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Biomedical subjects

C Y Pak

Publications and source records attributed to C Y Pak.

At least 235 records · Page 13Linked to original sources
PubMed1980

Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria.

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.

Adult↗
PubMed1980

Selective effects of thiazide therapy on serum 1 alpha,25-dihydroxyvitamin D and intestinal calcium absorption in renal and absorptive hypercalciurias.

The effect of long-term thiazide therapy (hydrochlorothiazide, 50 mg twice/day) on intestinal calcium (Ca) absorption and serum 1 alpha,25-dihydroxyvitamin D [1 alpha,25-(OH)2D] concentration was examined in 10 patients with renal hypercalciuria (RH), many of whom had hyperabsorption of Ca, and in 11 cases of absorptive hypercalciuria (AH), all of whom had intestinal hyperabsorption of Ca. In patients with RH, the intestinal Ca absorption decreased significantly during thiazide therapy (mean treatment period of 15 mo) from 0.68 +/- 0.09 SD to 0.56 +/- 0.10 (p less than 0.01), commensurate with the "correction" of the renal leak of Ca and secondary hyperparathyroidism. Furthermore, serum 1 alpha,25-(OH)2D decreased significantly from 5.2 +/- 2.2 SD ng/dl to 3.7 +/- 0.8 ng/dl (p less than 0.025) during thiazide therapy. In patients with AH, the intestinal hyperabsorption of calcium persisted during thiazide treatment (0.69 +/- 0.07 versus 0.69 +/- 0.06), despite restoration of normal urinary Ca. Serum 1 alpha,25-(OH)2D was virtually unchanged during treatment (4.5 +/- 1.4 ng/dl versus 4.7 +/- 0.9 ng/dl). The results support the hypothesis that the intestinal hyperabsorption of Ca in RH is a result of increased serum concentration of 1 alpha,25-(OH)2D secondary to the hyperparathyroid state, while that in AH may not be totally dependent on increased concentrations of 1 alpha,25-(OH)2D.

Adult↗
PubMed1980

A simple and reliable method for calcium balance using combined period and continuous fecal markers.

Calcium balances were determined in 13 patients during 2--4 3-day periods following both period marking (with carmine) and continuous marking (with polyethylene glycol or chromium). The reliability coefficient for the uncorrected fecal calcium (obtained from period marking) from one period to another was 0.82, whereas it was 0.97 for corrected fecal calcium (determined from recovery of continuous marker in 3-day fecal pools). Thus, the addition of continuous marking yielded a significantly more reliable measure of fecal calcium than obtainable by the use of period marking alone (p < 0.05); the error variance for corrected fecal calcium from one period to another was 3%, whereas it was 18% for uncorrected fecal calcium. It is concluded that a reliable measure of fecal calcium, and hence calcium balance, could be obtained by combined use of continuous and period markers, involving fecal collection over only one 3-day study period (marked by period marker), and correction of fecal calcium for the completeness of fecal collection (determined from continuous fecal marker).

Adult↗
PubMed1980

Renal oxalate excretion in calcium urolithiasis.

Urinary oxalate was determined in an ambulatory setting in 107 patients with an increased intestinal calcium absorption rate in whom stones formed, 34 patients with normal calcium absorption in whom stones formed and 34 control subjects without stones. Urinary oxalate excretion was not significantly different when the diet was changed from a random to a calcium-restricted diet. Moreover, urinary oxalate was not higher during summer months when intestinal calcium absorption may have been stimulated. Diet history disclosed that many patients with an increased calcium absorption rate had been on a moderate oxalate-restricted diet, often as part of a calcium-restricted regimen for the control of hypercalciuria. The results indicate that renal oxalate excretion in an ambulatory setting is not critically dependent on the state of calcium absorption and intake, and that the imposition of a low calcium dietary regimen in patients with an increased calcium absorption and in whom stones form does not necessarily augment oxalate excretion.

Adult↗
PubMed1980

Effect of 1,25-(OH)2D3 on jejunal absorption of magnesium in patients with chronic renal disease.

These studies were performed to see if jejunal malabsorption of magnesium in patients with chronic renal disease was influenced by therapy with 1 alpha, 25-dihydroxyvitamin D3 [1,25-(OH)2D3; 2 microgram/day by mouth for 7 days]. This treatment restored normal serum concentrations of the vitamin D metabolite from 0.9 +/- 0.2 to 4.2 +/- 0.6 ng/dl. Jejunal absorption of magnesium, measured by a triple-lumen constant-perfusion technique, was enhanced in each of the seven patients by this therapy. The mean value rose from 0.04 +/- 0.02 to 0.13 +/- 0.02 mmol . 30 cm-1 . h-1. This last value is similar to the magnesium absorption rate in untreated normal subjects. These results demonstrate that magnesium absorption in the human jejunum is dependent on vitamin D, and they show that 1 alpha,25-dihydroxyvitamin D3 therapy in patients with chronic renal failure is associated with an enhanced jejunal absorption of magnesium.

Adult↗
PubMed1980

Ability of 25-hydroxyvitamin D3 therapy to augment serum 1,25- and 24,25-dihydroxyvitamin D in postmenopausal osteoporosis.

Six women (mean age, 62 yr; range, 48--77 yr) who were considered to have postmenopausal osteoporosis, as demonstrated by radiological evidence of vertebral crush fractures, low intestinal calcium (Ca) absorption, and bone biopsies consistent with this diagnosis, received a pharmacological dose of 25-hydroxyvitamin D3 (25OHD3; 20 microgram/day) for 3 months. This treatment increased the serum concentration of 25OHD from 8.7 +/- 4.6 to 30.2 +/- 9.5 (SD) ng/ml (P less than 0.0025), increased the serum concentration of 24,25-dihydroxyvitamin D from 1.2 +/- 1.2 to 7.7 +/- 2.7 ng/ml (P less than 0.025) in three patients, and increased the serum concentration of 1,25-dihydroxyvitamin D from 2.1 +/- 1.7 to 4.3 +/- 1.5 ng/dl (P less than 0.025). Moreover, there were commensurate increases in fractional intestinal Ca absorption from 0.38 +/- 0.03 to 0.49 +/- 0.06 (P less than 0.025) and in urinary Ca from 69 +/- 31 to 127 +/- 67 mg/day (P less than 0.025). There were no significant changes in serum Ca (9.6 +/- 0.5 vs. 9.5 +/- 0.4 mg/dl), serum phosphorus (3.4 +/- 0.2 vs. 3.6 +/- 0.4 mg/dl) or alkaline phosphatase (87 +/- 27 vs. 91 +/- 30 IU/liter) before or after therapy. It is concluded that orally administered 25OHD3 is not only effective in raising the low intestinal Ca absorption observed in postmenopausal osteoporosis but also in increasing the serum concentrations of 24,25-dihydroxyvitamin D and 1,25-dihydroxyvitamin D.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

Effect of growth hormone administration: reciprocal changes in serum 1 alpha,25-dihydroxyvitamin D and intestinal calcium absorption.

The mechanism by which GH stimulates intestinal calcium absorption was explored. In this study, seven children with idiopathic GH deficiency were studied before and during GH therapy while they were maintained on the same metabolic diet. After 5-14 months of GH administration, fractional intestinal calcium absorption increased from 0.364 +/- 0.114 to 0.449 +/- 0.159 (P less than 0.01), and serum 1,25-dihydroxyvitamin D decreased from 63.7 +/ 19.3 to 46.7 +/ 17.8 pg/ml (P less than 0.025). Serum immunoreactive parathyroid hormone, urinary cAmp, serum 24,25-dihydroxyvitamin D, and 25-hydroxyvitamin D did not change significantly. The data suggest that GH does not directly influence parathyroid hormone or vitamin D metabolism. The possibility that relative intestinal resistance to 1,25-dihydroxyvitamin D exists in patients with GH deficiency is considered.

Adolescent↗
PubMed1980

Pathogenetic role of 1 alpha,25-dihydroxyvitamin D in sarcoidosis and absorptive hypercalciuria: different response to prednisolone therapy.

Intestinal hyperabsorption of calcium (Ca) is frequently observed in sarcoidosis and is characteristic of absorptive hypercalciuria (AH). The potential pathogenetic role of 1 alpha,25-dihydroxyvitamin D [1,25(OH)2D] in these two conditions was sought by a careful assessment of the circulating concentration of this vitamin D metabolite and various measures of Ca metabolism before and after prednisolone therapy. In eight patients with sarcoidosis, prednisolone treatment (50 mg/day for 8 days) produced a significant fall in serum 1,25(OH)2D [4.8 +/) 1.9 to 3.3 +/- 1.0 (SD) ng/dl; P less than 0.025], concomitant with a significant decrease in the fracitional intestinal Ca absorption (alpha) from 0.58 +/- to 0.14 to 0.46 +/- 0.13 (+/- SD; P less than 0.005). Urinary Ca and serum parathyroid hormone did not change significantly. However, in six patients with AH, prednisolone therapy resulted in a nonsignificant rise in serum 1,25(OH)2D from 3.6 +/- 0.7 to 4.4 +/- 1.0 ng/dl and no significant fall in alpha (from 0.73 +/- 0.08 to 0.70 +/- 0.10). Urinary Ca was significantly increased in AH patients from 230 +/- 35 to 343 +/- 74 (SD) mg/day (P less than 0.005), while serum parathyroid hormone rose slightly. Serum 1,25(OH)2D and alpha were significantly correlated (r = 0.543; P less than 0.05) for patients with sarcoidosis but not in AH patients. These results suggest that the hyperabsorption of calcium in sarcoidosis is dependent on the serum concentration of 1,25(OH)2D, while in AH it may result from additional vitamin D-independent processes.

Calcitriol↗
PubMed1980

Evidence justifying a high fluid intake in treatment of nephrolithiasis.

We quantitatively assessed the effect of urinary dilution on the crystallization of calcium salts. Urinary dilution was achieved in vitro (1 to 2 L/d) by addition of water to urine from six patients with renal stones and two normal subjects, and in vivo (1.023 to 2.383 L/d) by an increased ingestion of distilled water in four patients with nephrolithiasis and three normal subjects. Both forms of urinary dilution significantly reduced the urinary activity product ratio (state of saturation) of calcium phosphate (brushite), calcium oxalate, and monosodium urate. Moreover, the formation product ratio (limit of metastability or minimum supersaturation needed to elicit spontaneous nucleation) of calcium oxalate significantly increased, although that for brushite did not change significantly. Thus, there was a reduced propensity for crystallization of calcium salts. The results provide objective evidence for the beneficial role of an increased fluid intake in the management of nephrolithiasis.

Calcium Oxalate↗
PubMed1980

Ion binding by small molecular weight substances (1,000-10,000 daltons) in urine.

The reliability of calculated activity products as an index of the urinary saturation of calcium oxalate was tested by comparing the solubility of calcium oxalate in various urine preparations. Urine samples were collected from six control subjects and nine patients with nephrolithiasis. From each sample four urine preparations were prepared: centrifugation at 1400 g. 0.22-mu filtration, ultrafiltration through a 10,000 daltons cutoff filter, and ultrafiltration through a 1000 daltons cutoff filter. Each preparation was incubated with an excess of calcium oxalate to steady-state, and the activity product of calcium oxalate was calculated for the ambient solution. Our findings suggest that most calcium and/or oxalate conplexes in urine that are not recognizable by available computational techniques for activity products probably reside in the fraction of 1000 to 10,000 daltons.

Adult↗
PubMed1979

Effect of phenytoin on bone and vitamin D metabolism.

Calcium and vitamin D metabolism were evaluated in 5 adult epileptic patients before and during treatment with phenytoin. Significant decreases occurred in serum concentrations of calcium, albumin, and 25-hydroxy-cholecalciferol. The decreases in serum calcium paralleled those in serum albumin. Significant increases occurred in serum alkaline phosphatase and 1 alpha, 25-dihydroxycholecalciferol, in urinary hydroxyproline, and in the fractional gastrointestinal absorption of calcium. Urinary cyclic adenosine monophosphate and serum parathyroid hormone did not change. The results suggest that the bone disease resulting from phenytoin therapy may be associated with a deficiency of 25-hydroxycholecalciferol and not of 1 alpha, 25-dihydroxycholecalciferol, and that reduced gastrointestinal absorption of calcium or changes in parathyroid function may not be necessary for the development of bone disease.

Adult↗
PubMed1979

Pitfalls in parathyroid evaluation in patients with calcium urolithiasis.

Primary hyperparathyroidism is a major cause of calcium urolithiasis and is easily recognised when it is classically manifested. However, subtle presentations of primary hyperparathyroidism may cause confusion with other causes of calcium stone disease or cause diagnostic difficulty. Several pitfalls of parathyroid evaluation and treatment are illustrated by four cases of calcium urolithiasis. Cases 1 and 2 represent ineffective or useless parathyroid surgery rendered for renal hypercalciuria and absorptive hypercalciuria, respectively. Cases 3 and 4 had mild or intermittent hypercalcaemia. The correct diagnosis of primary hyperparathyroidism was made in Case 3 by parathyroid venous sampling and bone densitometry. In Case 4, the thiazide provocative test was used to establish the diagnosis of primary hyperparathyroidism.

Adult↗
PubMed1979

Quantitation of response to therapy in calcium urolithiasis.

The physico-chemical basis for the action of various drugs in calcium nephrolithiasis may be described in terms of changes produced in the urinary state of saturation (APR), limit of metastability (FPR), or in crystal growth. The validation of this scheme for drug action requires further correlation of objective responses to drug therapy, described in terms of urinary crystallisation, with the clinical response.

Calcium↗
PubMed1979

Selective jejunal hyperabsorption of calcium in absorptive hypercalciuria.

Calcium absorption in the jejunum and ileum of patients with absorptive hypercalciuria was studied by in vivo intestinal perfusion. Net calcium absorption in the jejunum was markedly increased at four luminal calcium concentrations (1 to 20 mM) in the patients with absorptive hypercalciuria when compared to that in normal subjects. In the ileum, net calcium absorption was only slightly increased in the patients with absorptive hypercalciuria. Experiments with radioactive calcium (47Ca) revealed increased unidirectional flux out of the jejunal lumen in the patients but no difference in the unidirectional flux into the lumen, when compared to that in normal control subjects. Net magnesium absorption was normal in the patients. These results suggest that hyperabsorption of calcium in patients with absorptive hypercalciuria is mainly due to enhanced calcium transport in the jejunum and that the defect is specific for calcium since magnesium is absorbed normally.

Adult↗
PubMed1979

Hypoparathyroidism.

Recent advances in our understanding of the physiologic actions of PTH and vitamin D have clarified certain aspects of the pathogenesis, classification, and management of hypoparathyroidism. Central to pathogenesis and categorization is the recognition that hypoparathyroidism may result from PTH deficiency, ineffectiveness, or resistance, with a resultant inability to stimulate adenylate cyclase in target tissues. This aberration in adenylate cyclase activity impairs certain physiologic responses such as renal phosphate excretion and renal calcium reabsorption that are required for proper calcium homeostasis. Also critical is the subnormal production of 1 alpha,25-dihydroxycholecalciferol (1,25-DHCC). Although the precise mechanism for the deficiency of 1,25-DHCC remains unclear, one may hypothesize that in hormone-deficient or hormone-ineffective hypoparathyroidism, decreased synthesis results from the absence of the two recognized stimuli for 1 alpha-hydroxylase--bioactive PTH and hypophosphatemia. Provision of either one of these stimuli would then be expected to restore 1,25-DHCC to normal levels, which could explain the calcemic response to PTH in these patients. There is some evidence that the synthesis of 1,25-DHCC may be "primarily" affected in PTH-resistant hypoparathyroidism, and thus may be unresponsive to any of the known stimuli. It remains conceivable, however, that during normocalcemic phases, such patients may improve their renal cyclic AMP and phosphaturic responses to PTH, with associated improvement in 1,25-DHCC synthesis. Certain acquired forms of PTH resistance such as hypomagnesemia and end-stage renal disease may also be associated with defective 1-hydroxylation. Whether occurring primarily or as a secondary process, the subnormal production of 1,25-DHCC may influence calcium and skeletal metabolism directly or by modifying response to PTH. The availability of 1,25-DHCC provides an effective and physiologically meaningful mode of therapy for most cases of hypoparathyroidism.

Acetazolamide↗
PubMed1979

Critical appraisal of oral calcium load test for indirect assessment of intestinal calcium absorption.

Two methods of oral calcium load or tolerance test for the indirect assessment of calcium absorption were compared. In 16 patients in whom the diagnosis of absorptive hypercalciuria was made independently, an exaggerated urinary total calcium excretion during four hours following calcium load, indicative of increased calcium absorption according to the method of Pak et al., was found in 15 patients. An abnormally high increment in urinary calcium during third and fourth hours post-calcium load, suggestive of enhanced calcium absorption by the criteria of Broadus et al., was encountered in 14 patients. However, an exaggerated urinary total calcium following calcium load was found in all 7 patients with renal hypercalciuria, whereas only 4 were shown to have an enhanced increment in calcium excretion. It is concluded that both methods are equally reliable in the detection of increased calcium absorption in absorptive hypercalciuria. However, the technique of Broadus et al. is probably superior to that of Pak et al. in the disclosure of increased calcium absorption in renal hypercalciuria.

Administration, Oral↗