Biomedical subjects
A Halabe
Publications and source records attributed to A Halabe.
Immune complex haemolytic anaemia associated with sulfasalazine.
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[Diabetes and hyperparathyroidism--a new connection between old diseases].
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[Interaction between oral anticoagulants and dietary factors].
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Effect of parathyroid adenoma excision on interleukin-6 (IL-6) and IL-2 receptor levels.
1,25-Dihydroxycholecalciferol [1,25(OH)2D], besides its role in calcium and phosphorus homeostasis, is also an important immunoregulatory molecule. Plasma levels of this hormone may be normal or elevated in patients with primary hyperparathyroidism. 1,25(OH)2D has been reported to inhibit production of the cytokines interleukin-2 (IL-2) and IL-6. In the present study, we examined the effect of parathyroid adenoma excision on serum IL-2 receptor (IL-2R) levels and the release and production of IL-2R and IL-6 by peripheral blood lymphocytes (each measurement was performed twice). Ten patients (5 females and 5 males aged 45 to 78 years) with primary hyperparathyroidism were enrolled in the study. The diagnosis of primary hyperparathyroidism was based on the presence of asymptomatic hypercalcemia, hypophosphatemia, and elevated serum intact PTH levels. Three weeks after removal of the parathyroid adenoma, there was a significant increase in the serum level of IL-2R, as well as the PHA-stimulated peripheral blood lymphocyte production of IL-6 and release of IL-2R. The results indicate that the removal of a parathyroid adenoma in patients with primary hyperparathyroidism causes a significant increase in IL-2R and IL-6 levels. The mechanism by which hyperparathyroidism may affect these cytokines and how they seem related to the levels of vitamin D is discussed.
Fat distribution in AIDS.
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[Biphosphonates as a treatment for arresting metastasis. A new indication?].
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Possible discrimination of Gitelman's syndrome from Bartter's syndrome.
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Hypoparathyroidism--a long-term follow-up experience with 1 alpha-vitamin D3 therapy.
OBJECTIVE: Previous studies have suggested that alpha-D3 therapy can cause deterioration in renal function. We have, therefore, examined the long-term effect of 1 alpha-hydroxyvitamin D3 (alpha-D3) administration upon renal function in hypoparathyroid patients. DESIGN: This is a prospective long-term follow-up study of alpha-D3 administration on hypoparathyroid patients at a mean daily dose of 1 microgram (range 0.5-2.5 micrograms) during a total of 2040 patient-months. PATIENTS: Seventeen unselected patients (14 females and 3 males), two with primary and 15 with post-surgical hypoparathyroidism. RESULTS: The significant effect of alpha-D3 on serum and urinary calcium was achieved during the first week of treatment and remained stable at the same range during the close follow-up of 2040 patient-months. No significant change was observed in the serum creatinine during the whole follow-up period. During follow-up, five women developed hypercalciuria and one patient developed hypercalcaemia that disappeared when the dose of the drug was reduced or discontinued. CONCLUSIONS: From our study we concluded that alpha-D3 is a safe and effective drug in the long-term therapy of hypoparathyroid patients.
Uric acid nephrolithiasis.
Uric acid is the end-product of purine nucleotide metabolism in man. The renal handling of urate is a complicated process, resulting in a fractional clearance of 8.2-10.3%. The anhydrous form is thermodynamically the most stable uric acid crystal. Uric acid is a weak acid that ionizes with a Pka at pH 5.75. At the normal acidic region, uric acid solubility is strongly increased by urinary pH. The prevalence of uric acid stones varies between countries, reflecting climatic, dietary, and ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran). The risk for uric acid stone formation correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. Hyperuricosuria is the major risk factor, the most common cause being increased purine intake in the diet. Acquired and hereditary diseases accompanied by hyperuricosuria and stone disease include: gout, in strong correlation with the amount of uric acid excreted, myelo- and lymphoproliferative disorders, multiple myeloma, secondary polycythemia, pernicious anemia and hemolytic disorders, hemoglobinopathies and thalassemia, the complete or partial deficiency of HGPRT, superactivity of PRPP synthetase, and hereditary renal hypouricemia. A common denominator in patients with idiopathic and gouty stone formers is a low urinary pH. Uric acid nephrolithiasis is indicated in the presence of a radiolucent stone, a persistent undue urine acidity and uric acid crystals in fresh urine samples. A radiolucent stone in combination with normal or acidic pH should raise the possibility of urate stones.(ABSTRACT TRUNCATED AT 250 WORDS)
Bartter's syndrome: evidence suggesting a distal tubular defect in a hypocalciuric variant of the syndrome.
Renal tubular function was examined in 5 adult patients aged 18-30 years with Bartter's syndrome associated with renal magnesium wasting and hypocalciuria. In the 3 patients studied during hypotonic saline diuresis, distal tubular fractional chloride reabsorption was lower than that reported in normal subjects. In response to a single intravenous dose of furosemide (40 mg), the increment in the excretion of sodium, chloride, and magnesium was equal to or greater than in normal subjects, while in 2 patients, in response to intravenous chlorothiazide (500 mg), the increment in sodium excretion was less than in normal subjects. Magnesium chloride infusion was undertaken in 2 patients in order to compare magnesium and calcium excretions at similar plasma magnesium levels in patients and in normal subjects. The patients exhibited magnesium wasting only at normal or low plasma magnesium levels, while calcium excretion was reduced in the patients at normal and elevated plasma magnesium levels. We conclude that in these patients the enhancement of renal magnesium reabsorption by hypomagnesemia is defective, and the hypomagnesemia is not the cause of the hypocalciuria. The tubule defect responsible for these abnormalities of magnesium and calcium excretion may be located beyond the side of action of furosemide, in the thiazide-sensitive segment of the distal convoluted tubule.
The effect of calcitriol on atrial natriuretic factor release from isolated atrium.
Previous studies in our laboratory have shown that patients with idiopathic hypercalciuria (IH) have low basal atrial natriuretic factor (ANF) levels in the plasma. These depressed ANF levels are associated with a high plasma calcitriol levels. In this study, we have evaluated the effect of acute calcitriol administration on ANF release in the isolated atrium. There was a gradual reduction of ANF release as the dosage of calcitriol increased from 1 ng to 10 ng. Beyond 10 ng, additional suppression of ANF release by calcitriol was not observed. These results indicate that acute calcitriol administration causes a significant decrease in ANF release. To further determine whether this reduction in ANF release is due to changes in plasma calcium, additional studies were conducted to examine the effect of acute changes in perfusate calcium on ANF release by isolated atria. Acute elevation of perfusate calcium caused an increase in ANF release, whereas a reduction significantly decreased the secretory rate. These observations suggest that calcitriol affects ANF release by a mechanism not dependent on changes in plasma calcium.
Accelerator mass spectrometry: application to study of aluminum kinetics in the rat.
The advent of accelerator mass spectrometry (AMS) now permits the ultrasensitive detection of extremely long-lived isotopes, including 14C, 26Al, and 41Ca. Until now, tracer studies of aluminum kinetics have not been possible because aluminum has only two isotopes, with half-lives of 6.5 min (29Al) and 7 x 10(5) yr (26Al), neither of which is suitable for conventional studies. In a novel experiment we have employed AMS to study aluminum kinetics in a normal rat and a 5/6-nephrectomized rat over a 3-wk period of intravenous injection of a tracer dose of 26Al. Kinetics were similar in the two animals; approximately 75% of intravenously injected tracer 26Al was excreted in the urine in the first 24 h as was approximately 80% after 3 wk. Renal clearance of 26Al was approximately 0.75 ml.min-1.kg body wt-1 in both rats. The results clearly demonstrate the potential of this technique for isotope tracer studies in animals as well as in humans.
Effect of chronic cisplatin administration on phosphate and glucose transport by the renal brush border membrane.
Cisplatin (CIS-diamine dichloroplatinum) is a highly nephrotoxic antineoplastic agent which may cause acute renal failure and renal tubular dysfunction. In the present study we have examined the effect of chronic cisplatin administration on sodium-dependent 32P-phosphate and 3H glucose transport by the renal brush border membrane vesicles (BBMV). Our results indicate that both transport mechanisms were significantly reduced at the BBMV following cisplatin therapy due to an increased Km (0.13 +/- 0.09 vs. 0.34 +/- 0.09 mM; p = less than 0.01) without significant change in Vmax (56 +/- 18 vs. 44 +/- 17 pM/mg/s). The results of these studies indicate that cisplatin causes a diffuse renal injury in the proximal segment of the nephron altering both transport mechanisms. Possible mechanisms of cisplatin nephrotoxicity are discussed.
Chronic hypomagnesemia caused by cisplatin: effect of calcitriol.
A group of six patients with hypomagnesemia (serum magnesium less than or equal to 0.5 mmol/L), previously given treatment with cisplatin for ovarian or testicular cancer, received calcitriol at a dose of 0.5 to 1.0 microgram/day for a period of 4 weeks to determine whether treatment with this vitamin D metabolite could improve their hypomagnesemia. In response to treatment, the serum magnesium concentration fell progressively in association with a rise in serum and urinary calcium levels and a decrease in parathyroid hormone level. In a single previous report, active vitamin D metabolites markedly improved renal magnesium wasting. However, in the present study, increases in serum and urinary calcium levels and suppression of parathyroid hormone, factors known to decrease magnesium reabsorption, presumably overwhelmed any direct effect calcitriol may have had to enhance magnesium reabsorption, so that the net effect was a marked exacerbation of the renal magnesium wasting.
The effect of verapamil and thiazide in the prevention of renal stone formation.
The effect of the calcium antagonist verapamil, and of thiazide, a well accepted treatment in the prevention of calcium oxalate renal stones, were examined in an experimental renal stone model. Calcium oxalate stones were induced by the synthetic metabolite of vitamin D3, the alpha-OH-vitamin D3 plus ethylene glycol fed rats. A significant decrease in urinary calcium and oxalate was observed following verapamil treatment. Thiazide significantly decreased urinary calcium, but unlike verapamil, did not decrease urinary oxalate. However, no differences in the radiological findings or in the calcium or magnesium content of the kidneys were observed. Although several animal models have been described for the study of calcium oxalate stones, none has yet been proven useful for the evaluation of stone therapy.
Atrial natriuretic factor levels in renal stone patients with idiopathic hypercalciuria and in healthy controls: the effect of an oral calcium load.
Ionized calcium is a stimulator for the release of several peptide hormones. Atrial natriuretic factor (ANF) is a peptide hormone released from atrial tissue in response to atrial distension or volume expansion. In the present study, we have examined the effect of an oral calcium load in healthy controls and renal stone patients with idiopathic hypercalciuria. Our results demonstrated that ANF release increased in both groups in response to a calcium load. However, idiopathic hypercalciuric patients presented lower basal ANF levels in the presence of high calcitriol levels. The role of calcitriol on ANF release remains to be evaluated.
"Idiopathic" hypercalciuria and hereditary hypophosphatemic rickets. Two phenotypical expressions of a common genetic defect.
Among 59 closely related members of one Bedouin tribe, we identified 9 who had the characteristic features of hereditary hypophosphatemic rickets with hypercalciuria (HHRH). We found "idiopathic" hypercalciuria in 21 of the 50 asymptomatic members. The biochemical abnormalities observed in these 21 subjects were qualitatively similar to those in the 9 with HHRH, but were quantitatively milder. The urinary calcium concentration was 0.43 +/- 0.14 mg per milligram of creatinine (mean +/- SD) in the patients with HHRH, 0.34 +/- 0.07 in the subjects with idiopathic hypercalciuria, and 0.14 +/- 0.05 in normal subjects from the same tribe. Tubular reabsorption of phosphorus and serum phosphorus concentrations were 3.0 and 4.3 SD units below the age-related mean, respectively, in HHRH, and 1.1 SD units below the normal mean for both variables in idiopathic hypercalciuria. Mean serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D) were 303 pg per milliliter in HHRH and 145 pg per milliliter in idiopathic hypercalciuria (upper normal limit, 110). We conclude that the subjects with hypercalciuria and the patients with HHRH shared a hereditary renal phosphate leak that led to hypophosphatemia, elevated serum concentrations of 1,25-(OH)2D, increased intestinal calcium absorption, and hypercalciuria. The magnitude of the hypophosphatemia, which regulates 1,25-(OH)2D levels, appears to determine which subjects will have hypercalciuria alone and which will also have bone disease.