putative parathyroid cell-surface calcium receptor that are plausible causes for the chromosome 3q variant of the familial hypercalcemia syndrome. Perhaps the other genes for this syndrome encode proteins representing hitherto-unknown regulators of systemic calcium metabolism independent of parathyroid cell calcium sensing or proteins involved in signal transduction from the calcium receptor.

Genetic Linkage↗