Successful Treatment of Dialysis Osteomalacia and Dementia, Using Desferrioxamine Infusions and Oral 1-Alpha Hydroxycholecalciferol

Hood, Sally A.; Clark, William F.; Hodsman, Anthony B.; Bolton, Charles F.; Cordy, P. E.; Anderson, C D; Leung, F Y

doi:10.1159/000166855

Cited by 17 publications

(2 citation statements)

References 19 publications

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“…Chelation of Al from bone followed by increased bone calcium deposition suggests that Al deposited in bone may impair bone calcium uptake. Reduction of serum calcium has also been described during deferoxamine treatment for AIassociated dialysis osteomalacia (6,(13)(14)(15)(16), including a preliminary report of a series of 51 patients (16). Lack of roentgenographic improvement in our patient may be explained by a duration of deferoxamine therapy of <4 months, the minimum needed to show improvement in dialysis patients (6), the constant resupply of Al in the TPN solution, and lack of adequate provision of calcium and/or phosphate.…”

Section: Resultsmentioning

confidence: 98%

Hypocalcemia Complicating Deferoxamine Therapy in an Infant with Parenteral Nutrition‐Associated Aluminum Overload

Klein,

Snodgrass,

Griffin

et al. 1989

J. pediatr. gastroenterol. nutr.

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Aluminum (Al) contaminates total parenteral nutrition (TPN) solutions given to infants, and high levels of Al have been demonstrated in their bone, serum, and urine. However, it is uncertain whether Al at current levels of contamination of TPN solutions is harmful to bone. We report an 8‐month‐old infant who developed osteopenic bone disease while receiving TPN, which did not respond to large amounts of calcium, phosphate, and vitamin D2. Serum and urine Al levels were greatly elevated and fell after a short course of deferoxamine. However, shortly after treatment began, serum calcium levels fell in the absence of hypercalciuria. We postulate that chelation of Al from this patient's bone permitted increased bone calcium uptake. This would suggest that Al at current levels of contamination of TPN solutions may impair bone calcium uptake and thus contribute to the pathogenesis or exacerbation of TPN‐related osteopenia.

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Section: Resultsmentioning

confidence: 98%

Hypocalcemia Complicating Deferoxamine Therapy in an Infant with Parenteral Nutrition‐Associated Aluminum Overload

Klein,

Snodgrass,

Griffin

et al. 1989

J. pediatr. gastroenterol. nutr.

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“…Multiple reports have documented the utility of deferoxamine in the therapy of dialysis encephalop athy.21,a, 42,[44][45][46]. H owever, universal clinical improvement has not been achieved; this may relate to the duration of symptoms.…”

Section: Aluminum Clearance By Hernodialysis and Deferoxaminementioning

confidence: 99%

Precipitation of Aluminum Encephalopathy in a Patient Receiving Deferoxamine

Owen

1989

Seminars in Dialysis

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A 68-year old woman with an 8-year history of endstage renal disease was referred for evaluation of an acute alteration in her mental status. Other than inadequately controlled hypertension, the patient had been well until approximately 9 years ago when she presented with ad-van& chronic renal failure and bilateral small, echogenic kidneys. Hemodialysis was initiated for uremic symptoms. Initially, the patient did well without additional significant medical problems. The staffcaring for her in the outpatient hemodialysis facility described her as an extremely coop erative and compliant patient.At age 65, she complained of increasingly severe pain involving the long bones of the lower extremities and the pelvis, ribs, and shoulders. Skeletal X-rays revealed marked osteopenia without changes consistent with osteitis fibrosa cystica. A serum parathyroid hormone level was obtained and found to be only mildly elevated. Serum alkaline phosphatase was also mildly elevated'and serum calcium normal. The patient's phosphorus had been well controlled with aluminum hydroxide (ALOH), but she had not received vitamin D supplements. The institution of dihydrotachysterol at doses of 0.25 mg/day or less resulted in moderately severe hypercalcemia to 14 mg/dl. Over the next year, the patient's symptoms worsened to the extent that she was unable to ambulate. At age 66 she underwent parathyroidectomy, and three and one-half modestly enlarged glands were removed. Vitamin D supplements were resumed, and lesser degrees of hypercalcemia were provoked. Despite these interventions, her osteopathy worsened. Skeletal radiographs of the hips and long bones now demonstrated pseudohctures, and skeletal scintigraphy was compatible with severe osteomalacia.Coincident with the diagnosis of osteomalacic osteodystrophy, the aluminum concentration in the deionized water supply to the dialysis unit was found to be 50 p g L . 48. Slatopolsky E, Weem C, Finch J, Lee W, Windus D, Delmez J The use of microencapsulated carbon in the removal of aluminum in dialysis patients. Proc Am Soc

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Aluminum intoxication in vitamin D-deficient rats: Studies of bone aluminum localization and histomorphometry before and after vitamin D repletion

Hodsman

Steer

Arsenault

1988

Journal of Bone and Mineral Research

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Aluminum accumulation by both dialysis patients and nonuremic patients, requiring chronic total parenteral nutrition, may be an etiological factor in the development of severe osteomalacia. To study the role of aluminum toxicity in bone, further experiments have been conducted in the nonuremic, vitamin D-deficient rat. Weanling rats were raised on vitamin D-deficient diets, and half received parenteral aluminum (5 mg/wk), for 30 days. In the first experiment low doses of 25-OH cholecalciferol (500 ng/week) were given subcutaneously for a further 30 days. Control rats were maintained on a similar protocol, but were supplemented with cholecalciferol (5 micrograms/week) from the outset until sacrifice at 60 days. In the second experiment a single bolus of cholecalciferol (5 micrograms) was given to study short-term changes in serum biochemistry and bone histology at 96 hr. Quantitative bone histomorphometric analyses of the proximal tibial metaphysis were made in all experimental groups. In the experimental vitamin D-deficient group, with the highest bone aluminum content (as assessed by extraction of whole bone aluminum), X-ray microanalysis was performed to determine the distribution of aluminum in bone tissue and bone cell organelles. The results showed that control rats treated with prolonged aluminum therapy (30 mg over 60 days) had evidence of both reduced osteoid matrix synthesis and mineralization. However, in vitamin D-deficient rats, there was no evidence that aluminum exacerbated the osteomalacic lesion, even though there was histochemical evidence of aluminum deposition at the bone-osteoid interface.(ABSTRACT TRUNCATED AT 250 WORDS)

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Successful Treatment of Dialysis Osteomalacia and Dementia, Using Desferrioxamine Infusions and Oral 1-Alpha Hydroxycholecalciferol

Cited by 17 publications

References 19 publications

Hypocalcemia Complicating Deferoxamine Therapy in an Infant with Parenteral Nutrition‐Associated Aluminum Overload

Hypocalcemia Complicating Deferoxamine Therapy in an Infant with Parenteral Nutrition‐Associated Aluminum Overload

Precipitation of Aluminum Encephalopathy in a Patient Receiving Deferoxamine

Aluminum intoxication in vitamin D-deficient rats: Studies of bone aluminum localization and histomorphometry before and after vitamin D repletion

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