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Biomedical subjects

U Alon

Publications and source records attributed to U Alon.

At least 109 records · Page 6Linked to original sources
PubMed1984

Excretory pattern of bile during phototherapy.

We studied the acute effects of phototherapy (PT) on bile flow and on the biliary excretion of bilirubin pigments and of bile salts in male homozygous Gunn rats (120-150 g). 13 rats received PT and 10 rats were kept in the dark. Bile was collected by cannulation of the common bile duct at hourly intervals from 1 h prior to PT till after 4 h of 'lights on'. Before treatment, all values were similar in both groups. After 4 h of lights on, mean plasma bilirubin fell from 145.3 +/- 4.3 to 99.2 +/- 2.7 mumol/l (p less than 0.01) in the PT rats, but did not change in the controls. During the lights-on period, PT rats had a significantly higher hourly bile volume, and a higher excretion of biliary bilirubin and bile salts than the controls (p less than 0.005). Over the total 4-hour lights-on period, the PT group had a higher mean output of bile than the controls (0.93 +/- 0.17 vs. 1.52 +/- 0.34 ml/4 h; p less than 0.005) and an increased excretion of bilirubin (0.08 +/- 0.016 vs. 0.148 +/- 0.01 mumol/4 h; p less than 0.005) and bile salts (35.1 +/- 3.7 vs. 55.2 +/- 12.5 mumol/4 h; p less than 0.005). The results show that PT of the Gunn rat is associated with a rise in bile flow and with an increased excretion of bile salts, in addition to an increased biliary bilirubin output.

Animals↗
PubMed1984

Effects of parathyroid hormone and 1,25-dihydroxyvitamin D3 on tubular handling of phosphate in hypophosphatemic rickets.

A controlled metabolic study to examine the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) treatment on the renal handling of phosphate was conducted in nine patients with X-linked dominant hypophosphatemic rickets, including one with autonomous secondary hyperparathyroidism. Administration of 1,25(OH)2D3 resulted in uniform reduction in serum PTH from 63.6 +/- 14.7 (SD) to 49.3 +/- 14.8 muleq/ml (P less than 0.01), elevation of the tubular threshold for phosphate (TmP/GFR) from 1.41 +/- 0.30 to 1.90 +/- 0.31 mg/dl (P less than 0.01) and increase in serum phosphate from 2.6 +/- 0.7 to 3.4 +/- 1.1 mg/dl (P less than 0.01) in eight PTH-suppressible patients. Four patients treated with phosphate before and during the study (group A) excreted significantly more phosphate than those not treated with phosphate (group B) (P less than 0.001). In the control period, group A also had depressed TmP/GFR and higher concentrations of serum phosphate and PTH. With 1,25(OH)2D3 treatment, serum phosphate in group A became remarkably higher than in group B, 4.28 +/- 0.99 vs. 2.55 +/- 0.31 mg/dl (P less than 0.02), whereas serum PTH and TmP/GFR were similar in both groups. A good inverse linear correlation was found between mean serum PTH and mean TmP/GFR of the groups before and after treatment (r = 0.947); whereas, no correlation was found between TmP/GFR and serum calcium. The patient with autonomous secondary hyperparathyroidism, who was also treated with phosphate, had the lowest TmP/GFR. Administration of 1,25(OH)2D3 had no effect on the serum PTH and phosphate concentrations or on TmP/GFR. We conclude that in patients with X-linked dominant hypophosphatemic rickets PTH modulates to some extent the tubular handling of phosphate, and that the importance of this mechanism increases with therapeutic phosphate supplementation. Simultaneous administration of 1,25(OH)2D3 suppressed PTH activity, raised serum phosphate concentrations, and elevated TmP/GFR.

Adolescent↗
PubMed1984

Progressive diaphyseal dysplasia: genetics and clinical and radiologic manifestations.

Progressive diaphyseal dysplasia was found in a three-generation family including 13 affected individuals, the largest family reported to date. Our study confirms that progressive diaphyseal dysplasia, also known as Engelmann's or Camurati-Engelmann disease, is an autosomal dominant disorder with variable osseous and muscular manifestations. Disease distribution among patients, within a given patient, or even in individual bones is unpredictable. The femur is the most commonly and severely affected bone and hence most useful for radiographic screening of possible patients. Radiographs provide a meaningful assessment of disease activity and extent. The severity of symptoms is generally proportionate to severity of involvement shown by roentgenography. Exophthalmos due to osteosclerotic dysplasia of the skull occurred in more than half of the patients with progressive diaphyseal dysplasia. Twelve-year follow-up of this family, with affected individuals ranging in age from 6 months to 12 years, indicates that progressive diaphyseal dysplasia may progress or become quiescent and be remarkably inactive despite advanced osteosclerosis and structural deformity.

Adolescent↗
PubMed1984

Additive hypocalciuric effects of amiloride and hydrochlorothiazide in patients treated with calcitriol.

To compare the effects of hydrochlorothiazide (HCTZ) alone and in combination with amiloride on urinary calcium excretion we performed 14 acute studies on 7 patients with vitamin-D-induced calciuria. Each patient was studied first with HCTZ alone, and 1-32 weeks later with the same or lower dose of HCTZ combined with amiloride. Administration of HCTZ alone did not change UCaV during the 1st day of therapy, and caused a significant reduction from 44.4 +/- 28.8 to 26.0 +/- 14.4 mg/m2/24 h (p less than 0.02) on the 4th day. In contrast, combined diuretic regimen caused a significant reduction in UCaV from 36.0 +/- 16.7 to 23.6 +/- 14.4 mg/m2/24 h (p less than 0.02) on the 1st day and further reduction to 13.3 +/- 6.9 mg/m2/24 h (p less than 0.01) on the 4th day. UCaV on the 4th day was significantly lower with the HCTZ-amiloride combination (p less than 0.05). The combined therapy caused a greater reduction in FECa/FENa than HCTZ alone on the 1st day (p less than 0.02) and on the 4th day (p less than 0.01). HCTZ-induced hyperkaluria, hypokalemia and alkalosis were prevented by the addition of amiloride. In another patient, low-dose HCTZ-amiloride had a maximal dissociative effect on FECa/FENa and was more effective than HCTZ given alone in a double dose. 3 patients were treated with the low-dose HCTZ-amiloride regimen for a total of 23 months. UCaV was kept persistently low.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1984

Hyperparathyroidism in patients with X-linked dominant hypophosphatemic rickets--application of the calcium infusion test as an indicator for parathyroidectomy.

Two children with X-linked dominant hypophosphatemic rickets treated with vitamin-D metabolites and phosphate supplementation, for prolonged periods, developed hyperparathyroidism with nephrocalcinosis. Calcium infusion tests were performed in both. In one patient, the initial test was done two weeks after all treatment was stopped. Only moderate decrease in the degree of the phosphaturia was recorded. However, a repeat test, performed after all medications were withheld for another four weeks, showed normal anti-phosphaturic response, and she continued to be treated conservatively. In the other patient, the test was done five weeks after withholding treatment. Failure to suppress the phosphaturia provided strong support for the diagnosis of tertiary hyperparathyroidism. He underwent total parathyroidectomy and the parathyroid histology confirmed the diagnosis. In both, control of parathyroid activity stopped the deterioration in kidney function and improved the response of the basic disorder to treatment. It is concluded that in patients with X-linked dominant hypophosphatemic rickets, the calcium infusion test is useful for the differentiation between secondary-reversible and tertiary-irreversible hyperparathyroidism. To avoid continued stimulation of the parathyroid glands by phosphate administration, we recommend that such calcium infusion test be performed and interpreted after at least six weeks have elapsed without phosphate or vitamin-D administration.

Adolescent↗
PubMed1983

Bacterial meningitis. Effect of antibiotic treatment on cerebrospinal fluid.

The effects of full short-term antibiotic treatment on cerebrospinal fluid (CSF) findings were studied retrospectively in 68 children with acute bacterial meningitis. The features of CSF at admission were compared with those of the CSF obtained after 44-68 hours of therapy. Except in one case with H. influenzae and one case with pneumococcal meningitis, all CSF cultures were negative in the repeat specimen. In three of 16 children with meningococcal meningitis, the CSF glucose levels became normal in the second specimen. In all remaining 65 children, however, full intravenous antibiotic treatment for 44-68 hours did not alter the biochemistry and cytology of the CSF, which retained its "bacterial" character. From these findings it may be discerned that partial antibiotic treatment is even less likely to distort a 'bacterial' CSF.

Adolescent↗
PubMed1983

Reversal of vitamin-D2-induced hypercalciuria by chlorothiazide.

To test the effects of chlorothiazide on vitamin-D2-induced hypercalciuria, we carried out 17 metabolic studies lasting 12 days each in adult Sprague-Dawley male rats. Three groups were studied: (A) control rats receiving only the vitamin-D2 vehicle; (B) vitamin-D2-treated rats receiving 50 IU/day; and (C) rats treated in the same manner as group B with the addition of chlorothiazide 20 mg/day for the last 6 days of the study. Urine was collected during the last 3 days, and a blood sample was obtained at the end of each study period. Analysis of the data showed that there were no significant differences between the groups in changes of serum calcium concentration (A, 6.1 +/- 0.1 mg/dl; B, 6.1 +/- 0.2 mg/dl; C, 6.0 +/- 0.2 mg/dl), serum creatinine concentration (A, 0.5 +/- 0.07 mg/dl; B, 0.52 +/- 0.08 mg/dl; C, 0.48 +/- 0.04 mg/dl), and creatinine clearance (A, 4.8 +/- 0.7 ml/min/kg; B, 5.2 +/- 1.2 ml/min/kg; C, 4.9 +/- 0.5 ml/min/kg). The administration of vitamin-D2 significantly increased the urinary calcium excretion from 6.7 +/- 1.0 mg/kg/day to 19.5 +/- 9.7 mg/kg/day (p less than 0.02), but the calciuria was inhibited in group C rats by the addition of chlorothiazide, which restored urinary calcium excretion to 6.8 +/- 2.5 mg/kg/day (p less than 0.02). Evaluation of the ratio of calcium/creatinine excretion (A, 0.19 +/- 0.03; B, 0.53 +/- 0.25; C, 0.20 +/- 0.07) and calcium/sodium excretion (A, 0.22 +/- 0.05; B, 0.48 +/- 0.25; C, 0.19 +/- 0.04) further confirmed these effects of vitamin-D2 and chlorothiazide on urine calcium excretion. We conclude that in rats conventional doses of vitamin-D2 consistently induce marked hypercalciuria, even without hypercalcemia, and that this hypercalciuria can be effectively prevented by chlorothiazide.

Animals↗
PubMed1983

Calcium and vitamin-D metabolism in nephrotic syndrome.

A child with long-standing steroid resistant minimal-change nephrotic syndrome developed mild muscular weakness. Laboratory studies demonstrated reduction in both protein-bound and ionized calcium concentrations which were accompanied by high serum PTH and low urinary calcium excretion. These findings were related to the marked sustained reduction in the serum concentrations of 25-hydroxyvitamin-D3 and 1,25-dihydroxyvitamin-D3. Relief of the muscular weakness and normalization of serum ionized calcium and PTH were realized with oral administration of 1,25-dihydroxyvitamin-D3 at 0.25 mcg per day. These beneficial effects persisted for over one year of follow-up.

Calcifediol↗
PubMed1982

Pathogenesis of salt retention in dogs with chronic bile-duct ligation.

1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL). 2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 +/- 62 vs 960 +/- 58 mumol/min in the control period before CBDL (P less than 0.001). This antinatriuresis was associated with a significant rise in plasma aldosterone concentration, from 52.5 +/- 5.5 pg/ml before CBDL to 177 +/- 50 pg/ml after CBDL (P less than 0.02). Ascites was present in all salt-retaining CBDL dogs. 3. Bilateral adrenalectomy resulted in disappearance of ascites and in a rise in the natriuretic response to extracellular volume expansion. Urinary sodium excretion was 770 +/- 124 mumol/min, a value significantly higher than in the CBDL dogs with intact adrenals (P less than 0.001). Sodium balance studies in the adrenalectomized CBDL dogs during chronic deoxycorticosterone acetate (DOCA) treatment (25 mg/day) showed that in these animals there was failure to escape from the mineralocorticoid-induced sodium retention. Glomerular filtration rate and renal plasma flow did not change during the studies. 4. The present evidence supports the thesis that sodium retention in the CBDL dog results from a dual mechanism: (a) excess of circulating aldosterone and (b) and extra-adrenal factor which prevents escape from the salt-retaining effect of mineralocorticoids, in the CBDL dogs, thereby perpetuating the antinatriuresis in these animals.

Adrenalectomy↗
PubMed1982

The effect of intrarenal infusion of bile on kidney function in the dog.

1. Obstructive jaundice sensitizes the kidney to anoxic damage. To clarify further this phenomenon the effect of unilateral infusion of bile on kidney function was studied. The contralateral intact kidney served as control. 2. Intrarenal infusion of diluted bile (1:10) resulted in an ipsilateral fourfold increase in mean rate of urinary flow (P less then 0.01), threefold increase in mean fractional excretion of sodium (P less then 0.05) and more than 50% increase in mean rates of potassium excretion (P less then 0.05). Urinary flow rate and electrolyte excretion returned to baseline upon cessation of bile infusion. The mean clearances of inulin and rho-aminohippurate were unchanged during intrarenal bile infusion. 3. Intrarenal infusion of isotonic taurocholate solution (20 mmol/l) mimicked the diuretic, natriuretic and kaliuretic effects of diluted bile, whereas intrarenal infusion of bilirubin did not cause any change in the excretion of electrolytes. 4. It is concluded that increase in circulating bile acids rather than hyperbilirubinaemia may alter kidney function during obstructive jaundice. Acute cholaemia may cause volume depletion by increasing urinary salt loss. This in turn may aggravate the direct nephrotoxicity of circulating bile compounds.

Animals↗
PubMed1982

Effect of isolated cholaemia on systemic haemodynamics and kidney function in conscious dogs.

1. Systemic haemodynamics and kidney function were studied in the same dogs before and 14 days after choledochocaval anastomosis. 2. All dogs became deeply jaundiced whereas parenchymal liver function remained unchanged as assessed biochemically. 3. After choledochocaval anastomosis there was a decrease in mean arterial pressure (118 +/- 18 to 98 +/- 13 mmHg, P less than 0.005), and total peripheral resistance (4073.8 +/- 620.0 to 3327.6 +/- 244.9 kPa 1-1 s kg, P less than 0.01), whereas mean cardiac index and plasma volume corrected for body weight did not change. 4. Despite their disturbed systemic haemodynamics the cholaemic dogs and normal mean glomerular filtration rate and renal plasma flow. Maximal ability to concentrate and dilute the urine was, however, impaired during cholaemia. 5. It is concluded that cholaemia per se causes peripheral vasodilatation, hypotension and renal tubular dysfunction. Similar phenomena in jaundiced patients may contribute to their susceptibility to postoperative shock and acute renal failure.

Animals↗