The weight of the parathyroid glands

Gilmour, J. R.; Martin, William J.

doi:10.1002/path.1700440218

Cited by 122 publications

(54 citation statements)

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“…We have previously (Ellis and Peart, 1972) It is well established that there is secondary parathyroid hyperplasia in chronic renal failure (Pappenheimer and Wilens, 1935;Gilmour and Martin, 1937;Castleman and Mallory, 1937;Herbert, Miller, and Richardson, 1941;Gilmour, 1947;Roth and Marshall, 1969 (Ellis and Knight, 1969). Like others (Gilmour, 1947;Christie, 1967) we have observed increased numbers of oxyphil cells in the parathyroid glands of some patients with chronic renal failure particularly those with Gilmour type IV nodular hyperplasia where aggregates of these cells form nodules easily visible to the naked eye.…”

Section: Discussionmentioning

confidence: 99%

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

1973

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SYNOPSISThe histopathology of bone is described in 60 patients with chronic renal failure due to a variety of renal diseases. Changes of azotaemic renal osteodystrophy included osteitis fibrosa, osteomalacia, and osteosclerosis. Quantitative histology using a point-counting technique revealed a significant increase in total bone, mineralized bone, and osteoid in comparison with a control group of 68 individuals. Osteitis fibrosa due to secondary hyperparathyroidism occurred in 93 %, osteomalacia in 40%, and osteosclerosis in 30% of patients. Woven bone formation was a characteristic feature and was related to the severity of osteitis fibrosa. There were significant correlations between the weights of parathyroid glands and the number of osteoclasts, amounts of woven bone, and marrow fibrosis in the ilium. Hyperparathyroidism caused degradation of mineralized bone but the loss was balanced or exceeded by the aggradation of woven mineralized bone. Woven bone formation together with excess osteoid gave rise to osteosclerosis. The histological findings indicate that hyperparathyroidism and osteitis fibrosa usually occur early in chronic renal failure and that osteomalacia develops subsequently.Chronic renal failure may be accompanied by bone disease (Stanbury, 1957(Stanbury, , 1972 and the changes, which include osteitis fibrosa due to secondary hyperparathyroidism, osteomalacia and osteosclerosis, may conveniently be termed renal osteodystrophy (Liu and Chu, 1943). Although it is recognized that the clinical effects of such changes may be severe in childhood (Claireaux, 1953;Haust, Landing, Holmstrand, Currarino, and Smith, 1964) 20 December 1972. in this study it appeared that there were histological differences between the bone changes in dialysed and non-dialysed patients. The latter tended to show osteitis fibrosa, osteomalacia, and a normal or raised total bone mass with normal or elevated amounts of mineralized bone. In contrast, in the bones of dialysed patients there was a loss of mineralized lamellar bone and total bone after about one or two years on dialysis. In others, following more prolonged dialysis, the total bone mass was elevated due to excess osteoid formation whilst the amount of mineralized bone remained low. The bones of dialysed patients in general also showed less severe changes of osteitis fibrosa (Ellis and Peart, 1971).To determine whether or not these differences were real it became necessary to quantitate the amounts of mineralized bone and osteoid present and the severity of the osteitis fibrosa. Critical quantitative histological studies of the mineralized and non-mineralized bone in renal failure were lacking until Garner and Ball (1966) reported their findings in 42 controls and in 18 selected cases of azotaemic renal osteodystrophy using a pointcounting technique to study undecalcified sections of iliac crest. As a basis for our quantitative observations in renal failure we have similarly studied the 83

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Section: Discussionmentioning

confidence: 99%

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

1973

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“…These findings are consistent with parathyroid gland enlargement (25) and suggest that the rise in circulating PTH associated with aging may in part be a consequence of gland hypertrophy. Despite this inference, however, data from autopsy studies indicate that parathyroid gland volume in human subjects remains nearly constant between the ages of 30 and 80 yr (1,12). To test the hypothesis that parathyroid gland volume increases with postmaturational aging in the rat, and to determine whether the putative increase in gland volume is associated with hypocalcemia or linked to renal insufficiency, we measured the volume of the parathyroid glands, the glomerular filtration rate Address for reprint requests and other correspondence: B. Halloran, Veterans Affairs Med.…”

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confidence: 91%

Parathyroid gland volume increases with postmaturational aging in the rat

Halloran¹,

Udén

Duh

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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To examine the pathophysiology of the age-related rise in the plasma concentration of parathyroid hormone (PTH), we studied the relationships among plasma immunoreactive PTH (iPTH), parathyroid gland volume, parathyroid cell proliferation rate, renal function, and blood Ca 2ϩ in male Fischer 344 rats aged 6-28 mo. Plasma iPTH increased 2.5-fold between 6 and 28 mo and correlated with parathyroid gland volume (r ϭ 0.87). Gland volume began to increase as early as 6-12 mo of age and by 28 mo was threefold greater than at 6 mo. Gland expansion was a consequence of hyperplasia stimulated in part by an increase in cell proliferative activity late in life. Blood Ca 2ϩ and plasma inorganic phosphorus did not change significantly with age. Glomerular filtration rate decreased with age but only after the age of 24 mo. Unlike what has been observed in the human, these data suggest that the age-related increase in plasma iPTH in the rat is linked to parathyroid gland hyperplasia and that early gland growth does not appear to be associated with hypocalcemia or renal insufficiency, but rather to developmentally related metabolic changes. Later in life (Ͼ24 mo), the increase in parathyroid cell proliferation rate, further hyperplastic expansion of the gland, and increase in iPTH secretion appear to be associated with renal insufficiency. parathyroid hormone; renal function; glomerular filtration rate THE SERUM CONCENTRATIONS of immunoreactive (3,9,11,16,23,24,28,31) and bioactive (8) parathyroid hormone (PTH) increase with postmaturational aging in humans and rats. Bone turnover also increases with aging and correlates directly with the rise in circulating PTH, suggesting that the mild hyperparathyroidism of aging may contribute to bone loss in the elderly (6,19). In the Fischer 344 (F344) rat, the serum concentration of PTH begins to increase as early as 12 mo of age, and by 24 mo of age (the mean life span for the F344 rat) is as much as 5 times higher than in 6-mo-old animals (3, 16, 28).In the rat, the age-related increase in serum PTH reflects increased secretion. Fox and Mathew (10) measured the metabolic clearance rate of PTH in 6-and 25-mo-old animals and showed that clearance of PTH does not change with age.The age-related rise in PTH secretion has been interpreted to reflect the decrease in renal function associated with aging (20), decreased intestinal calcium absorption (21), decreased renal conservation of calcium (19), and/or senescent changes intrinsic to the parathyroid secretory cell itself (4,24,27). Whatever the underlying pathology, a consistent feature of the change in PTH secretory dynamics with aging has been an increase in the PTH minimum and maximum secretory rates (9,18,24). Fox (9) reports that minimum and maximum PTH secretion rates are higher in older than in younger animals, and Ledger et al. (18) demonstrated that minimum and maximum serum concentrations of PTH are higher in elderly than in young women. We have shown that the minimum suppressible level of PTH during calcium infusion is two-to th...

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“…U toku razvoja nodusa u štitastoj žlezdi mogu biti spljoštene, me utim, svoj normalan oblik ponovo dobijaju odvajanjem od površine nodusa. Prose na veli ina kre e se oko 5x3x1 mm prema Gilmouru (22) i Wangu (23), dok se prema istim autorima težina kre e u opsegu 10-78 mg, sa prose nom od 40 mg. Paratiroidne žlezde su inkapsulirane, oštrih ivica, glatke i sjajne površine. Naj eš e ih nalazimo potpuno ili delimi no uronjene u masno tkivo tako da zajedno sa njim formiraju "masnu loptu" zbog njihovog posebnog a niteta prema masnom tkivu, od koga se lako mogu odvojiti.…”

Section: Paratiroidne žLezdeunclassified

Surgical anatomy of thyroid and parathyroid glands and basic principles of operative technique

Paunović¹,

Živaljević²,

Gorić³

et al. 2012

Med gl Ins stit Zlatibor

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Sažetak: Štitasta žlezda je najve i endokrini organ i ima najve u u estalost oboljenja u odnosu na druge endokrine organe. Uspešno operativno le enje kako benignih tako i malignih oboljenja štitaste žlezde povezano je s adekvatnom preoperativnom pripremom, preciznom operativnom tehnikom i poznavanjem hirurške anatomije. Komplikacije koje se mogu javiti zbog nepoznavanja hirurške anatomije štitaste i paraštitastih žlezdi trajno ugrožavaju zdravlje operisanog i ine ga doživotnim invalidom. Potrebno je zato da hirurg koji operiše štitastu žlezdu i/ili paraštitaste žlezde poseduje neophodno znanje o hirurškoj anatomiji ovih endokrinih organa bez obzira na sada široku dostupnost aparata koji omogu avaju bolju vizuelizaciju operativnog polja, koagulaciju krvnih sudova, kao i intraoperativni neuromonitoring.Štitasta žlezda je najve i endokrini organ u odraslog oveka, težina u zdrave osobe iznosi oko 17gr (1), pokriva anterolateralni deo gornjih trahealnih prstenova (od II do IV) i larinksa. Predstavlja bilobarni organ, iji su desni i levi lobus me usobno spojeni trakom istmi nog žlezdanog tkiva. Svaki lobus nalazi se u prostoru izme u traheje i ezofagusa medijalno, karotidne lože pozadi, i sternokleidomastoidnog, sternohioidnog i sternotiroidnog miši a napred i lateralno.Ukoliko se sternotiroidni i sternohioidni miši i moraju prese i i transverzalno tokom tiroidektomije (radi bezbednog pristupa krvnim sudovima gornjeg pola), to treba u initi visoko u nivou krikoidne hrskavice, što obezbe uje prezervaciju njihovog motornog nerva (ansa nervi hypoglossi). Klini ki, nema funkcionalnih posledica zbog presecanja ovih miši a (1). * Centar za endokrinu hirurgiju, Klinika za endokrinologiju, dijabetes i bolesti metabolizma,

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The weight of the parathyroid glands

Cited by 122 publications

References 0 publications

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

Parathyroid gland volume increases with postmaturational aging in the rat

Surgical anatomy of thyroid and parathyroid glands and basic principles of operative technique

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