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M J Favus

Publications and source records attributed to M J Favus.

At least 37 records · Page 2Linked to original sources
PubMed1993

Response of genetic hypercalciuric rats to a low calcium diet.

A fundamental mechanism for hypercalciuria in genetic hypercalciuric rats appears due to a primary increase in intestinal calcium absorption. However previous studies could not exclude additional mechanisms to account for the hypercalciuria. To determine if enhanced bone mineral dissolution either as a primary abnormality or secondary to a defect in renal tubule calcium reabsorption is responsible for a component of the augmented calcium excretion we studied rats continually inbred for hypercalciuria. Nineteenth generation adult female idiopathic hypercalciuric (IH) and non-inbred control (Ctl) rats were fed 13 g/day of a normal calcium diet (0.6% calcium, NCD) for 10 days. Urine calcium excretion over the last seven days was greater in IH (34 +/- 2 mg/7 day) than in Ctl (2.9 +/- 0.3, P < 0.01) rats. Some rats in each group were continued on the same diet while others were fed a low calcium diet (0.02% calcium, LCD) for an additional 10 days; balance measurements were made over the final seven days. With LCD, urine calcium excretion was approximately 8-fold higher in IH compared to Ctl (13 +/- 2 mg/7 day vs. 1.6 +/- 0.1, IH vs. Ctl, respectively, P < 0.01). In IH rats percent calcium absorption was greater (59 +/- 3% vs. 45 +/- 3, IH vs. Ctl, P < 0.01), however calcium retention was negative (-1.9 +/- 2.0 mg/7 day vs. 6.5 +/- 0.5, IH vs. Ctl, P < 0.01) compared to Ctl rats. The fall in urine calcium excretion when IH rats are fed LCD indicates that enhanced intestinal calcium absorption is a primary mechanism of the hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Computerized radiographic analysis of osteoporosis: preliminary evaluation.

Measurement of bone mass is important in determining the risk for fracture and in following the course of patients undergoing therapy for osteoporosis. Bone mineral densitometry (BMD) is a good predictor of fracture risk, but there is considerable overlap in BMD measurements between individuals with fracture risk and those without. In this study, computerized texture analysis of the trabecular pattern on conventional spine radiographs was used to evaluate bone structure as a determinant of fracture risk. Standard lumbar spine radiographs of 43 individuals were analyzed and compared with BMD measurements obtained with dual-photon absorptiometry. This method was more effective than BMD in differentiation of patients with fractures elsewhere in the spine from those with no fracture. These preliminary results suggest that this method of bone structure analysis, combined with BMD, may lead to a more sensitive and specific predictor of osteoporosis and risk of fracture.

Adult↗
PubMed1993

Increased intestinal vitamin D receptor in genetic hypercalciuric rats. A cause of intestinal calcium hyperabsorption.

In humans, familial or idiopathic hypercalciuria (IH) is a common cause of hypercalciuria and predisposes to calcium oxalate nephrolithiasis. Intestinal calcium hyperabsorption is a constant feature of IH and may be due to either a vitamin D-independent process in the intestine, a primary overproduction of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], or a defect in renal tubular calcium reabsorption. Selective breeding of spontaneously hypercalciuric male and female Sprague-Dawley rats resulted in offspring with hypercalciuria, increased intestinal calcium absorption, and normal serum 1,25(OH)2D3 levels. The role of the vitamin D receptor (VDR) in the regulation of intestinal calcium absorption was explored in 10th generation male genetic IH rats and normocalciuric controls. Urine calcium excretion was greater in IH rats than controls (2.9 +/- 0.3 vs. 0.7 +/- 0.2 mg/24 h, P < 0.001). IH rat intestine contained twice the abundance of VDR compared with normocalciuric controls (536 +/- 73 vs. 243 +/- 42 nmol/mg protein, P < 0.001), with no difference in the affinity of the receptor for its ligand. Comparable migration of IH and normal intestinal VDR on Western blots and of intestinal VDR mRNA by Northern analysis suggests that the VDR in IH rat intestine is not due to large deletion or addition mutations of the wild-type VDR. IH rat intestine contained greater concentrations of vitamin D-dependent calbindin 9-kD protein. The present studies strongly suggest that increased intestinal VDR number and normal levels of circulating 1,25(OH)2D3 result in increased functional VDR-1,25(OH)2D3 complexes, which exert biological actions in enterocytes to increase intestinal calcium transport. Intestinal calcium hyperabsorption in the IH rat may be the first example of a genetic disorder resulting from a pathologic increase in VDR.

Animals↗
PubMed1993

Structure-function requirements of parathyroid hormone for stimulation of 1,25-dihydroxyvitamin D3 production by rat renal proximal tubules.

PTH stimulates synthesis and secretion of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in renal proximal tubule cells through activation of the protein kinase-A (PKA) or the protein kinase-C (PKC) signaling pathway. The relative contribution of the two transducing systems was explored using PTH fragments with selective activation of either PKA or PKC. Rat renal proximal tubules were isolated by Percoll centrifugation, and PKA and PKC activities were measured after treatment with synthetic fragments and analogs of PTH. Rat PTH-(1-34), [Nle8,Nle15,Tyr34]bovine PTH-(3-34), and human PTH-(13-34) increased PKC activity in a dose-dependent manner. All fragments tested stimulated PKC at physiological concentrations (10(-11)-10(-10) M). Rat PTH-(1-34) (10(-7) M) increased PKA activity 4.5-fold, but other fragments failed to stimulate PKA between 10(-12)-10(-6) M. Human PTH-(28-34) stimulation of PKC was variable from experiment to experiment. All four PTH fragments tested increased 1,25-(OH)2D3 secretion by perifused renal proximal tubules at the lowest concentrations that stimulated PKC activity. The adenylate cyclase inhibitor 2',5'-dideoxyadenosine (10(-4) M) reduced PTH-(1-34)-stimulated PKA activity by 60%, but failed to block the rise in 1,25-(OH)2D3 secretion. The results of these studies demonstrate that PTH fragments that contain the PKC translocating domain stimulate 1,25-(OH)2D3 secretion, whereas elimination of the PKA activation domain does not alter the potency of the analogs' 1,25-(OH)2D3-stimulating activity. These results support the concept that PKC translocation may be required for PTH stimulation of 1,25-(OH)2D3 secretion.

Animals↗
PubMed1992

The use of pharmacologic agents to study mechanisms of intestinal calcium transport.

The mechanism of vitamin D-dependent intestinal calcium transport has been explored in experimental animals in vivo and in vitro with the aid of pharmacologic agents that inhibit steps in the translocation process. Glucocorticoids in vivo, but not in vitro, inhibit the mucosal-to-serosal flux (Jms) of calcium and thus reduce net calcium absorption. Chronic metabolic acidosis inhibits calcium transport in vivo through inhibition of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] production and by a direct effect in vitro on the enterocyte to decrease calcium Jms. Cellular functions that may be involved in the transport process have been inhibited in vitro, including brush border calcium uptake by calcium channel blockers; calmodulin-dependent Ca-activated ATPase by trifluoperazine; calcium binding to vitamin D-dependent calcium-binding protein (CaBP, calbindin) by theophylline and acidic lysosomal vesicle function by quinacrine, chloroquine and ammonium chloride. The results of these studies demonstrate the consequences of selectively inhibiting steps thought to be involved in calcium transport and suggest new directions for further research in elucidating mechanisms of cellular calcium transport.

Animals↗
PubMed1992

Role of protein kinase C in parathyroid hormone stimulation of renal 1,25-dihydroxyvitamin D3 secretion.

PTH is a major regulator of renal proximal tubule 1,25(OH)2D3 biosynthesis. However, the intracellular pathways involved in PTH activation of the mitochondrial 25-hydroxyvitamin D3-1 alpha-hydroxylase (1-OHase) remain unknown. PTH can activate both the adenylate cyclase/protein kinase A (PKA) and the plasma membrane phospholipase C/protein kinase C (PKC) pathways. The present study was undertaken to determine whether PKC may mediate PTH activation of renal 25-hydroxyvitamin D3-1 alpha-hydroxylase activity. Rat PTH 1-34 fragment in vitro translocated PKC activity from cytosolic to soluble membrane fraction from freshly prepared rat proximal tubules. Physiologic concentrations (10(-11)-10(-10) M) of rat PTH 1-34 fragment increased PKC translocation three- to fourfold while PKA activity ratio increased at PTH 10(-7) M. PTH stimulation of PKC and PKA was reduced in the presence of staurosporine (10 nM) by 41 and 29%, respectively. Sangivamycin (10 and 50 microM) also reduced PTH-stimulated PKC translocation, but did not alter PKA activity ratio. In vitro perifusion of renal proximal tubules with PTH (10(-11) M) increased 1,25(OH)2D3 steady-state secretion two- to fourfold. Sangivamycin at the same concentration that inhibited PKC translocation by 52% completely inhibited PTH-stimulated 1,25(OH)2D3 secretion. The present studies indicate that the phospholipase C/PKC pathway may mediate PTH stimulation of mammalian renal proximal tubule 1,25(OH)2D3 secretion.

Animals↗
PubMed1992

Evidence that activation of protein kinase-C can stimulate 1,25-dihydroxyvitamin D3 secretion by rat proximal tubules.

PTH stimulates mammalian renal proximal tubule cell synthesis and secretion of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] by a Ca-dependent process. In the present study regulation of 1,25-(OH)2D3 secretion by PTH, phorbol ester 12-O-tetradecanoylphorbol 13-acetate, the Ca ionophore A23187, and calcitonin was evaluated in perifused rat proximal tubule cells isolated by collagenase digestion and centrifugation through Percoll. Tubules from rats fed a low Ca diet secreted 1,25-(OH)2D3 at a rate 2.5 times that of tubule cells from rats fed a normal Ca diet. Perifusion of tubules with human PTH-(1-34) (10(-7) M) induced an immediate and sustained increase in 1,25-(OH)2D3 secretion. Perifusion with either A23187 or 12-O-tetradecanoylphorbol 13-acetate caused transient increases in hormone secretion, while both agents perifused simultaneously resulted in a sustained increase in 1,25-(OH)2D3 secretion. Perifusion of tubule cells with the protein kinase-C (PKC) inhibitor staurosporine blocked the PTH-induced increase in 1,25-(OH)2D3 secretion. Calcitonin had no effect on 1,25-(OH)2D3 secretion rates. The results of the present studies show that an activator of PKC increases 1,25-(OH)2D3 secretion by mammalian proximal tubule cells and suggest that the phospholipase-C/PKC signalling system may mediate PTH stimulation of 1,25-(OH)2D3 secretion.

Alkaloids↗
PubMed1990

Acidosis inhibits 1,25-(OH)2D3 but not cAMP production in response to parathyroid hormone in the rat.

Parathyroid hormone (PTH) is a major activator of renal proximal tubule 25-hydroxyvitamin D3-1-hydroxylase (1-OHase). Chronic metabolic acidosis (CMA) inhibits 1-OHase and reduces circulating 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] levels in rats fed a low-Ca diet (LCD, 0.002% Ca). To examine the cellular mechanism whereby CMA inhibits 1-OHase, PTH-dependent renal 1-OHase activity and cAMP were measured in proximal tubules isolated from rats fed LCD for 14 days and made acidotic by the addition of 1.5% ammonium chloride to the drinking water. Serum 1,25-(OH)2D3 and proximal tubule 1-OHase activity and cAMP content were lower in acidotic rats. hPTH-(1-34) (10(-7) M) in vitro increased cAMP content to equivalent concentrations in tubules from rats with CMA and from nonacidotic controls; however, PTH increased 1-OHase activity only in tubules from nonacidotic animals. Although forskolin increased tubule cAMP content to equivalent levels in tubules from acidotic and nonacidotic rats, 1-OHase activity declined in tubules from nonacidotic rats and remained suppressed in acidotic tubules. The results suggest that chronic metabolic acidosis inhibits the PTH activation of 1-OHase through alteration of one or more steps in a cAMP-independent messenger system. PTH and forskolin can increase cAMP production by acidotic and nonacidotic proximal tubules; however, 1-OHase activity is not restored to normal in acidotic tubules and nonacidotic tubule 1-OHase may be inhibited.

Acidosis↗
PubMed1989

Regulation of 1,25-dihydroxyvitamin D3 by calcium in the parathyroidectomized, parathyroid hormone-replete rat.

Parathyroid hormone (PTH) is a major stimulus for the renal production of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Elevated arterial blood ionized calcium ([Ca2+]) depresses serum 1,25-(OH)2D3 in nonparathyroidectomized rats even when serum PTH is maintained at high levels by infusion. However, suppression by [Ca2+] of endogenous PTH, causing the fall in 1,25-(OH)2D, cannot be excluded. To determine whether [Ca2+] regulates 1,25-(OH)2D3 in the absence of a variation in PTH, we parathyroidectomized (PTX) rats (post-PTX calcium levels less than 7.0 mg/dl), inserted arterial and venous catheters, and then replaced PTH using an osmotic pump. We varied [Ca2+] by infusing either 75 mM sodium chloride (control), 0.61 mumol/min of EGTA (EGTA), or calcium chloride at 0.61 mumol/min (low calcium) or 1.22 mumol/min (high calcium) for 24 h 5 days after surgery. Blood was then drawn from the rat through the arterial catheter. Compared with the control, [Ca2+] fell with EGTA, remained constant with the low-calcium infusion, and rose with the high-calcium infusion. 1,25-(OH)2D3 was correlated inversely with [Ca2+] in all four groups together (r = -0.635, n = 34, p less than 0.001), within the control group alone (r = -0.769, n = 11, p less than 0.002), and within the EGTA group alone (r = -0.774, n = 10, p less than 0.003). Serum phosphorus, PTH, and arterial blood pH were not different in any group, and none correlated with serum 1,25-(OH)2D3. We conclude that 1,25-(OH)2D3 levels are regulated by [Ca2+] independently of serum PTH, phosphorus, and acid-base status, all of which support the hypothesis that [Ca2+] is a principal regulator of serum 1,25-(OH)2D3 in the rat.

Animals↗
PubMed1989

Familial forms of hypercalciuria.

The pathogenesis of calcium oxalate stone formation in patients with idiopathic hypercalciuria remains incompletely understood. Several lines of evidence suggest that inherited abnormalities of mineral metabolism may contribute to stone formation, including high frequency of calcium stone disease and hypercalciuria in first degree relatives of stone formers, similar phenotypic expression of hypercalciuria of the absorptive variety in several members of an affected kindred, and breeding of male and female hypercalciuric rats increases the magnitude and frequency of hypercalciuria among offspring. The causes of hypercalciuria are reviewed and possible molecular mechanisms are discussed.

Animals↗
PubMed1989

Effect of hypercalcemia-producing tumor on 1,25(OH)2D3 biosynthesis in athymic mice.

Serum 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels are low in patients with malignancy-associated hypercalcemia (MAH), whereas murine models of MAH have high circulating 1,25(OH)2D3. To determine the effects of a hypercalcemia-producing tumor on circulating 1,25(OH)2D3, in vitro 25-hydroxyvitamin D1-hydroxylase (1OHase) activity was measured in kidneys from BALB/c athymic mice implanted with a hypercalcemia-producing human lung tumor. Twelve days of low-phosphorus diet (LPD) in control animals lowered serum phosphorus to levels found in tumor-bearing mice fed normal phosphorus diet (NPD; 4.1 +/- 0.3 vs. 4.4 +/- 0.7 mg/dl, P = NS) and increased 1OHase activity (1.6 +/- 0.2 vs. 3.9 +/- 0.7 pmol.mg protein-1.5 min-1, NPD vs. LPD, P less than 0.05). 1OHase activity was greater in tumor-bearing animals fed NPD compared with control animals fed LPD (8.4 +/- 0.6 vs. 3.9 +/- 0.7 pmol.mg protein-1.5 min-1, P less than 0.01). High-phosphorus intake suppressed 1OHase activity in both control and tumor-bearing animals. Seven days of parathyroid hormone infusion in control animals fed NPD raised serum calcium (9.4 +/- 0.2 vs. 13.3 +/- 1.6 mg/dl, P less than 0.05) and suppressed 1OHase activity (0.25 +/- 0.02 vs. 0.02 +/- 0.002 pmol.mg protein-1.5 min-1, P less than 0.001). The inverse relationship of serum phosphorus and 1OHase activity was much steeper in the tumor-bearing animals, with greater enzyme activity at comparable levels of serum phosphorus. The present study indicates that 1) factors produced by the tumor stimulate 1OHase activity, and 2) hypophosphatemia is required for expression of enhanced enzyme activity.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1989

Effects of chronic metabolic alkalosis on Ca2+, PTH and 1,25(OH)2D3 in the rat.

The effect of chronic metabolic alkalosis on arterial blood ionized calcium concentration ([Ca2+]) and the levels of serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] is difficult to predict. Although a fall in pH directly decreases [Ca2+], chronic alkalosis reduces urine calcium excretion, which could elevate [Ca2+]. [Ca2+] modulates the serum level of PTH and the level of 1,25(OH)2D3 directly and through PTH. To determine the effect of chronic metabolic alkalosis on [Ca2+], PTH, and 1,25(OH)2D3, rats were made alkalemic by feeding a chloride-deficient diet (LCl) or LCl with 75 mM NaHCO3 in the drinking water (LCl + HCO3-) and compared with controls fed a chloride-replete diet (NCl). Compared with NCl, after 8 days of LCl and LCl + HCO3- arterial pH and PTH rose and [Ca2+] fell. Serum 1,25(OH)2D3 tended to rise with LCl and rose with LCl + HCO3-. Serum 1,25(OH)2D3 was correlated inversely with [Ca2+] (r = -0.510, n = 54, P less than 0.001) and with pH (r = -0.291, n = 57, P less than 0.03) but not with PTH or phosphorus. Stepwise regression analysis indicated that [Ca2+] accounted for the majority of the variance of serum 1,25(OH)2D3. Chronic metabolic alkalosis induced by a low-chloride diet and HCO3- appears to increase serum PTH and 1,25(OH)2D3 through a fall in [Ca2+].

Alkalosis↗
PubMed1989

Effects of 1,25(OH)2D3 on enterocyte basolateral membrane Ca transport in rats.

One, twenty-five dihydroxyvitamin D3 [1,25(OH)2D3], commonly known as calcitriol, stimulates intestinal Ca absorption through increased activity of a cellular transport process. To determine whether transcellular Ca transport involves energy-dependent Ca efflux across enterocyte plasma membrane in vitamin D-sufficient rats, in vitro bidirectional Ca fluxes were measured under short-circuited conditions across proximal duodenum from rats fed diets adequate in vitamin D and containing a normal Ca diet (NCD), a low Ca diet (LCD), or fed NCD and injected with 50 ng of 1,25(OH)2D3 daily for 4 days before study. LCD or 1,25(OH)2D3 increased Ca net flux [Jnet, mucosal-to-serosal flux minus the serosal-to-mucosal flux] by increasing Ca mucosal-to-serosal flux (Jm----s) (mean +/- SE, NCD vs. LCD vs. 1,25(OH)2D3, 16 +/- 4 vs. 179 +/- 18 vs. 82 +/- 21 nmol.cm-2. h-1, P less than 0.0001). Initial ATP-dependent Ca uptake rates by duodenal basolateral membrane vesicles (BLMV) was greater in vesicles from rats fed NCD compared with LCD and not different from NCD injected with 1,25(OH)2D3. These studies suggest that in vitamin D-replete animals, 1,25(OH)2D3 increases epithelial Ca Jm----s by mechanisms that do not involve ATP-dependent BLM Ca efflux. ATP-dependent Ca exit from the cell under these conditions may play a role in intracellular Ca homeostasis rather than Ca absorption.

Animals↗
PubMed1989

Effects of quinacrine on calcium active transport by rat intestinal epithelium.

To determine the possible role of acidic lysosomal vesicles in the transcellular transport of Ca, bidirectional Ca fluxes were measured across intestinal segments in vitro in the absence of electrochemical gradients. Mucosal addition of the weak base quinacrine (0.2 mM) caused a 67% decline in the mucosal-to-serosal Ca flux (Jm----s) across duodenum (175 +/- 34 vs. 58 +/- 9 nmol.cm-2.h-1, P less than 0.007) and reduced cecal Ca Jm----s (177 +/- 15 vs. 45 +/- 4, P less than 0.0001). Higher concentrations of up to 2.0 mM caused no further decline in cecal Ca Jm----s. Inhibition of cecal Ca Jm----s by mucosal chloroquine (0.1 mM) or ammonium chloride (10 mM) varied from 37 to 50%. Addition in vitro of quinacrine to enterocyte basolateral membrane vesicles failed to inhibit ATP-dependent Ca uptake. The present studies demonstrate that agents that collapse lysosomal pH gradients inhibit transcellular Ca transport. These observations are consistent with the hypothesis that Ca destined for transcellular transport is functionally associated with acidic lysosomes and that these organelles play an important role in transepithelial Ca translocation.

Ammonium Chloride↗
PubMed1989

Elevated Ca2+ does not inhibit the 1,25(OH)2D3 response to phosphorus restriction.

Phosphorus restriction and parathyroid hormone (PTH) are the most potent stimuli for 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] biosynthesis. Elevated arterial blood ionized calcium (Ca2+) inhibits the PTH-stimulated pathway for 1,25(OH)2D3 production. To determine whether the increase in Ca2+ due to chronic metabolic acidosis (CMA) would prevent stimulation of 1,25(OH)2D3 by dietary phosphorus restriction, rats were fed either a normal (NPD, 0.65%)- or low (LPD, 0.1%-phosphorus diet for 10 days. Ammonium chloride (NH4Cl) was added (1.5%) to the drinking water of some rats (CMA) while others served as nonacidemic controls. LPD increased serum 1,25(OH)2D3 levels in the absence of CMA and CMA did not affect the increase of 1,25(OH)2D3. LPD decreased serum phosphorus and increased Ca2+. Serum 1,25(OH)2D3 levels were correlated inversely with serum phosphorus and directly with Ca2+. Using stepwise linear regression the correlation between phosphorus and 1,25(OH)2D3 accounted for the majority of the variance contributed by both phosphorus and Ca2+ (F = 12.30, P less than 0.001). Increased Ca2+ induced by CMA does not inhibit the rise in serum 1,25(OH)2D3 during LPD, indicating that during phosphorus restriction Ca2+ does not inhibit production of 1,25(OH)2D3. Thus the mechanism whereby PTH and phosphorus restriction stimulate 1,25(OH)2D3 production differ; increased Ca2+ blocks the PTH-mediated rise in 1,25(OH)2D3 but does not alter the 1,25(OH)2D3 response to phosphorus restriction.

Ammonium Chloride↗
PubMed1989

Evidence that mouse renal proximal tubule cells produce nephrocalcin.

Nephrocalcin (NC) is a glycoprotein inhibitor of calcium oxalate monohydrate crystal growth present in urine and kidney tissue. To determine if kidney cells can produce NC, we have isolated proximal tubules from mouse kidney and cultured them in a serum-free medium containing supplements. The tubules accumulate p-aminohippurate and respond with increase in adenosine 3',5'-cyclic monophosphate to parathyroid hormone but not to arginine vasopressin. They produce 1,25 dihydroxyvitamin D3 when 25 hydroxyvitamin D3 is added as substrate. Medium conditioned for 3 days reacted by direct enzyme-linked immunosorbent assay (ELISA) with a rabbit antiserum to human urinary NC; the same antiserum was localized to the cells using immunoperoxidase staining. Using ion exchange and molecular sieve chromatography, we purified a glycoprotein calcium oxalate crystal-growth inhibitor the chromatographic behavior and amino acid and carbohydrate compositions of which closely resembled that of purified human urinary NC. Its dissociation constant toward the calcium oxalate crystal was 0.4-10 X 10(-7) M. Purified fractions of the protein cross-reacted with the antiserum tested by ELISA. Cultured proximal tubule cells produce a molecule that resembles NC from human urine, rat urine, and rat kidneys; proximal tubule is a probable site of NC production in vivo.

Animals↗
PubMed1989

Recurrent parathyroid cystic disease.

Cystic masses of the neck may represent thyroid, parathyroid, thyroglossal duct or branchial cleft cysts. Analysis of the cyst fluid may establish the etiology. Elevated levels of parathyroid hormone can be found in parathyroid cysts without concomitant hyperparathyroidism. A high concentration of cholesterol without the finding of thyroglobulin or parathyroid hormone in the fluid aspirated from a lateral neck mass suggests a branchial cleft cyst.

Adult↗