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Biomedical subjects

F L Coe

Publications and source records attributed to F L Coe.

At least 109 records · Page 6Linked to original sources
PubMed1983

Effects of trifluoperazine, ouabain, and ethacrynic acid on intestinal calcium transport.

Bidirectional steady-state calcium fluxes were measured in vitro under short-circuited conditions in segments of rat duodenum and descending colon. The calcium-activated ATPase (Ca-ATPase) inhibitor trifluoperazine (TFP, 0.1 mM) reduced net calcium absorption in both tissues by decreasing the absorptive flux from mucosa to serosa (Jm leads to s) without consistently altering the secretory flux from serosa to mucosa. 1,25-Dihydroxyvitamin D3 administration (50 ng/day for 4 days) increased net calcium absorption by increasing Jm leads to s, and TFP reduced Jm leads to s to the same extent across tissues from vehicle- or 1,25-dihydroxyvitamin D3-treated animals. Na-K-ATPase inhibitors ouabain and ethacrynic acid both reduced short-circuit current without affecting calcium fluxes. These data suggest that Ca-ATPase, located in the basolateral membrane of intestinal epithelial cells, plays a role in the transepithelial transport of calcium. More general effects of TFP on intestinal epithelium may also contribute to the reduction in calcium fluxes. Duodenal and descending colon calcium transport appears independent of transcellular sodium transport mediated by Na-K-ATPase.

Animals↗
PubMed1983

Effects of pH on bone calcium and proton fluxes in vitro.

Bone mineral is thought to decompose during acute and chronic metabolic acidosis and thereby contribute to buffering of the acid load. We cultured neonatal mouse calvariae for 3 h and found calcium efflux from bone when the medium pH was below 7.40, calcium influx into bone when the pH was above 7.40, and no net flux at pH 7.40. The calcium flux varied to the same extent when medium pH was altered by a primary change in the medium bicarbonate concentration or in the partial pressure of carbon dioxide. Calcium and proton fluxes were inversely correlated (r = -0.713, P less than 0.001), and the slope of the linear regression indicated that between 16 and 21 neq of proton entered the calvariae in exchange for each neq of calcium that left. In 24-h cultures, acid medium also caused net calcium efflux from bone, and alkaline medium caused net influx. PTH increased calcium efflux at acid but not at alkaline medium pH. Sodium azide resulted in net influx of calcium into bone at all values of medium pH. Calcium release by cultured calvariae in response to low medium pH is associated with proton buffering; over 3 h the stoichiometry indicates that little buffering is due to the dissolution of calcium-containing crystals. Effects of medium pH on calcium release are amplified by PTH, and calcium efflux can be prevented by the metabolic inhibitor sodium azide.

Animals↗
PubMed1982

Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study.

We evaluated 522 patients with idiopathic, recurrent calcium nephrolithiasis using a comprehensive clinical and laboratory protocol, and obtained additional laboratory measurements during their subsequent years of treatment in our program. In 57 patients, a new calcium stone ultimately formed during treatment (relapse), whereas 189 others have been free of recurrence during at least two years (average 4.3 +/- 2.2 [SD] years) of follow-up. Compared with the patients who remained stone-free, the patients with relapse (1) had a shorter interval between the time they entered our program and the time their last recurrent, pretreatment stone formed; (2) excreted more calcium *in mg/kg of body weight pr 24 hours) in their urine during treatment (2.79 +/- 1.08 versus 2.39 +/- 0.98 [SD] for relapse and stone-free); and (3) increased their urine volume less during treatment compared with pretreatment values (delta in liters per 24 hours was -0.02 +/- 0.48 versus 0.23 +/- 0.54 for relapse and stone-free). The two groups were otherwise the same. All comparisons used only data obtained prior to relapse. A discriminant function using only these three characteristics correctly identified 72 percent of patients with relapse and 67 percent of those who remained stone-free.

Allopurinol↗
PubMed1982

Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects.

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.

Calcitriol↗
PubMed1982

Pathogenesis and clinical course of mixed calcium oxalate and uric acid nephrolithiasis.

By direct measurement, urine from patients who form calcium oxalate stones was supersaturated abnormally with respect to calcium oxalate monohydrate but not supersaturated with respect to undissociated uric acid. Urine from patients who form uric acid stones was supersaturated excessively with undissociated uric acid but not calcium oxalate. Patients who form both calcium oxalate and uric acid stones, however, produce urine that is supersaturated with respect to both solid phases. Low urine pH was the primary factor that increased supersaturation with respect to undissociated uric acid. The formation of both calcium oxalate and uric acid stones appears to be explained by a dual abnormality of urine supersaturation.

Calcium Oxalate↗
PubMed1982

Effects of chlorothiazide on 1,25-dihydroxyvitamin D3, parathyroid hormone, and intestinal calcium absorption in the rat.

Previous studies have shown that thiazide diuretic agents reverse secondary hyperparathyroidism and reduce circulating 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and intestinal calcium absorption rates in patients with idiopathic hypercalciuria of the renal-leak variety. We have investigated whether thiazides can reverse the secondary increase in serum parathyroid hormone (PTH) and 1,25(OH)2D3 levels or intestinal calcium absorption induced by feeding rats a diet low in calcium (LCD, 0.02% calcium) but adequate in phosphorus and vitamin D. We found that LCD increased circulating immunoreactive PTH [chow vs. LCD, 0.52 +/- 0.06 vs. 1.06 +2- 0.1 (SE) ng/ml, P less than 0.001], 1,25(OH)2D3 (chow vs. LCD, 101 +/- 15 vs. 325 +/- 38 pg/ml, P less than 0.001), calcium uptake by everted gut sacs from duodenum, ileum, and descending colon, and net calcium absorption by descending colon studied in Ussing chambers in vitro. Chlorothiazide (CTZ) prevented the increase in PTH during LCD (chow + CTZ vs. LCD + CTZ, 0.69 +/- 0.07 vs. 0.73 +/- 0.06, NS) but not the increase in 1,25(OH)2D3 (chow + CTZ vs. LCD + CTZ, 88 +/- 10 vs. 277 +/- 31, P less than 0.002) or intestinal calcium transport. The drug caused no change in serum 1,25(OH)2D3 or intestinal calcium absorption in rats fed normal chow. In rats given exogenous 1,25(OH)2D3 to stimulate intestinal calcium absorption, CTZ reduced urine calcium excretion greatly but did not alter intestinal calcium absorption.

Administration, Oral↗
PubMed1982

Effects of metabolic acidosis on PTH and 1,25(OH)2D3 response to low calcium diet.

To study the effects of chronic metabolic acidosis on the metabolism of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] rats were given either a low calcium diet (LCD) (0.002% calcium) or chow (1.2% calcium); ammonium chloride (NH4Cl) was added (1 or 1.5%) to the drinking water of some rats eating LCD or chow while others served as nonacidotic controls. LCD increased circulating 1,25(OH)2D3 levels from 46 +/- 14 to 204 +/- 24 pg/ml (P less than 0.001) in the absence of NH4Cl; 1.5% NH4Cl prevented the increase in 1,25(OH)2D3 (25 +/- 6 vs. 27 +/- 8 pg/ml (P, NS) but 1% NH4Cl did not (50 +/- 12 vs. 161 +/- 23 pg/ml; P less than 0.001). Acidosis suppressed neither serum immunoreactive parathyroid hormone (PTH) nor urine cAMP response to LCD. Although total serum calcium and phosphorus showed no regular changes with NH4Cl, acidosis raised blood ionized calcium in rats fed either chow or LCD, and serum 1,25(OH)2D3 levels were inversely correlated with ionized calcium (r = 0.714; P less than 0.001) during LCD. Chronic NH4Cl acidosis prevented serum 1,25(OH)2D3 from rising during LCD, independent of changes in PTH secretion, cAMP generation, or serum phosphorus. The absence of a 1,25(OH)2D3 response may be due to increased ionized calcium produced by acidosis.

Acidosis↗
PubMed1982

Formation of a single calcium stone of renal origin. Clinical and laboratory characteristics of patients.

Of 859 consecutive patients with calcium renal stones, 182 had formed only one stone before entering our program. Ninety-three (51.1%) had idiopathic hypercalciuria or hyperuricosuria; 36 (19.8%) others had a systemic disorder producing stones. The remainder, 53 (29.1%) patients, had no metabolic disorder. The frequency of hypercalciuria was lower than among patients with multiple stones. Compared with recurrent stone formers, patients with single stones were older when they passed their stones, suffered higher rates of complication such as surgery, cystoscopy, and urinary tract infection, and had a lower frequency of idiopathic hypercalciuria. During treatment, 11% formed a new stone in an average follow-up period of three years, a relapse rate similar to that of multiple stone formers; however, those patients with single stones who did relapse formed new stones at lower rates than multiple stone formers. Compared with recurrent stone formers, patients with solitary stones were more often treated with diet alone. Since there were no substantial differences between solitary and recurrent stone disease, patients who have formed a single stone should be evaluated and they should be treated no differently from other patients with stone disease.

Adult↗
PubMed1981

Nephrolithiasis: causes, classification, and management.

The specific biochemical cause of calcium stone formation can now be reliably identified in close to 80% of cases. By permitting treatment to be targeted to the underlying condition, this has, in recent years, resulted in a documented reduction in stone recurrence. Less common types of nephrolithiasis--uric acid, cystine, and struvite stone formation--are also discussed and their management outlined.

Adult↗