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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↗
PubMed1974

Mast cells in parathyroid glands of hyperparathyroidism.

Parathyroid glands from cases of hyperparathyroidism have been examined with particular attention to mast cells. In ;normal' glands accompanying an adenoma they were common, although there was a wide range in their frequency, whereas in pathological tissue, both adenoma and hyperplasia, mast cells were scarce. This difference between glands was examined with respect to alterations in gland size, to variations in the amount of interstitial tissue, to degrees of overactivity, and to anatomical development of the glands. No conclusions can be drawn with regard to the significance of mast cells in parathyroid tissue.

Adenoma↗
PubMed2000

PTHrP enhances the secretory response of PTH to a hypocalcemic stimulus in rat parathyroid glands.

BACKGROUND: The secretion of parathyroid hormone (PTH) from the parathyroid glands might be regulated by autocrine/paracrine factors, and a feedback regulatory mechanism of PTH on the secretion of PTH has been suggested. Because of the existence of a common receptor between PTH and PTH-related peptide (PTHrP), the aim of the present study was to examine the possible effects of PTHrP 1-40 and 1-86 on PTH secretion in rats. METHODS: In vivo, the effect of PTHrP on Ca++-regulated PTH secretion was examined by the induction of hypocalcemia and hypercalcemia by an infusion of EGTA and Ca++, with and without PTHrP. The eventual effects of PTHrP on the peripheral metabolism of PTH were examined by infusion of human PTH (hPTH) with and without PTHrP. hPTH was measured by an intact hPTH assay not cross reacting with rat PTH or PTHrP. To examine whether near physiological levels of circulating PTH have an autoregulatory effect in vivo on PTH secretion from the parathyroid gland, an acute reduction of the circulating PTH was induced by an acute unilateral parathyroidectomy (UPTX). PTH secretion from the remaining parathyroid gland was followed in response to EGTA-induced hypocalcemia. In vitro investigations on the effect of PTHrP 1-40 on PTH secretion from whole rat parathyroid glands incubated in media containing a calcium concentration of 0.6 or 1.35 mmol/L were performed to confirm whether the effect of PTHrP was directly on the gland. The rat PTH assay was examined for cross reaction with PTHrP. RESULTS: In vivo, the same rate of decrease of plasma Ca++ was induced in the experimental groups. The maximal response of PTH to hypocalcemia (218 +/- 16 pg/mL, N = 6) was significantly enhanced by PTHrP 1-40 (525 +/- 79 pg/mL, N = 6) and by PTHrP 1-86 (465 +/- 29 pg/mL, N = 6, P < 0.001). No effect of PTHrP on PTH secretion was found during normocalcemia or hypercalcemia. UPTX resulted in a 50% reduction of PTH secretion, and no compensatory increase of PTH was observed. PTHrP had no effect on the metabolism of PTH. In vitro, low-Ca++-induced PTH secretion was significantly augmented by 300% (P < 0.01) when the medium contained PTHrP 1-40. PTHrP did not cross react with the PTH assay. CONCLUSIONS: PTHrP significantly enhanced the low-Ca++-stimulated PTH secretion in vivo and in vitro. An autocrine/paracrine role of PTHrP in the parathyroid glands is suggested. An autoregulatory effect of circulating PTH on the PTH secretion from parathyroid glands seems unlikely. The "maximal secretory capacity" of the parathyroid glands induced by hypocalcemia in vivo and in vitro is not the maximum, as PTH secretion can be increased even further, by several-fold.

Animals↗
PubMed2000

Hyperparathyroidism after thyroid surgery and autotransplantation of histologically normal parathyroid glands.

BACKGROUND: Parathyroid autotransplantation is a well-established method to prevent hypoparathyroidism during parathyroid and thyroid operations. The reported success rate of parathyroid autotransplantation ranges from 75% to 100%. Recurrent hyperparathyroidism may develop after parathyroid autotransplantation, especially after the transplantation of hyperplastic or adenomatous parathyroid tissue. Hyperparathyroidism recurs most frequently after subtotal parathyroidectomy or total parathyroidectomy and autotransplantation, in patients with renal failure and secondary hyperparathyroidism, and in patients with familial primary hyperparathyroidism or MEN I or MEN II syndrome. We report three patients who experienced primary hyperparathyroidism after autotransplantation of normal parathyroid tissue during thyroid operations (two patients) or after a long period of hypoparathyroidism. STUDY DESIGN: We reviewed our records from 1983 to May 1998 and identified three patients in whom hyperparathyroidism developed after thyroid operations. RESULTS: One patient had a thyroidectomy with left modified radical neck dissection for papillary thyroid cancer, followed by radioiodine ablative therapy. Two patients had thyroid operations for benign thyroid disease. One of these patients had a history of radiation exposure for acne, and in the other one secondary hyperparathyroidism arose 6 years after a thyroidectomy for hyperthyroidism. CONCLUSIONS: Our study documents that hyperparathyroidism may develop after autotransplantation of histologically normal parathyroid tissue and after a period of hypoparathyroidism after thyroid operations. For this reason, it is important to mark the site of the parathyroid transplantation.

Adult↗
PubMed1991

Effects of melatonin on the ultrastructure of the golden hamster parathyroid gland.

Ultrastructural changes of the parathyroid glands of melatonin-treated golden hamsters were studied. Many chief cells in the parathyroid glands after 1 hour of administration of melatonin contained poorly-developed Golgi complexes associated with a few prosecretory granules and numerous lipid droplets as compared with those of the control animals. The morphology of the parathyroid glands after 5 hours of administration resembled that of the control animals. Many chief cells in the parathyroid glands after 24 hours of administration had well-developed Golgi complexes and cisternae of the granular endoplasmic reticulum, numerous prosecretory granules, a few lipid droplets and many secretory granules in the peripheral cytoplasm as compared with those of the control animals. The ultrastructure of the parathyroid glands after 48 hours of administration was almost similar to that of the control animals. It is considered that melatonin affects the secretory activity of the parathyroid gland.

Animals↗
PubMed1995

Accessory carotid body within the parathyroid gland III of the chicken.

In the chicken, the cranial and caudal parathyroid glands (parathyroid gland III and IV), which are connected to each other, are located adjacent to the carotid body. In the present study, we found that a mass of glomus cells surrounded by a thick layer of connective tissue was frequently distributed within the parathyroid gland III. The glomus cells in the parathyroid III, as well as those of the carotid body, expressed intense immunoreactivity for serotonin, chromogranin A, and tyrosine hydroxylase but no immunoreactivity for neuropeptide Y. The cells possessed long cytoplasmic processes containing dense-cored vesicles of 70-220 nm in diameter, and were in close association with sustentacular cells. In and around the glomus cell clusters of the parathyroid III, dense networks of varicose fibers showed immunostaining with the monoclonal antibody TuJ1 to a neuron-specific class III beta-tubulin isotype, c beta 4. Furthermore, the distribution was also detected of numerous galanin-, vasoactive intestinal peptide (VIP)-, substance P-, and calcitonin gene-related peptide (CGRP)-immunoreactive fibers.

Animals↗
PubMed2004

The origin of the parathyroid gland.

It has long been held that the parathyroid glands and parathyroid hormone evolved with the emergence of the tetrapods, reflecting a need for new controls on calcium homeostasis in terrestrial, rather than aquatic, environments. Developmentally, the parathyroid gland is derived from the pharyngeal pouch endoderm, and studies in mice have shown that its formation is under the control of a key regulatory gene, Gcm-2. We have used a phylogenetic analysis of Gcm-2 to probe the evolutionary origins of the parathyroid gland. We show that in chicks, as in mice, Gcm-2 is expressed in the pharyngeal pouches and the forming parathyroid gland. We find that Gcm-2 is present not only in tetrapods but also in teleosts and chondrichthyans, and that in these species, Gcm-2 is expressed within the pharyngeal pouches and internal gill buds that derive from them in zebrafish (Danio rerio), a teleost, and dogfish (Scyliorhinus canicula), a chondrichthyan. We further demonstrate that Gcm-2 is required for the formation of the internal gill buds in zebrafish. We also have identified parathyroid hormone 1/2-encoding genes in fish and show that these genes are expressed by the gills. We further show that the gills express the calcium-sensing receptor, which is used in tetrapods to monitor serum calcium levels. These results indicate that the tetrapod parathyroid gland and the gills of fish are evolutionarily related structures, and that the parathyroid likely came into being as a result of the transformation of the gills during tetrapod evolution.

Amino Acid Sequence↗
PubMed1991

Response of the parathyroid gland to infusion of human parathyroid hormone-(1-34) [PTH-(1-34)]: demonstration of suppression of endogenous secretion using immunoradiometric intact PTH-(1-84) assay.

Alterations in the sensitivity of the parathyroid gland to both stimulative and suppressive stimuli may be partially responsible for skeletal changes that occur with age, estrogen deficiency, osteoporosis, and estrogen treatment of osteoporosis. We sought to define the changes in intact PTH-(1-84) secretion in normal premenopausal and postmenopausal, osteoporotic and estrogen-treated osteoporotic women during the infusion of human (h) PTH-(1-34). hPTH-(1-34) was infused at 0.55 U/kg.h for 24 h, with serum sampling every 4 h. Serum was analyzed for calcium (ionized and total), hPTH-(1-34), and PTH-(1-84). Basal chemistries were no different among groups, except for serum phosphorus, which was highest in osteoporotic women (1.31 vs. 1.07 mmol/L in premenopausal; P less than 0.02), and hPTH-(1-34), which was slightly higher in normal postmenopausal women (19.31 vs. 13.24 ng/L in estrogen treated; P less than 0.02). No differences in PTH-(1-84) were found among groups. hPTH-(1-34) rose similarly in all patient groups, while the calcemic response was somewhat more sluggish in estrogen-treated women, although statistically significant differences were not found. PTH-(1-84) declined rapidly in all patient groups, although estrogen-treated women had a smaller maximal decrease in PTH-(1-84), and the slope of the decremental change in PTH-(1-84) was lower in estrogen-treated women than in osteoporotic or normal postmenopausal women. Untreated osteoporotic women had less suppression of PTH-(1-84) than normal postmenopausal women at every calcium level. Estrogen treatment decreases the calcemic effects of infused hPTH-(1-34) and at the same time reduces calcium-induced suppression of parathyroid secretion. It is possible that such changes in the set-point of the gland contribute to the alterations in bone turnover that result in osteoporosis and the mechanisms by which estrogen prevents bone loss.

Calcium↗
PubMed1993

[The role of ultrasonography in the diagnosis of enlarged parathyroid glands].

The ultrasonographic diagnosis of parathyroid glands was introduced by the Japanese in 1975. Only after more perfect machines have been introduced, first of all by advancement of "real-time" technique, this method started being used as a routine. The paper shows results of ultrasonographic investigation in 200 patients separated into two groups. In the first group 100 patients were examined with a clinical suspect of primary hyperparathyroidism from which in 30 the existence of parathyroid gland adenoma was diagnosed. Scintigraphy of parathyroid glands was performed in the smaller group of patients; the comparison of these two methods was done, and in 77.7% cases coincidence was found. In the group of 10 operated patients comparison of the two mentioned methods was carried out, with surgical or pathohistologic findings and the coincidence was complete. In the second group 100 patients were examined belonging to the chronical program of hemodialysis, from which in 24 cases existence of swollen parathyroid glands was found. Comparison of ultrasonographic and scintigraphic findings was also done and the coincidence was 68.75%. At the end, the importance of ultrasonography in the first diagnostic stage of swollen parathyroid glands was pointed out.

Adenoma↗
PubMed2004

Disorders of the parathyroid glands.

The three calcitropic hormones, parathyroid hormone (PTH), 1,25-dihydroxycholecalciferol and calcitonin are together responsible for calcium homeostasis in the mammal. Feline PTH is an 84 amino acid, single chain polypeptide with a molecular weight of 9449, which is secreted by the parathyroid glands. The principle secretagogue for PTH is a low plasma ionised calcium concentration, although both 1,25-dihydroxycholecalciferol and phosphate have significant roles in regulating PTH secretion. The ability to accurately measure circulating PTH in the cat has simplified the evaluation of disorders of calcium metabolism in this species. In primary parathyroid disorders the lesion is located within the parathyroid gland, with parathyroid secretion being inappropriate to the prevailing mineral balance. By contrast, in secondary conditions a pathological state out with the parathyroid gland alters mineral homeostasis and the parathyroid gland responds in an appropriate manner. The measurement of circulating PTH may then be used to determine if PTH secretion is appropriate to the prevailing calcium concentrations to differentiate primary from secondary disorders. Although primary hyper and hypoparathyroidism are generally considered rare endocrine conditions of the cat, the ability to measure PTH has led to their increasing recognition.

Animals↗
PubMed1990

Effects of pinealectomy on the ultrastructure of the golden hamster parathyroid gland.

Ultrastructural changes of the parathyroid glands of pinealectomized golden hamsters were investigated. The main changes in the parathyroid glands 1 hour and 1 day after pinealectomy compared with the control and sham-operated groups were an increase of the Golgi complexes, cisternae of the granular endoplasmic reticulum and large vacuolar bodies. In addition, many chief cells contained numerous prosecretory granules in the Golgi areas and many secretory granules in the peripheral cytoplasm. The morphology of the parathyroid glands 7 and 30 days after pinealectomy resembled that of the control parathyroid glands. These results suggest that pinealectomy affects the secretory activity of the parathyroid gland.

Animals↗
PubMed1994

Thoracoscopic excision of enlarged mediastinal parathyroid glands.

BACKGROUND: Most abnormal parathyroid glands can be removed through the neck, but those deep in the chest have required sternotomy or thoracotomy. To avoid the morbidity of these open procedures, ectopic parathyroid glands deep in the chest were removed with video-assisted thoracoscopy. METHODS: Two patients with persistent primary and two with persistent secondary hyperparathyroidism had technetium-thallium scintigraphy and computed tomography of the chest to localize their ectopic glands. Video-assisted thoracoscopy was used for operative removal of these glands in each patient. RESULTS: Parathyroid scans identified a mediastinal gland that was confirmed and localized precisely by the computed tomography scan. An enlarged ectopic gland weighing 1 to 2 gm was removed from each patient with normalization of serum calcium level. Glands were found by the main pulmonary artery, aortopulmonary window, ascending aorta, and aortic arch. One patient had recurrent disease 9 months later. CONCLUSIONS: Removal of parathyroid glands deep in the chest with video-assisted thoracoscopy is a safe and successful alternative to median sternotomy.

Adenoma↗
PubMed1988

Effects of isoproterenol on the fine structure of the hamster parathyroid gland.

Ultrastructural changes of the parathyroid glands of isoproterenol-treated golden hamsters were investigated. Many chief cells in the parathyroid glands after 5 and 10 minutes of administration of isoproterenol contain well-developed Golgi complexes and granular endoplasmic reticulum, numerous prosecretory granules, and many secretory granules in the peripheral cytoplasm as compared with the control animals. Many chief cells in the parathyroid glands after 1, 3, 6 and 12 hours of administration have poorly-developed Golgi complexes, granular endoplasmic reticulum, many secretory granules and numerous lipid droplets as compared with the control animals. The morphology of the parathyroid gland after 30 minutes and 24 hours of administration resembles that of the control animals. It is considered that isoproterenol affects the secretory activity of the parathyroid gland.

Animals↗
PubMed1996

Experimental autotransplantation of the parathyroid gland.

The lateral parathyroid gland of the rabbit was resected and autotransplanted under an ear skin flap. A skin flap at the opposite side was used as control. The success of autotransplantation was established by microangiography of the transplant and by measuring plasma concentrations of parathyroid hormone (PTH), calcium and phosphorus. After 4 months the animals were killed and the transplant was studied histologically and by electron microscopy. Fourteen animals were included in the study. There was an increase in PTH derived from the transplanted gland after 4-6 postoperative days. All animals developed hypocalcaemia during the 3 days after transplantation. There were no significant changes in serum phosphorus. Transplantation did not alter the morphology of the distribution of the cells in the transplanted gland, which functioned normally after the fourth postoperative day.

Animals↗
PubMed1995

Effect of parathyroid hormone and calcitonin on cholinergic markers in rat parathyroid gland.

The effect of parathyroid hormone (PTH) and calcitonin on 3H-choline uptake and on 3H-acetylcholine synthesis by rat parathyroid glands were examined. Incubation of tissue for 120 min with PTH or calcitonin resulted in an inverted bell-shaped, dose-dependent inhibition of 3H-choline uptake, with a maximal effect at 10(-9) M concentration. The effect of PTH on parathyroid choline uptake was blunted by preincubation with the PTH antagonist NLe(8-18)-PTH (3-34) amide. PTH brought about a dose-dependent inhibition of 3H-choline conversion to 3H-acetylcholine, with significant effects at 10(-8) M concentration or higher. This inhibitory effect of PTH on 3H-acetylcholine synthesis was blocked by co-incubation with the PTH antagonist NLe(8-18)-PTH (3-34) amide. Only at a 10(-7) M concentration calcitonin was effective to impair the in vitro conversion of radioactive choline into 3H-acetylcholine by parathyroid fragments. The results indicate that, in vitro, PTH, and to a less extent, calcitonin, inhibit cholinergic activity in rat parathyroid glands.

Acetylcholine↗