Vitamin D deficiency is common in the elderly, especially in the housebound and in geriatric patients. The establishment of strict diagnostic criteria is hampered by differences in assay methods for 25-hydroxyvitamin D. The synthesis of vitamin D3 in the skin under influence of UV light decreases with aging due to insufficient sunlight exposure, and a decreased functional capacity of the skin. The diet contains a minor part of the vitamin D requirement. Vitamin D deficiency in the elderly is less common in the United States than elsewhere due to the fortification of milk and use of supplements. Deficiency in vitamin D causes secondary hyperparathyroidism, high bone turnover, bone loss, mineralization defects, and hip and other fractures. Less certain consequences include myopathy and falls. A diet low in calcium may cause an increased turnover of vitamin D metabolites and thereby aggravate vitamin D deficiency. Prevention is feasible by UV light exposure, food fortification, and supplements. Vitamin D3 supplementation causes a decrease of the serum PTH concentration, a decrease of bone turnover, and an increase of bone mineral density. Vitamin D3 and calcium may decrease the incidence of hip and other peripheral fractures in nursing home residents. Vitamin D3 is recommended in housebound elderly, and it may be cost-effective in hip fracture prevention in selected risk groups. (Endocrine Reviews 22: 477–501, 2001)

Vitamin D Deficiency and Secondary Hyperparathyroidism in the Elderly: Consequences for Bone Loss and Fractures and Therapeutic Implications

Pentoxifylline (oxpentifylline) is an orally active haemorheological agent for the treatment of peripheral vascular disease, cerebrovascular disease and a number of other conditions involving a defective regional microcirculation. Pentoxifylline acts primarily by increasing red blood cell deformability, by reducing blood viscosity and by decreasing the potential for platelet aggregation and thrombus formation. Extensive open and placebo-controlled studies have shown that pentoxifylline 600 to 1200 mg/day for at least 6 weeks is associated with subjective and objective improvements in 60 to 100% of patients with peripheral vascular disease. The most commonly assessed clinical parameter, walking distance, is usually improved by about 100%, although much greater improvements have also been documented. Other parameters which have been clearly improved include lower limb rest pain, paraesthesia, muscle blood flow, cramps and leg ulcers. Pentoxifylline has produced consistently better results than placebo, and in those studies using comparative drugs, better results than nylidrin, adenosine and naftidrofuryl. In patients with cerebrovascular disorders, open studies with pentoxifylline, usually at a dosage of 600 to 1200 mg/day (300 to 600 mg/day in Japan), have shown marked overall clinical improvements in about 85% of patients. Symptomatic improvements in rehabilitation psychometric tests, neuromotor and speech deficits and other subjective symptoms have accompanied increased cerebral blood flow, particularly to ischaemic areas. Pentoxifylline would appear to be useful in most types of cerebrovascular disease including transient ischaemic attacks, sequelae of cerebral thrombosis and haemorrhage, and chronic ischaemic disorders. In patients with chronic cerebrovascular disease pentoxifylline 600 to 1200 mg/day conferred significant clinical benefit compared with placebo and in isolated studies proved to be superior to drugs such as co-dergocrine mesylate, adenosine and pyrithioxine. Preliminary studies indicate that pentoxifylline may also prove useful in vaso-occlusive crises of sickle cell disease, some hearing disorders, disorders of eye circulation, high altitude sickness and asthenozoospermia. Pentoxifylline is usually well tolerated when administered as the conventional controlled release formulation, gastrointestinal symptoms (about 3%) being the most common complaint, although these and other adverse effects have not occurred to a significantly greater extent than with placebo. Thus, pentoxifylline offers a well-tolerated and effective alternative to the treatment options available for patients with peripheral vascular disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Pentoxifylline. A review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic efficacy.

The ovariectomized rat model of postmenopausal bone loss

Bone metabolism and disease in chronic kidney disease

Note: This article was originally published with an incorrect version of the Acknowledgments, which appeared on p. 218 of the print version. The correct version of the Acknowledgments appeared on pp. 1–2. The corrected article is available below.

/pdf/human-health-risk-assessment-for-aluminium-aluminium-oxide-5dfetd69xm.pdf

Human Health Risk Assessment for Aluminium, Aluminium Oxide, and Aluminium Hydroxide

Vitamin D. Basic research and its clinical application.

SUMMARY

In vitamin D deficient rats the influence of diphenylhydantoin (DPH) and phenobarbital (PB) pretreatment on intestinal uptake of 45calcium and on the activity of CaBP was studied. The DPH rats show in contrast to the PB and control rats a significantly reduced intestinal uptake of 45calcium. However, the activity of CaBP was similar in all investigated groups. These results suggest a possibly special effect of DPH on the development of the calcium and bone disorders that have been observed in patients treated with anticonvulsant drugs.



RESUME

On a etudie chez des rats qui manquaient de vitamine D, l'effet d'un pre-traitement avec de la diphenylhydantoine (DPH) et du phenobarbital (PB) sur l'absorption intestinale de calcium 45 et sur l'activite du CaPB.



Les rats qui avaient du DPH, en opposition aux rats de controle et aux rats avec PB, avaient une absorption intestinale de calcium 45 significativement reduite.



L'activite du CaPB etait cependant semblable chez tous les groupes. Ces resultats suggerent un effet possible particulier de la DPH sur l'origine des troubles du calcium et du metabolisme des os, qui ont ete observes chez des patients en traitement avec des produits anticonvulsivants.

Influence of diphenylhydantoin and phenobarbital on intestinal calcium transport in the rat.

A comparative study of long-term haemodialysis patients investigated the effects of calcium acetate and calcium carbonate on concentrations of serum phosphate, calcium, and parathyroid hormone. It was demonstrated that both substances led to a significant decrease in phosphate and serum parathyroid hormone. Administration of calcium acetate reduced the serum phosphate concentration in 7 weeks from an initial value of 2.08 +/- 0.53 mmol/l to 1.51 +/- 0.39 mmol/l (P less than 0.01). Following a 1-week wash-out period, calcium carbonate reduced the serum phosphate concentration in the same patients from 1.99 +/- 0.62 mmol/l to 1.34 +/- 0.40 mmol/l (P less than 0.01). Of particular significance, however, is the fact that in relation to daily elementary calcium intake, calcium acetate was a considerably more effective binder of intestinal phosphate than calcium carbonate. During administration of calcium acetate only 1.02 g of elementary calcium were required daily in order to reduce the serum phosphate concentration. The same patients, however, required 1.88 g of elementary calcium during calcium carbonate therapy. Complementary studies investigated the influence of an accompanying calcitriol medication. In this instance, too, calcium acetate was shown to be more effective; although the patients developed hypercalcaemia with calcium acetate, this happened more often with calcium carbonate. In summary it can be said that daily calcium loading of the uraemic organism under calcium acetate therapy is reduced by nearly half as compared to calcium carbonate therapy, and that this can be achieved with the same effective decrease of the serum phosphate concentration.

The Treatment of Uraemic Hyperphosphataemia with Calcium Acetate and Calcium Carbonate: A Comparative Study

During a 19-month period we determined the incidence of bacterial infection among 39 patients treated with desferrioxamine who had end-stage renal disease and were undergoing maintenance hemodialysis. Twenty-three received desferrioxamine because of aluminum-related bone disease, and 16 because of iron overload. A control group of 193 patients on maintenance hemodialysis but without desferrioxamine was used. No difference was found in the incidence of septicemia or of all bacterial infections between the patients with aluminum-related bone disease treated with desferrioxamine and the control patients (0.12 vs. 0.12 septicemia per patient-therapy-year, p greater than 0.05; 0.23 vs. 0.26 bacterial infections per patient-therapy-year, p greater than 0.05). The incidence of septicemia in patients treated with desferrioxamine for iron overload, however, was almost three times that in the control patients (0.36 vs. 0.12 septicemia per patient-therapy-year, p less than 0.01). To assess the effect of iron overload itself, we determined the frequency of bacterial infection in patients on regular hemodialysis who have never received desferrioxamine. These were subdivided into three groups according to serum ferritin level which indicated normal or low iron stores (Group I: serum ferritin 10-330 micrograms/l, n = 125), moderate (Group II: serum ferritin 331-1000 micrograms/l, n = 49) or more advanced iron overload (Group III: serum ferritin 1001-2000 micrograms/l, n = 10). Compared to patients with normal or low serum ferritin levels (Group I), we found a significantly higher rate of bacterial infection among patients in Group II compared with Group I (0.18 vs. 0.34 infections per patient-therapy-year, p less than 0.05) and Group III compared with Group I (0.18 vs. 0.58 infections per patient-therapy-year, p less than 0.01). These results suggest that treatment with desferrioxamine does not favour the development of septicemia or bacterial infection independently of iron overload and that iron overload itself may predispose patients on regular hemodialysis to bacterial infection.

Iron Overload, but not Treatment with Desferrioxamine Favours the Development of Septicemia in Patients on Maintenance Hemodialysis

This report is about a 23-year-old man who required hemodialysis in connection with an acute renal failure resulting from uric acid nephropathy without hyperuricemia. After recovering renal function he showed extreme hypouricemia (0,1–0,3 mg/dl) and elevated uric acid clearance (100–300 ml/min). The fractional excretion of uric acid (Cua/Cer) could be suppressed by oral pyrazinamide and enhanced by probenecid. As no other renal tubular or metabolic abnormalities were detected, it is suggested that a markedly increased renal tubular urate secretion was responsible for the hypouricemia and also for the rare side-effect of an uric acid nephropathy in this patient.

K. Schaefer

Papers

Vitamin D. Basic research and its clinical application.

Influence of diphenylhydantoin and phenobarbital on intestinal calcium transport in the rat.

The Treatment of Uraemic Hyperphosphataemia with Calcium Acetate and Calcium Carbonate: A Comparative Study

Iron Overload, but not Treatment with Desferrioxamine Favours the Development of Septicemia in Patients on Maintenance Hemodialysis

Acute renal failure due to uric acid nephropathy in a patient with renal hypouricemia