Oral Aluminum Hydroxide Research Articles

Outcome of Tumor Lysis Syndrome with Hydration and Alkalinization in Children with Acute Lymphoblastic Leukemia

Objective: To observe the out come of tumor lysis syndrome (TLS) following treatment with hydration and alkalinization in children with acute lymphoblastic leukemia.Methodology: This is an observational study which included 30 diagnosed ALL children who were at high risk of developing TLS in the Department of Pediatric Hematology & Oncology, BSMMU, from January 2010 to July 2010. Result: The mean (±SD) age was found 10.2±2.9 years and maximum (46.7%) numbers were found between 11 to 15 years. Male female ratio was 2.3:1. High risk patients for developing TLS presented with huge organomegaly such as hepatomegaly, splenomegaly, and lymphadenopathy associated with fever, anemia, and bony tenderness. For diagnosis of Acute Lymphoblastic Leukemia (ALL) bone marrow study was done in all patients and immunophenotyping in 40.0% patients. Hydration, Alkalinization, Tab Allopurinol and Oral Aluminum hydroxide were used in all study patients while treatment. WBC and serum uric acid were found higher in all patients during baseline investigation. After hydration and Alkalinization serum potassium, serum phosphate, serum calcium and serum creatinine level were normal within 72 hours and serum uric acid within day five. Mortality was found 6.7% and the cause of mortality was septicemia. DOI: http://dx.doi.org/10.3329/bjms.v11i4.12598 Bangladesh Journal of Medical Science Vol. 11 No. 04 Oct’12

Effect of Oral Aluminium Hydroxide on Iron Absorption from Iron(III)-hydroxide Polymaltose Complex in Patients with Iron Deficiency Anemia

The study was carried out as an open-label, laboratory-blind, single-dose, randomized, two-period crossover, isotope efficacy study. Twenty-two patients with iron-deficiency anemia were enrolled in the study. The study consisted of two treatment phases of 15 days each, including blood sample measurements for Fe-59 activity. The 2 treatments were given orally. Treatment A was Fe-59 labeled iron(III)-hydroxide polymaltose complex (IPC, Maltofer), equivalent to 100 mg elemental iron given orally, and Treatment B consisted of Treatment A combined with 600 mg aluminium hydroxide (CAS 21645-51-2) (10 ml). No differences between the two treatment groups with regard to the erythrocyte uptake were found, and thus IPC can be used with aluminium hydroxide, if necessary.

Radiation-induced esophagitis: A double-blind randomized clinical trial of aluminum hydroxide plus magnesium hydroxide plus oxetacaine suspension versus aluminum hydroxide plus magnesium hydroxide suspension

9100 Background: To assess whether oral administered oxetacaine-containing suspension is effective in treating acute radiation- induced esophagitis in cancer patients. Methods: A double-blind, prospective-randomized clinical trial was conducted across 20 radiotherapy institutions in Germany. Patients [pts.] with head and neck or thoracic cancer without dysphagia/odynophagia received definitive or postoperative radiotherapy [RT] with or without chemotherapy including at least 5 cm of the esophagus in the high dose volume. Pts. were randomized to receive oral aluminum hydroxide plus magnesium hydroxide plus oxetacaine (Tepilta [T]) suspension or aluminum hydroxide plus magnesium hydroxide suspension without oxetacaine (Magaldrat [M]) as first-line treatment for acute radiation-induced esophagitis. Primary endpoint was the interval between begin of RT and failure of first-line treatment of esophagitis defined as need for additional systemic analgesics. Data on pts.’ symptoms were collected during and for at least 2 weeks after treatment. Results: A total of 158 pts. were randomized, of whom 103 had take at least one dose of the study medication for acute esophagitis = grade 2 (CTC). Of the 105 pts., 51 were randomized to receive T and 52 M. The cumulative incidence of acute esophagitis = grade 2 (CTC) was 25% for the T and 22% for the M arm. Kaplan-Meier analysis showed a statistically significant difference between the two groups regarding the need for systemic analgesics under consideration of the intake time in favor of T (p = 0.032). No statistically significant difference was found between the two groups regarding the secondary endpoints need respective delay of additional parenteral nutrition (p = 0.28 respective p = 0.12), and pts.`s and investigator`s estimation of global effectivity of the study medication (0.08 and 0.12). Conclusions: This trial demonstrated a statistically significant delay of the intake time for systemic analgesics in pts. randomized to receive oral aluminum hydroxide plus magnesium hydroxide plus oxetacaine suspension. No significant financial relationships to disclose.

Sodium ferrous citrate does not cause aluminum retention in rats with experimentally induced renal failure

Accumulation of aluminum (Al) in the brain and bone has been implicated in the development of encephalopathy and osteodystrophy in patients with renal failure, and it has been reported that citric acid enhances Al absorption and retention. Oral iron supplementation is usually carried out with recombinant human erythropoietin (rHuEPO) therapy in end-stage renal disease (ESRD) patients. Accordingly, there is a possibility that Ferromia (sodium ferrous citrate, tetrasodium biscitrato iron (II), E0708), which is used for the treatment of iron deficiency anemia, might accelerate Al absorption and retention. To investigate this possibility, we administered oral aluminum hydroxide [Al(OH)3] [50mg Al/kg body weight (BW)] with or without E0708 (48mg/kg BW or 480mg/kg BW) to 5/6-nephrectomized rats (n = 27) five times per week for 16 weeks, and determined the Al content of the serum, liver, cerebral cortex, and femoral bone by flameless atomic absorption spectroscopy. The low dose of E0708 corresponded approximately to the clinical dose, and its low and high doses contained 34.5mg/kg BW and 345.0mg/kg BW, respectively, of citric acid. In addition, we gave 5/6-nephrectomized rats Al(OH)3 with citric acid at 35mg/kg BW, which was identical to the citric acid dose of the low-dose regimen of E0708. The weight gain, serum urea nitrogen, and creatinine levels indicated that the rats developed mild to moderate renal failure. There was no significant increase of the Al content in the serum or organs of the Al(OH)3, + E0708-treated rats when compared with the Al(OH)3-treated rats and Al(OH)3 + citric acid-treated rats. These findings suggest that the usual clinical dose of E0708 does not promote Al retention in rats with mild to moderate renal failure or normal rats.

The contribution of acidosis to renal osteodystrophy

A 5-year-old boy was admitted to the hospital 19 years ago for repair of primary hypospadias. The serum creatinine was 1.2 mg/dl; the BUN, 33 mg/dl; and the bicarbonate concentration, 23 mEq/liter. The creatinine clearance, determined from a 24-hour urine collection, was 75 mI/mm/I .73 m2. An intravenous pyelogram demonstrated a faint nephrogram on the right and no nephrogram on the left. Renal function was markedly diminished bilaterally with dysplastic pelvicalyceal systems and renal dysplasia affecting the left renal parenchyma more than the right. A voiding cystourethrogram demonstrated a distended and irregular bladder with massive bilateral reflux, distended calyces and pelves, and tortuous, dilated ureters. After voiding and standing, most of the contrast medium was drained from the upper collecting system; however, the bladder contained 500 ml of residual urine. A urologist advised against surgery because the patient had never had a urinary tract infection. Over the next several years, the patient's renal function progressively declined. Thirteen years ago, the serum creatinine was 3.9 mgldl; phosphate, 5.5 mgldl; calcium, 8.8 mg/dl; and bicarbonate, 22 mEq/liter. Aluminum hydroxide was administered, as was vitamin D. Six months later, the serum creatinine was 4.9 mgldl; phosphate, 6.1 mg/dl; calcium, 8.6 mg/dl; and bicarbonate, 20 mEq/liter. Oral sodium bicarbonate was given and the aluminum hydroxide was increased. In spite of marked increases in oral aluminum hydroxide and sodium bicarbonate, the serum phosphate level ranged from 5.2 to 7.4 mgldl (mean, 6.2 mg/dl over 2 years) and the bicarbonate ranged from 16 to 23 mEq/liter (mean, 20.7 mEq/liter) as the serum creatinine increased to 9.8 mg/dl over the next 18 months. Approximately ii years ago, peritoneal dialysis was begun. The patient was evaulated for transplantation at 3 major university centers, but each required that bilateral nephrectomy be performed prior to transplantation; the patient and his family refused. Nine years ago, the patient's mode

Calcinosis Cutis in Juvenile Dermatomyositis Responsive to Aluminum Hydroxide Treatment

Calcinosis cutis is a frequent complication of juvenile dermatomyositis; however, its treatment remains unsatisfactory. We report a case of calcinosis cutis in juvenile dermatomyositis which was successfully treated with oral aluminum hydroxide. Almost complete clearing of calcinosis was observed after 8 months of therapy. There were no adverse effects from therapy. Aluminum hydroxide is worth trying in treating calcinosis cutis.

Serum aluminium measurement by DC plasma emission spectrometry.

A serum aluminium assay has been established using a DC plasma emission spectrometer and calibration with serum based standards. The assay is linear between 0.20 and 18.0 mumol/L aluminium. The procedure gives good analytical recovery and precision. The assay was validated by comparison(s) with an electrothermal atomic absorption (ETAAS) procedure which showed good agreement. Serum aluminium concentrations have been compared in normal individuals, in undialysed chronic renal failure patients with or without aluminium hydroxide treatment, and in dialysed patients treated with oral aluminium hydroxide. Non-dialysed patients had higher serum aluminium concentrations if treated with aluminium hydroxide. Haemodialysis patients had the highest serum aluminium concentrations whilst those on peritoneal dialysis had levels similar to those of the non-dialysed chronic renal failure group.

Of Mouse and Man: The Hypophosphataemic Genes

X-linked hypophosphataemia is the most frequent cause of familial rickets resistant to treatment with physiological amounts of vitamin D [1-3]. It is also one of the great mysteries of metabolic bone disease, since so little is known about phosphate regulation. However in the past decade research on phosphate transport in this disorder has been considerably illuminated by studies on the hypophosphataemic animal homologue, the Hyp mouse, whose mutant locus is at the distal end of the X chromosome [4]. Since not all physicians hold the mouse in high regard theclinical relevance of this work may have been undervalued; but recent discoveries now bring hypophosphataemic man and mouse together and provide a fascinating metabolic story. Not only has the human X-linked hypophosphataemic gene been localized [5-7] but another murine hypophosphataemic gene (called Gy) has been described, in which both hearing and the vestibular apparatus are defective [8]. What is the significance of these findings? What further lessons can be learnt from the mouse? And where should we go from here? Inherited hypophosphataemia, and the rickets it usually causes, differs from all other forms of rickets, from acquired hypophosphataemia (often associated with specific tumours [9]), and also from phosphate depletion, as with excessive oral aluminium hydroxide [10]. Growth failure, widespread calcification of the tendons and ligaments [2, 11] which may lead to spinal stenosis and paraplegia [12] and absence of proximal myopathy, possibly related to normal intramyofibrillar inorganic phosphate concentration [13], distinguish X-linked hypophosphataemia. Although in this disease disturbances of parathyroid hormone and vitamin D metabolism have been sought, and sometimes found [14], this experiment of Nature certainly appears to be a primary disorder of phosphate transport and as such has the potential to teach us a lot about phosphate metabolism. Important steps have been taken to identify the gene causing X-linked hypophosphataemia using the techniques of modern molecular biology. Multilocus linkage analysis was performed using a series of cloned X-chromosome genetic markers in 16 informative hypophosphataemic families from Britain, Canada and America [5, 7, 15]. These families had at least three generations in whom individuals were affected in a pattern consistent with X-linked dominant inheritance. The mutant locus was mapped to the short arm of the human X chromosome and its position could be related to the Hyp locus in the mouse by a scheme involving rearrangement of homologous blocks of genes [5]. This was the first dominant disease gene to be mapped to the

The Effects of Zero Magnesium Dialysate and Magnesium Supplements on Ionised Calcium Concentration in Patients on Regular Dialysis Treatment

The effect of oral magnesium carbonate or aluminium hydroxide on serum ionised calcium, total calcium, aluminium and magnesium, was assessed in 31 patients with chronic renal failure, during and after one haemodialysis. The behaviour of ionised calcium and total calcium was the same in both groups. Each showed a slight fall during dialysis, which was not significant. Serum total calcium was 0.2-0.3 mmol/l (0.8-1.2 mg/dl) greater throughout the period of dialysis in the group taking aluminium hydroxide. Serum magnesium and aluminium were both lower in the group treated with magnesium carbonate. In the group taking magnesium carbonate, serum magnesium concentrations fell markedly during dialysis, but otherwise were maintained within the reference range by the use of a magnesium-free dialysate. These results show the effectiveness of magnesium carbonate oral phosphate-binding agents and zero magnesium dialysate in reducing serum aluminium without affecting the behaviour of serum calcium fractions during dialysis.

SUBSTITUTION OF ALUMINIUM SALTS BY MAGNESIUM SALTS IN CONTROL OF DIALYSIS HYPERPHOSPHATAEMIA

For two years all 28 patients undergoing hospital haemodialysis were switched from a dialysate magnesium (Mg) of 0·85 mmol/l to one containing none. Oral aluminium hydroxide was discontinued, and magnesium carbonate was substituted as a phosphate binder. After 24 months on this regimen predialysis aluminium concentration had fallen significantly. There was no significant change in predialysis phosphate, which remained above the normal range; nor was there evidence of increased secondary hyperparathyroidism as judged by parathyroid hormone immunoassay and biochemical or clinical criteria. Predialysis Mg concentrations tended to fall towards the normal range. Aluminium-containing phosphate binders seem to be unnecessary for the control of dialysis hyperphosphataemia. Magnesium carbonate may be an alternative and less toxic compound.

CALCIUM AND PHOSPHORUS METABDLISM IN CHILDREN WITH RENAL FAILURE: THE EFFECT OF DIFFERENT DIALYSIS MODALITIES

Abnormalities of calcium and phosphorus metabolism and hyperparathyroidism are major problems for children with renal failure. It is hoped that dialysis will reverse these problems and prevent the progression of renal osteodystrophy.Children starting either hemodialysis(HD,n=18), intermittent peritoneal dialysis (IPD, n=16)or continuous ambulatory peritoneal dialysis(CAPD,n=12)and remaining on the same modality for 6 months were compared for serum calcium(Ca), phosphorus (P), alkaline phosphatase (A-p), parathyroid hormone(PTH)and the oral aluminum hydroxide dose (Al-d) required. All children received dihydrotachysterol or calcitriol.Children started dialysis with abnormalities in Ca and P metabolism and although serum Ca and P improved on dialysis, PTH and Al-d did not decrease. In addition, there was no significant difference in any parameters between the different dialysis modalities. Therefore, earlier and more aggressive medical treatment prior to dialysis and early transplant in children may be the best approach to normalize Ca and P metabolism, since dialysis offers little benefit.

Comparison of Control of Serum Phosphate Levels during Continuous Ambulatory Peritoneal Dialysis and during Hemodialysis

Recent reports have suggested that oral aluminium hydroxide carries the risk of aluminium toxicity. We have compared the aluminium hydroxide dose and serum levels of phosphate and aluminium in 27 CAPD and 26 hemodialysis patients. Despite a more liberal protein intake and lower aluminium hydroxide dose, the CAPD patients achieved the same serum phosphate level as those on hemodialysis. While the reason for more efficient serum phosphate control with CAPD is uncertain, the better control gives CAPD an advantage in patients in whom it is particularly important to minimise exposure to aluminium.

Accumulation of Aluminum in a Nondialyzed Uremic Child Receiving Aluminum Hydroxide

A child with renal insufficiency was treated with the oral phosphate binder aluminum hydroxide from age 6 to 31 months. The prescribed dose of elemental aluminum varied from 31 to 108 mg/kg/d. Concurrently the patient developed vitamin D-resistant osteomalacia which failed to improve with parathyroidectomy. Encephalopathy with myoclonic seizures, loss of speech, and motor impairment also occurred. Serum and bone aluminum levels were elevated at 334 micrograms/L (normal 7 +/- 3 micrograms/L) and 156 mg/kg (normal 3.3 +/- 2.9 mg/kg), respectively. This case demonstrates that aluminum may accumulate in tissue of children receiving oral aluminum hydroxide. The accumulation of aluminum may have contributed to the vitamin D-resistant osteomalacia and the encephalopathy in this patient. Children receiving aluminum-containing antacids as phosphate binders should be monitored for aluminum accumulation and signs of aluminum intoxication.

Clinical and experimental studies with oral aluminium hydroxide

Experimental studies in 10 paraplegic patients showed highly significant reduction in urinary saturation associated with the oral administration of aluminium hydroxide. Only 50 per cent of urine samples from five patients with calculous disease were actually undersaturated, however. During clinical studies in 12 patients with renal calculous disease, four had recurrence or growth of calculi while receiving medication, three had no recurrence during therapy, but new stones appeared after the medication was stopped, and five had no growth or recurrence either during therapy or after its cessation.

Renal response to alterations in dietary phosphate in the young beagle.

Hyperphosphatemia is present in the young of many species compared to adult animals. We studied the renal response to alterations in dietary phosphate in 4- to 7-day-old beagle puppies. Puppies were phosphate restricted with oral aluminum hydroxide gel (Group I) or phosphate loaded with oral sodium phosphate (Group II). Puppies in both groups had hyperphosphatemia (Group I 8.6, Group II 12.2 mg/dl) relative to dogs (3.4--4.8 mg/dl). Plasma phosphate concentration (P) and rate of excretion of phosphate (Ep) were independent of glomerular filtration rate (GFR). At any filtered load of phosphate Ep was greater and rate of reabsorption less in Group II independent of P. The maximal rate of phosphate reabsorption (TmP) was higher in Group I (100 micrograms/ml GFR) than Group II (26 micrograms/ml GFR). Negative values for phosphate reabsorption in 4 animals support the presence of a secretory mechanism for phosphate. Relative hyperphosphatemia in the puppy is not secondary to a renal limitation in phosphate excretion. The 1- to 2-week-old puppy adjusts renal reabsorption of phosphate to maintain a concentration of phosphate in plasma higher than in the adult animal. The renal alterations in response to variations in dietary phosphate occur independently of plasma phosphate concentration, GFR, or filtered load of phosphate.

Control of secondary hyperparathyroidism during long-term hemodialysis

The hyperparathyroidism which occurs during long-term hemodialysis of patients with chronic renal failure has been successfully controlled without the need for subtotal parathyroidectomy. Utilizing a highly sensitive radioimmunoassay for plasma parathyroid hormone (iPTH), it was found that iPTH was correlated negatively with dialysate calcium concentration and positively with plasma phosphate concentration. Manipulation of these factors separately demonstrated that iPTH could be significantly decreased in two to three weeks by simultaneously decreasing plasma phosphate and increasing dialysate calcium. On the basis of calcium flux studies across the dialyzer, it was determined that the optimal calcium concentration in the dialysate was 8 mg/100 ml. Ten patients were treated by initially decreasing their plasma phosphate to less than 6 mg/100 ml (by giving them oral aluminum hydroxide) and using dialysis against a calcium concentration of 8 mg/100 ml. All patients have manifested a substantial and progressive decrease in plasma iPTH toward normal, with alleviation of bone pain and absence of complications, during use of this regimen.

Treatment of calcinosis universalis with aluminium hydroxide.

A 9-year-old boy with calcinosis universalis due to dermatomyositis was treated with oral aluminium hydroxide with excellent response.

COMPLICATIONS AFTER PARATHYROIDECTOMY

1. Convulsions causing fractures complicated the post-operative course of two patients after parathyroidectomy. 2. One patient with primary hyperparathyroidism and osteitis fibrosa developed tetany which was controlled with difficulty with the usual measures to correct hypocalcaemia. The convulsion occurred during hypomagnesaemia. This seemed the main immediate cause of symptoms and was easily corrected when recognised. 3. The second patient had been subjected to total parathyroidectomy for treatment of renal glomerular osteodystrophy. The complications were entirely due to hypocalcaemia and the usual treatment was inadequate until oral aluminium hydroxide was given. 4. Further experience shows that aluminium hydroxide can be a valuable addition to other measures for dealing with hypocalcaemia due to the "hungry bones" phenomena.

Oral aluminium hydroxide in the treatment of hyperphosphatemia and acidosis in acute and chronic renal insufficiency.

Acta Medica ScandinavicaVolume 172, Issue 1 p. 75-78 Oral Aluminium Hydroxide in the Treatment of Hyperphosphatemia and Acidosis in Acute and Chronic Renal Insufficiency Tore Lindholm, Tore Lindholm University Medical Clinic (Renal Clinic), Lund, SwedenSearch for more papers by this author Tore Lindholm, Tore Lindholm University Medical Clinic (Renal Clinic), Lund, SwedenSearch for more papers by this author First published: January/December 1962 https://doi.org/10.1111/j.0954-6820.1962.tb07129.xCitations: 13AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume172, Issue1January/December 1962Pages 75-78 RelatedInformation