Search PubMed⌕ Search

Biomedical subjects

C Y Pak

Publications and source records attributed to C Y Pak.

At least 253 records · Page 14Linked to original sources
PubMed1979

Treatment of calcium urolithiasis with diphosphonate: efficacy and hazards.

The effect of treatment of renal stone formation with 5 to 20 mg./kg. per day oral disodium ethane-1-hydroxy-1,1-diphosphonate for up to 30 months was examined in 12 patients with active renal (calcium) stone disease. The over-all incidence of stone passage decreased from 17.8 stones per year per patient before treatment to 7.7 stones per year per patient during therapy. Of the 12 patients 7 passed fewer stones or no stones during treatment. However, the incidence of stone passage was not changed substantially by disodium ethane-1-hydroxy-1,1-diphosphonate in 5 patients. Symptoms of muscle weakness and pain in the back, hips and shoulders occurred in 3 patients during treatment, 2 patients had an increase in serum alkaline phosphatase and 1 patient had a decrease in bone density. Although disodium ethane-1-hydroxy-1,1-diphosphonate may be clinically useful to manage calcium urolithasis in certain patients its over-all use is limited because of its ineffectiveness in some patients and owing to its potential to induce osteomalacia.

Administration, Oral↗
PubMed1979

Physiological basis for absorptive and renal hypercalciurias.

Idiopathic hypercalciuria constitutes two major variants-absorptive hypercalciuria, characterized by a primary intestinal hyperabsorption of calcium, and renal hypercalciuria, in which renal tubular reabsorption of calcium is primarily impaired. The two forms of hypercalciuria may be distinguished from each other, since a) parathyroid function is stimualted in renal hypercalciuria, but normal or suppressed in absorptive hypercalciuria, b) the renal leak of calcium is present in renal hypercalciuria, but not in absorptive hypercalciuria, c) intestinal calcium absorption is probably increased primarily in absorptive hypercalciuria, and secondarily in renal hypercalciuria (from parathyroid hormone excess), d) the increased calcium absorption in renal hypercalciuria probably results from the parathyroid hormone-dependent stimulation of 1,25-dihydroxyvitamin D synthesis, whereas that in absorptive hypercalciuria may be vitamin D-independent, e) the response of the two conditions to certain treatments is unique, and f) the sequelae of parathyroid hormone excess, such as low bone density and negative calcium balance, may be present in renal hypercalciuria, but not in absorptive hypercalciuria. These findings provide a physiological basis for the consideration of absorptive and renal hypercalciurias as distinct and separate entities.

Benzothiadiazines↗
PubMed1979

Kidney stones: various forms and treatment.

Calcium urolithasis is not a homogeneous entity, but is a result of many etiologies, with different physicochemical and physiological backgrounds. This diversity of presentation requires an appreciation of specific diagnostic criteria, and a selection of an appropriate treatment regimen for each cause.

Calcium↗
PubMed1979

Effect of parathyroidectomy on serum 1 alpha,25-dihydroxyvitamin D and intestinal calcium absorption in primary hyperparathyroidism.

Serum concentration of 1 alpha,25-dihydroxyvitamin D [1,25(OH)2D] and intestinal absorption were measured before and after parathyroidectomy in 11 patients with primary hyperparathyroidism. Serum 1,25(OH)2D was high preoperatively (P less than 0.001) and normal postoperatively. Ca absorption was elevated preoperatively (P less than 0.001) and decreased significantly after parathyroidectomy (P less than 0.001). However, 5 of 11 patients had a persistent hyperabsorption of Ca postoperatively, despite normal serum 1,25(OH)2D. The results suggest that factors other than 1,25(OH)2D contribute to the maintenance of high intestinal Ca absorption in hyperparathyroid patients in the postoperative state.

Adult↗
PubMed1979

An unique form of osteomalacia associated with end organ refractoriness to 1,25-dihydroxyvitamin D and apparent defective synthesis of 25-hydroxyvitamin D.

A 28-yr-old woman presented with hypocalcemia, hypophosphatemia, secondary hyperparthyroidism, and biopsy-proven osteomalacia despite treatment with vitamin D2, (17.5 mg/day). Three weeks after vitamin D2 treatment was stopped, she was found to have a low normal serum 25-hydroxyvitamin D (25OHD) and high serum 1 alpha, 25-dihydroxyvitamin D [1,25(OH)2D] of 18.6 ng/ml and 21.2 ng/dl, respectively. The fractional intestinal calcium absorption was low at 0.26. Treatment with 25OHD3 (20--50 micrograms/day) corrected the hypocalcemia and secondary hyperparathyroidism, raised intestinal calcium absorption, and reversed the skeletal lesions of osteomalacia. Serum 25OHD concentration rose to 51 ng/ml, while 1,25(OH)2D remained elevated. This case illustrates the probable operation of dual abnormalities in vitamin D metabolism. An impaired end organ responsiveness to 1,25(OH)2D was suggested by a low intestinal calcium absorption in the face of high serum 1,25(OH)2D. Moreover, there may have been a defective vitamin D-25-hydroxylase, since there was a relative refractoriness to treatment with large doses of vitamin D2, an inappropriately low serum 250HD after vitamin D2 therapy, and a responsiveness to treatment with 25OHD3.

Adult↗
PubMed1979

A patient with pseudohypoparathyroidism with increased serum calcium and 1 alpha, 25-dihydroxyvitamin D after exogenous parathyroid hormone administration.

The cause for the normal calcemic response to exogenous parathyroid hormone (PTH) was explored in a case of pseudohypoparathyroidism. The diagnosis of pseudohypoparathyroidism in this 29-yr-old woman was well established, since she had hypocalcemia (6.6 mg/dl), hyperphosphatemia (5.0 mg/ dl), high serum immunoreactive PTH, and negligible urinary cAMP response to exogenous PTH. Treatment with Amphojel slightly increased serum calcium (to 7.4 mg/dl) and lowered serum phosphorus (to 4.1 mg/dl) without altering the serum concentration of 1 alpha, 25-dihydroxyvitamin D [1,25(OH)2D]. After im administration of parathyroid extract (400 U/day for 4 days), serum calcium increased to 9.2 mg/dl, commensurate with significant elevations in serum 1,25(OH)2D (from 1.2 to 2.6 ng/dl) and fractional (intestinal) calcium absorption (from 0.22 to 0.43). The results suggest that the synthesis of 1,25(OH)2D upon PTH challenge was relatively intact and may have accounted for the normal calcemic response.

Adult↗
PubMed1979

Antihypertensive comparison of furosemide with hydrochlorothiazide for black patients.

Furosemide and hydrochlorothiazide were compared for treatment of black patients with mild to moderate hypertension in a randomized, open-label, crossover study design. Hydrochlorothiazide produced a significantly greater fall in mean arterial (24.7 vs 16.0 mm Hg, P less than .01) and diastolic (17.3 vs 10.1 mm Hg, P less than .01) blood pressure (BP) in 16 patients. Addition of methyldopa in nine patients produced a significantly greater fall in mean arterial (38.8 vs 31.9 mm Hg, P less than .05) and diastolic (28.9 vs 23.4 mm Hg, P less than .05) BP with hydrochlorothiazide vs furosemide. Renin status was categorized before and after treatment. Patients with low and normal renin activity were equally responsive to both diuretics. Hydrochlorothiazide caused a greater reduction in plasma potassium (0.26 mEg/L). Serum parathyroid hormone was not chronically elevated with furosemide. In this study, hydrochlorothiazide was more effective than furosemide for treatment of mild to moderate hypertension in black patients; renin classification did not predict diuretic responsiveness.

Adult↗
PubMed1979

Attenuation by monosodium urate of the inhibitory effect of glycosaminoglycans on calcium oxalate nucleation.

The interaction between mucopolysaccharide (glycosaminoglycans) and monosodium urate, with respect to their effects on spontaneous precipitation of calcium oxalate, was explored in vitro. Heparin and, to a lesser extent, chondroitin sulfate were found to inhibit calcium oxalate precipitation. The formation product ratio (FPR, limit of metastability or the minimum supersaturation required for spontaneous nucleation) of calcium oxalate was increased 29 per cent by 0.05 mg of heparin per liter, and by 70 per cent with 1 mg of heparin per liter. The increment produced by heparin was much less pronounced when the solution containing the mucopolysaccharide was preincubated with crystalline monosodium urate. Pretreatment of the solution containing heparin (0.05 mg per liter) by monosodium urate (0.5 mg per ml) virtually eliminated the inhibitory action of heparin. Studies with radioactive heparin indicated that monosodium urate binds heparin. In contrast, the inhibitory effect of chondroitin sulfate was unaltered by prior exposure to monosodium urate. The results indicated that monosodium urate may attenuate the inhibitor activity of certain mucopolysaccharides such as heparin and facilitate the calcium oxalate precipitation. The findings provide further support for the important etiologic role of hyperuricosuria in the formation of calcium oxalate stones.

Calcium Oxalate↗
PubMed1979

Effect of parathyroidectomy on crystallization of calcium salts in urine of patients with primary hyperparathyroidism.

The effect of parathyroidectomy on the crystallization of calcium salts in urine was examined in seven stone-forming patients with primary hyperparathyroidism. After parathyroidectomy, urinary calcium decreased significantly from 205 +/- 30 to 67 +/- 11 mg per day (P less than 0.01); there were no significant changes in urinary phosphorus, oxalate, magnesium, sodium, potassium, uric acid, pH, or total volume. The urinary activity product ratio (state of saturation) of brushite (CaHPO4.2H2O) and calcium oxalate decreased significantly from 1.34 +/- 0.14 to 0.75 +/- 0.18 and from 3.20 +/- 0.56 to 1.53 +/- 0.21 respectively (P less than 0.05), owing principally to the decline in urinary calcium. Moreover, the urinary formation product ratio of calcium oxalate, which reflects the minimum supersaturation required for spontaneous nucleation, increased significantly after parathyroidectomy, from 7.19 +/- 1.19 to 12.99 +/- 1.69 (P less than 0.001). The results indicate that parathyroidectomy restores the normal urinary environment with respect to saturation and inhibitor and/or promoter activity.

Calcium↗
PubMed1978

Renal oxalate excretion following oral oxalate loads in patients with ileal disease and with renal and absorptive hypercalciurias. Effect of calcium and magnesium.

Intestinal absorption of oxalate was assessed indirectly from the increase in renal oxalate excretion following the oral administration of 5 mmol of stable oxalate. When sodium oxalate alone was given without divalent cations to patients in the fasting state, the urinary oxalate increased promptly (within 2 hours). The increase was more prominent and sustained in those with ileal disease (ileal resection or jujunoileal bypass); thus, 35 per cent of the orally administered oxalate eventually appeared in the urine in the group with ileal disease, 8 per cent in the group with stones (renal and absorptive hypercalciurias) and 9 per cent in the control group. This hyperexcretion of oxalate could be largely, but not totally, ameliorated by the concurrent oral administration of divalent cations. Although urinary oxalate decreased significantly following the oral administration of calcium or magnesium, hyperoxaluria persisted in most patients. The results suggested that the hyperabsorption of oxalate in ileal disease cannot be accounted for solely by an increased absorbable oxalate pool associated with calcium-fatty acid complexation. Moreover, although urinary oxalate decreased, urinary calcium increased concurrently when either calcium or magnesium was given. Thus, there was no significant change or increase in the urinary state of saturation with respect to calcium oxalate.

Administration, Oral↗
PubMed1978

Selective effects of thiazide on intestinal absorption of calcium and adsorptive and renal hypercalciurias.

The effect of long-term thiazide therapy on the intestinal Ca absorption was measured in 10 well-defined cases of absorptive hypercalciuria with intestinal hyperabsorption of Ca and 8 with renal hypercalciuria ("renal leak" of Ca), many of whom had hyperabsorption of Ca. In most cases of absorptive hypercalciuria, the intestinal hyperabsorption of Ca persisted during treatment, despite restoration of normal urinary Ca. In contrast, the intestinal Ca absorption decreased significantly during thiazide therapy in 7 of 8 patients with renal hypercalciuria commensurate with the "correction" of the renal leak of Ca and secondary hyperparathyroidism. The results support the hypothesis that the intestinal hyperabsorption of Ca in absorptive hypercalciuria may be primary, whereas that in renal hypercalciuria may be associated with the hyperparathyroid state.

Adult↗
PubMed1978

Effects of magnesium oxide on the crystallization of calcium salts in urine in patients with recurrent nephrolithiasis.

The effect of oral administration of magnesium oxide on the crystallization in urine of calcium oxalate and brushite was determined in 4 cases of recurrent calcium nephrolithiasis. Each patient was evaluated while on a constant metabolic diet before, during and after therapy with magnesium (1,000 mg. magnesium as magnesium oxide per day). During magnesium therapy urinary hydrogen ion concentration increased by approximately 0.5 unit in all 4 patients and urinary calcium increased about 50 mg. per day in 2. Urinary oxalate decreased significantly in 1 patient and urinary phosphorus was reduced in 2. The urinary activity product ratio of brushite (state of saturation) increased, owing largely to the rise in urinary hydrogen ion concentration but that of calcium oxalate was not changed significantly by magnesium treatment. Although urinary magnesium increased significantly there was no significant change in the urinary formation product ratio (limit of metastability) or the rate of crystal growth of brushite or calcium oxalate. Thus, no beneficial effect of magnesium therapy could be demonstrated in this short-term study.

Administration, Oral↗
PubMed1978

The hypercalciuria of diabetes mellitus: its amelioration with insulin.

Calcium and phosphous metabolism was investigated in 20 patients with diabetes mellitus when their diabetes was under poor metabolic control and again once optimal glycaemic control was achieved with aggressive insulin therapy. Ten of the twenty uncontrolled diabetics had hypercalciuria; insulin therapy returned calcium excretion to normal in five. Twenty-four hour calcium excretion fell in all but two patients when optimal diabetic control was achieved and calcium excretion was positively correlated with glucose excretion. Urinary cyclic AMP excretion, which was in the high normal range during poor control, decreased significantly during optimal insulin therapy. These data suggest that the hypercalciuria of uncontrolled diabetes may be a form of renal hypercalciuria which could result in parathyroid stimulation which might contribute to the development of osteopenia in patients with diabetes mellitus.

Adult↗
PubMed1978

An exaggerated augmentation of renal calcium excretion after oral glucose ingestion in patients with renal hypercalciuria.

The calciuric response to an oral glucose load (100 g) was determined in 16 patients with calcium oxalate urolithiasis (seven with renal hypercalciuria and nine with absorptive hypercalciuria) and seven normal subjects. The rates of renal calcium excretion increased significantly after glucose ingestion in all three groups. The calciuric response in patients with absorptive hypercalciuria and intestinal hyperabsorption of calcium was indistinguishable from that of normal subjects. However, the calcium excretions were significantly higher during 1 hr preceding and 3 hr after glucose ingestion in patients with renal hypercalciuria (with presumed "renal leak" of calcium) than in normal subjects. The increment in the calcium excretion rate was also higher in patients with renal hyperacalciuria, particularly during the 2nd hour of glucose ingestion. The results provide a further support for the concept of different etiologies of renal and absorptive hypercalciurias.

Adult↗