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Biomedical subjects

C Y Pak

Publications and source records attributed to C Y Pak.

At least 199 records · Page 11Linked to original sources
PubMed1983

Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts.

Effects of potassium citrate therapy (60 mEq/day) on urinary chemistries and crystallization were compared to those of sodium citrate treatment in five patients with uric acid lithiasis. Both alkali treatments significantly increased urinary pH (P less than 0.001), from 5.35 +/- 0.18 SD to 6.68 +/- 0.14 for potassium citrate and 6.73 +/- 0.20 for sodium citrate. During potassium citrate therapy, urinary calcium significantly declined from 154 +/- 47 mg/day to 99 +/- 23 mg/day (P less than 0.01) and urinary citrate rose from 398 +/- 119 mg/day to 856 +/- 103 mg/day (P less than 0.001). The urinary saturation (activity product ratio) of calcium oxalate decreased from 3.21-fold to 1.69-fold saturation (P less than 0.01), and the inhibitor activity against calcium oxalate precipitation (formation product ratio) significantly increased. However, sodium citrate therapy did not significantly decrease urinary calcium (to 139 +/- 24 mg/day), although it increased urinary citrate substantially (to 799 +/- 89 mg/day, P less than 0.01). Urinary environment became supersaturated with respect to brushite (calcium phosphate) and monosodium urate. The inhibitor activity against calcium oxalate precipitation was not significantly altered for the whole group; in two patients, it decreased by more than 30%. The results indicate that (1) both alkali therapies are equally effective in preventing uric acid stone formation because of their ability to increase urinary pH, and (2) potassium citrate may prevent the complication of calcium nephrolithiasis in patients with uric acid stones, whereas sodium citrate may not.

Adult↗
PubMed1983

Long term 25-hydroxyvitamin D3 therapy in postmenopausal osteoporosis: demonstration of responsive and nonresponsive subgroups.

Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25OHD3) therapy is effective in raising the impaired intestinal calcium absorption (alpha) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 micrograms/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in alpha for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise alpha in response to 25OHD3 therapy. In those who responded (n = 7), alpha increased from 0.36 +/- 0.05 to 0.49 +/- 0.08 (+/- SD; P less than 0.005) while no significant change was observed for the nonresponders (0.44 +/- 0.03 to 0.48 +/- 0.07). During therapy, there were significant increases in serum 25OHD and 24,25-dihydroxyvitamin D [25,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 +/- 8 to 39 +/- 13 pg/ml; P less than 0.01), but not in nonresponders (25 +/- 11 to 28 +/- 8 pg/ml). Between-group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 +/- 0.3 vs. 2.2 +/- 0.8 ng/ml; P less than 0.005) and alpha (0.36 +/- 0.05 vs. 0.44 +/- 0.03; P less than 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum I,25-(OH)2D which was significantly higher in the responders (39 +/- 13 vs. 28 +/- 8 pg/ml; P less than 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise alpha in response to 25OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with menopausal osteoporosis, renal 25OHD3-1 alpha-hydroxylase may be impaired.

24,25-Dihydroxyvitamin D 3↗
PubMed1983

Evidence for bone remodeling but lack of calcium mobilization response to parathyroid hormone in pseudohypoparathyroidism.

Twenty-eight patients with hypoparathyroidism were classified into PTH-deficient (HP; n = 14) or PTH-resistant [pseudohypoparathyroid (PHP); n = 14] groups on the basis of serum PTH level and urinary cAMP response to PTH infusion. Bone density (BD; bone mineral content/bone width) was determined by 125I photon absorptiometry in the distal third of the radius of each patient. After 3 days of equilibration on a constant diet, fasting serum Ca, 1,25-dihydroxyvitamin D [1,25-(OH)2D] and 24-h urinary hydroxyproline (OHP) were measured during 4 control days and 4 treatment days [Lilly Parathyroid Extract (PTE); 100 U, im, every 6 h]. In HP, the mean BD was 0.772 +/- 0.016 (+/- SE) g/cm2, which was similar to the value obtained in a normal control group matched for age, sex, and race. In PHP, the mean BD was 0.633 +/- 0.017 g/cm2, which was 15 +/- 2% less than the normal value (P less than 0.005). Diminished BD was present in all patients with PHP, even in the absence of radiographic changes. Mean basal OHP excretion in PHP was more than twice that in HP (34.9 +/- 5.5 vs. 13.8 +/- 1.3 mg/day; P less than 0.005). Both groups had significant and comparable increases in urinary OHP excretion in response to PTE (9.1 +/- 2.1 mg/day for HP; 8.1 +/- 2.2 mg/day for PHP; P less than 0.005 for each). However, unlike the patients with HP, those with PHP did not have increases in serum 1,25-(OH)2D or a normal calcemic response to PTE. Thus, the bone-remodeling response to PTH remains intact in the majority of patients with PHP, but the mineral mobilization response, which may require 1,25-(OH)2D, is defective.

Adolescent↗
PubMed1983

Effect of amiloride with or without hydrochlorothiazide on urinary calcium and saturation of calcium salts.

To assess the therapeutic role of amiloride in calcium nephrolithiasis, seven patients with renal stones were evaluated before and after 1 month of treatment each with amiloride (2.5 mg twice daily), hydrochlorothiazide (25 mg, twice daily), and both drugs at the same dosages. Although amiloride alone reduced urinary calcium in only two patients, it caused a slightly more prominent decline in urinary calcium when added to hydrochlorothiazide treatment in five patients. The urinary saturation of stone-forming salts (brushite and calcium oxalate) decreased significantly during treatment with hydrochlorothiazide alone or in combination with amiloride. Although the decrease in brushite saturation was slightly more marked with the combined treatment, the reduction in calcium oxalate saturation was equivalent during the two treatment phases. Although serum potassium was significantly reduced during combined treatment with amiloride and hydrochlorothiazide, this reduction was not as prominent as that occurring during treatment with hydrochlorothiazide alone. The results suggest that the addition of amiloride to hydrochlorothiazide treatment in calcium nephrolithiasis may be advantageous, because of its stimulation, though slight, of the thiazide-induced reduction of urinary calcium and saturation of calcium phosphate and because it may avert the development of severe hypokalemia.

Adult↗
PubMed1983

Assay of urinary oxalate: six methodologies compared.

To assess how well results by different methods for urinary oxalate determinations agree with each other in a clinical setting, we compared six different assays: Hodgkinson and Williams (Clin Chim Acta 36:127-132, 1972), enzymatic, modified Hodgkinson and Williams, gas chromatography, ion chromatography, and "high-pressure" liquid chromatography. For the entire group of samples, the mean value by each method agreed relatively closely, although the enzymatic procedure produced a somewhat higher value. All six methods had large coefficients of variation within (8-58%) and between (15-88%) assays. In addition, analytical recovery by most assays was more than 100% of the added oxalate. Analytical recovery of 10 micrograms of oxalate added per milliliter of urine specimen ranged from 86 to 237%; for 20 micrograms/mL it was 83 to 320%. Thus for the six methods evaluated, no single method appeared to be superior to the others.

Chromatography, Gas↗
PubMed1983

Physiological and physiochemical correction and prevention of calcium stone formation by potassium citrate therapy.

Long-term effects of potassium citrate therapy (usually 60 mEq/day) were examined in 53 patients with renal stones (11 with uric acid lithiasis with complication of calcium stones, 10 with hypocitraturia as the sole abnormality, and 28 with hypocitraturia occurring with other abnormalities such as absorptive hypercalciuria, renal tubular acidosis, hyperuricosuric calcium oxalate nephrolithiasis, and enteric hyperoxaluria). Potassium citrate was given alone in 29 patients, added to thiazide and/or allopurinol treatments in 12 patients who continued to form stones on these treatments, and begun concurrently with thiazide and/or allopurinol in 12 patients with hypocitraturia and other defects (hypercalcuria and/or hyperuricosuria). In all three groups of patients, urinary citrate and pH significantly increased during potassium citrate treatment. Urinary saturation of calcium oxalate significantly declined while that of brushite remained unchanged. The propensity for the spontaneous nucleation of calcium oxalate, determined from the minimum amount of added oxalate required to elicit precipitation, declined. The treatment was effective in preventing new stone formation in all three groups. Stone passage rate declined from 5.14-7.41 stones/patient year before potassium citrate treatment to 0.66-1.33 stones/patient year during treatment, and 75.0-91.7% of patients were in remission. In patients who relapsed on other treatments (with passage of 5.14 stones/patient year), the addition of potassium citrate to the ongoing treatment program reduced stone formation to 1.33 stones/patient year and caused remission in 91.7% of patients. In 14 of 33 patients with preexisting radiopaque stones, there was radiological evidence of a reduced number of stones after 8 months-2 years of potassium citrate treatment. In conclusion, potassium citrate restores normal urinary citrate, decreases saturation and propensity for spontaneous nucleation of calcium oxalate, and inhibits new stone formation.

Adult↗
PubMed1983

Absorption of phosphate in the jejunum of patients with chronic renal failure before and after correction of vitamin D deficiency.

To examine the role of vitamin D in human phosphate absorption, we studied patients with chronic renal disease on hemodialysis, before and after correction of vitamin D deficiency. Thirty-centimeter segments of jejunum were perfused with test solutions containing varying concentrations of phosphate; phosphate absorption rate and electrical potential difference were measured. The data reveal that dialysis patients have depressed phosphate absorption, but the degree of this depression is modest, compared to the extent of their depressed calcium absorption. Therapy with 1,25-(OH)2D3 for 1 wk restored phosphate absorption rate to near normal. With or without 1,25-(OH)2D3 therapy, phosphate absorption was not influenced by calcium in the perfused test solutions. Examination of kinetic data suggests that the vitamin D deficiency of chronic renal failure causes a reduction by half in the rate of active phosphate absorption. By contrast, our data suggest that vitamin D deficiency does not alter passive phosphate absorption. By aspirating jejunal contents after ingestion of different foods, with and without aluminum hydroxide, the physiologic luminal phosphate concentration was found to vary between 0.7 and 12.2 mM. At the lower end of this range, phosphate absorption would be mediated entirely by active transport; at the higher phosphate concentrations, phosphate absorption would be mainly mediated by passive transport.

Adult↗
PubMed1982

Decreased serum 24,25-dihydroxyvitamin D concentration during long-term anticonvulsant therapy in adult epileptics.

Serum concentrations of 25-hydroxyvitamin D (25-OHD), 24,25-dihydroxyvitamin D [24,25-(OH)2D], and 1 alpha, 25-dihydroxyvitamin D [1, 25-(OH)2D] were measured in 30 ambulatory adult epileptic patients during long-term anticonvulsant treatment with phenytoin, phenobarbital, or carbamazepine. For the entire group, serum 24,25-(OH)2D was decreased (p less than 0.0005) as compared to normal subjects to a mean value of 0.7 +/- 0.1 (SEM) ng/ml. However, serum 1, 25-(OH)2D was increased at 50 +/- 7 pg/ml (p less than 0.025). Serum 25-OHD declined insignificantly to 19 +/- 3 ng/ml. All three drugs caused a significant reduction of serum 24,25-(OH)2D concentrations. A significant decrease in serum 25-OHD was observed only for the phenobarbital-treated patients. Serum 1, 25-(OH)2D was high in patients receiving phenytoin or carbamazepine but not in those taking phenobarbital. The findings suggest that while various anticonvulsant drugs appear to exert different effects on vitamin D metabolism, a universal finding is diminished serum 24,25-(OH)2D. The results support the notion that 24,25-(OH)2D deficiency may play an important role in the pathogenesis of anticonvulsant-induced osteomalacia.

Adolescent↗
PubMed1982

Should patients with single renal stone occurrence undergo diagnostic evaluation?

Diagnostic evaluation was conducted on 34 patients with a single episode of renal stone formation. Absorptive hypercalciuria as disclosed in 55.9 per cent (23.5 percent type I and 32.4 per cent type II), renal hypercalciuria in 11.8 per cent, primary hyperparathyroidism in 2.9 per cent, hyperuricosuric calcium oxalate nephrolithiasis in 8.8 per cent and no metabolic abnormality in 20.6 per cent. Compared to the group with recurrent stone formation the group with a single stone episode had just as severe biochemical abnormalities or laboratory results, such as hypercalciuria and exaggerated calciuric response to oral calcium load in absorptive hypercalciuria, high fasting urinary calcium and cyclic adenosine monophosphate in renal hypercalciuria, hyperuricosuria in hyperuricosuria calcium oxalate nephrolithiasis and low urine volume in no metabolic abnormality. The results suggest that the same physiological and environmental disturbances characterize stone formation in patients with a single stone episode as in those with recurrent stone formation and indicate the need for diagnostic evaluation.

Adult↗
PubMed1982

Tamm and Horsfall glycoprotein does not promote spontaneous precipitation and crystal growth of calcium oxalate in vitro.

Tamm and Horsfall glycoprotein was isolated from urine of patients with renal stones and from normal control subjects, and tested for its effects on the crystallization of calcium oxalate in vitro. Preparations from both groups (10-100 micrograms./ml.) caused slight inhibition of spontaneous precipitation and crystal growth of calcium oxalate. No promotion was found.

Calcium Oxalate↗
PubMed1982

Partial biochemical and physicochemical characterization of organic macromolecules in urine from patients with renal stones and control subjects.

From the urine of patients with calcium nephrolithiasis, and of control subjects, we isolated organic substances according to molecular size and tested them for effects on calcium oxalate precipitation. Nine subgroup materials of varying sizes were prepared by ultrafiltration and Sephadex G-200 column chromatography from 10 stone-formers, as well as from 10 control subjects. Uromucoid was found in large materials of both groups, whereas glycosaminoglycans were detected in large- and medium-sized materials of both groups. The small materials were devoid of uromucoid and glycosaminoglycans, but contained protein and uronic acid, a finding suggesting that they may be glycoproteins. The daily excretion of the uromucoid-rich material was greater, but that of the small glycoproteins was lower in stone-formers than in control subjects. The largest-sized material from stone-formers was devoid of any activity on calcium oxalate precipitation. All of the remaining materials (at a concentration of 5 mg/dl) exerted inhibition on calcium oxalate precipitation. The inhibition rose progressively with the decreasing size of organic materials. The calculated total inhibitor activity for the stone-forming group was 36% lower than that obtained in the control group.

Adult↗
PubMed1982

The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism.

Earlier studies have shown that an oral sodium (Na) load may induce hypercalciuria in previously normocalciuric subjects and may also increase intestinal calcium (Ca) absorption. To probe the cause of the increased intestinal Ca absorption, we simultaneously measured parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], and fractional intestinal 47Ca absorption before and after a salt load. Eleven normal subjects and two patients with postsurgical hypoparathyroidism were placed on a 10 meq Na, 400 mg Ca per day diet for 10 days, followed by another 10-day period in which the same diet was supplemented by 240 meq Na daily. Measurements were performed on the final 3 days of each phase. In the normal subjects, urinary Na excretion increased from 7 +/- 2 to 226 +/- 8 meq/day (mean +/- SEM), urinary Ca rose from 110 +/- 14 to 167 +/- 16 mg/day, serum parathyroid hormone (PTH) increased from 20 +/- 1 to 22 +/- 1 muleq/ml, serum 1,25-(OH)2D rose from 38 +/- 4 to 51 +/- 7 pg/ml, and fractional intestinal 47Ca absorption increased from 0.39 +/- 0.03 to 0.49 +/- 0.03 (P less than 0.05 for all changes). Serum Ca corrected for total protein did not change (9.9 +/- 0.1 to 9.8 +/- 0.1 mg/dl). The patients with hypoparathyroidism who were maintained on vitamin D therapy also showed increases in urinary Na (20 +/- 12 to 245 +/- 11 meq/day) and urinary Ca (271 +/- 48 to 305 +/- 43; P less than 0.05). However, there were no increases in serum PTH (13 +/- 1 to 11 +/- 1 muleq/ml), serum 1,25-(OH)2D (44 +/- 1 to 40 +/- 6 pg/ml), or intestinal Ca absorption (0.41 +/- 0.03 to 0.42 +/- 0.05). Corrected serum Ca decreased from 9.4 +/- 0.2 to 8.6 +/- 0.2 mg/dl. We conclude that in normal subjects, Na-induced renal hypercalciuria is accompanied by increased 1,25-(OH)2D synthesis and enhanced intestinal Ca absorption. Since this adaptive mechanism did not occur in two patients with hypoparathyroidism, mediation by PTH is suggested.

Adult↗