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At least 739 records · Page 41Linked to original sources
PubMed1997

X-linked hypophosphatemia: normal renal function despite medullary nephrocalcinosis 25 years after transient vitamin D2-induced renal azotemia.

Nephrocalcinosis (NC) detected by ultrasound is a recognized abnormality for some patients with X-linked hypophosphatemia (XLH) who received vitamin D2 and inorganic phosphate therapy, but is commonly observed in XLH patients treated with 1,25-dihydroxyvitamin D3 and inorganic phosphate supplementation. Nevertheless, long-term follow-up of kidney function in XLH patients with NC detected ultrasonographically has not been reported. We investigated two women with XLH, ages 31 (patient 1) and 39 (patient 2) years, each of whom had suffered at least one documented episode of vitamin D2-induced hypercalcemia and renal azotemia during childhood. Patient 2 had also been treated with inorganic phosphate. No medications for XLH had been taken during adulthood. Renal ultrasonography at our institution demonstrated marked bilateral medullary NC in both women. No other explanation was found for their NC that apparently occurred several decades earlier from medical therapy for XLH. Detailed studies (including creatinine clearance, beta2-microglobulin excretion, and fasting urinary osmolality and acidification) revealed no impairment of kidney function in either patient. Our findings indicate that subradiographic medullary NC acquired during medical therapy for XLH may persist for decades, but with no adverse renal sequelae. Definitive (long-term) assessment of kidney function in the XLH population with NC, however, will be necessary to fully understand the risk of current medical treatment for this most common heritable form of rickets.

Adult↗
PubMed2002

Pathological long-bone fractures in residents with cerebral palsy in a long-term care facility in South Africa.

A high incidence of long-bone fractures has been observed in children and young adults with quadriplegic cerebral palsy in residential care. This study aimed to determine factors that contribute to these fractures and to institute preventive treatment. Twenty individuals (12 males, eight females) of a cohort of 88 residents with spastic quadriplegia in residential care in Gauteng, South Africa who had sustained fractures were compared with a random sample of age-matched control participants (10 males, 10 females) from the same facility. Participants ranged in age from 6 to 29 years (median 17.5 years). The majority of fractures were in the upper extremities. There was radiological and biochemical evidence of rickets and osteomalacia in both groups. However, the severity of the disease was more pronounced in the group with fractures. There was a significant relation (p=0.002) between the number of fractures and the use of anticonvulsant therapy (ACT). Three months of vitamin D administration (calciferol 5000 iu/day) resulted in a marked clinical improvement. There were no fractures during this period in either group. In addition, the mean serum calcium (Ca) and phosphate (Pi) levels increased (Ca from 2.17 to 2.35 mmol/L and Pi from 1.13 to 1.66 mmol/L) and mean total alkaline phosphatase level decreased (from 1123 to 423 U/L). We concluded that vitamin D deficiency was the major factor contributing to the occurrence of fractures in this population. Unless sunlight exposure can be guaranteed, vitamin D supplementation should be considered for children and adults in residential care, especially if they are on ACT, even in areas with year-round sunshine.

Adolescent↗
PubMed1974

Some properties of calciferol as a rodenticide.

The potentiality of calciferol (alone and combined with warfarin) for the control of commensal rats and mice has been examined in the laboratory. Nearly all animals fed on 0.1% calciferol for 2 days died. Though illness usually reduced food intake after the first 24 hr. there was no sign of aversion to the poison at 0.1% - which is considered to be the lowest concentration suitable for use against Rattus norvegicus, R. rattus and Mus musculus in the field. There was some indication that resistance to warfarin in R. norvegicus may be correlated with susceptibility to calciferol. Toxicity tests with calciferol combined with warfarin indicated an additive effect between the compounds. No evidence for synergism was found however, although elsewhere there is some evidence for this.

Animals↗
PubMed1974

Field trials of calciferol combined with warfarin against wild house-mice (Mus musclus L.).

A combination of calciferol (vitamin D(2)) and warfarin, each at 0.025% in medium oatmeal bait, failed to control six of seven house-mouse (Mus musculus L.) populations infesting urban and farm buildings. In three further treatments with both calciferol and warfarin at 0.05% in dehusked canary seed bait plus 5% corn oil, mortality, estimated from the consumption of pre- and post-treatment census bait, ranged between 94.2 and 97.4%. Finally, among sixteen treatments done with calciferol at 0.1% and warfarin at 0.025% in various cereal baits, the best results (97.0-100%) were obtained in six treatments where the bait-base was whole canary seed; this was so whether the poison bait was applied directly or after a 3-day pre-baiting period. It is concluded that calciferol at 0.1% plus warfarin at 0.025% is an effective combination against house-mice, especially when used with whole canary seed. The role played by warfarin in the poison mixture needs to be investigated further.

Animals↗
PubMed1974

Field trials of calciferol against warfarin resistant infestations of the Norway rat (Rattus norvegicus Berk).

The effectiveness of calciferol (vitamin D(2)) against Rattus norvegicus was investigated in field trials on twenty-three farms with rat infestations partly resistant to warfarin. At 0.01% combined with warfarin at 0.025% no rodenticidal effect of the calciferol was discernible. At 0.025% with warfarin at the same concentration, results were better, but not appreciably better than is often obtained with warfarin alone against resistant rat populations. When the concentration of calciferol was stepped up to 0.1%, four out of five treatments in which the poison was applied directly gave complete control. The fifth may have partly failed because of poison shyness caused by under-baiting. Five out of six more treatments done after ;pre-baiting' were also successful. The sixth failed for reasons unconnected with the choice of poison.Six further infestations that were not responding adequately to warfarin treatments were quickly controlled when, in three instances, calciferol at 0.1% was used instead and, in three more, it was used together with warfarin. It is concluded that calciferol at 0.1% is an effective poison against R. norvegicus either combined with warfarin or not, but that because at 0.1% its effect is subacute rather than chronic, there may be a case in some environments for using it only after pre-baiting.

Animals↗
PubMed1983

Laboratory tests of seven rodenticides for the control of Meriones shawi.

The response of Meriones shawi to seven rodenticides was investigated in laboratory feeding tests. The species proved to be much less susceptible to anticoagulants than most other species of rodent pests. Brodifacoum (at 0.005%), although giving complete mortality after only 8 days' continuous feeding, was more toxic than warfarin (0.025%), coumatetralyl (0.0375%), difenacoum (0.005%) and bromadiolone (0.005%). Calciferol (0.1%), though toxic, was significantly unpalatable. Zinc phosphide (5.0%) presented for 2 days in a choice test against unpoisoned food gave 80% mortality and appears to be the most suitable of these compounds for the control of M. shawi in the field.

4-Hydroxycoumarins↗
PubMed1984

Laboratory trials of five rodenticides for the control of Mesocricetus auratus Waterhouse.

The efficacy of five rodenticides for use in bait against the golden hamster (Mesocricetus auratus Waterhouse) was investigated in the laboratory. The species proved to be resistant to warfarin (up to 0.5%) and difenacoum (0.005%), but brodifacoum (0.005%) gave complete mortality after three days' feeding. Calciferol (0.1%), though toxic, was significantly unpalatable. Zinc phosphide (5.0%) presented in a choice test for two days against unpoisoned feed gave 100% mortality, and appears to be the most suitable of these compounds for the control of M. auratus in the field.

4-Hydroxycoumarins↗
PubMed1983

Vitamin D deficiency--a new cause of cochlear deafness.

Ten patients are reported with bilateral cochlear deafness which was associated with vitamin D deficiency. The features of these cases are discussed following an overview of the clinical aspects and diagnosis of vitamin D deficiency. The most likely pathogenesis is localized demineralization of the cochlea resulting in secondary morphological changes. Replacement therapy resulted in unilateral hearing improvement in two of the four patients in whom the response to treatment could be assessed. This suggests a previously unrecognized causal correlation between vitamin D deficiency and cochlear deafness. Impaired vitamin D activity may be important in the aetiology of otosclerosis, presbyacusis and the deafness associated with chronic renal failure. Vitamin D deficiency should be considered in the differential diagnosis of unexplained bilateral cochlear deafness. It is important, as this 'new' metabolic type of sensorineural deafness may be reversible, and may also lead to the diagnosis of early osteomalacia before more serious generalized skeletal symptoms can occur.

Adult↗
PubMed1986

Hearing-loss and calciferol deficiency.

Vitamin D (calciferol) deficiency has recently been claimed to cause cochlear hearing-loss (Brookes and Morrison, 1981; Brookes, 1983, 1984). In view of the therapeutic and pathophysiological implications of this finding, a confirmatory study was undertaken in the Department of Neuro-otology at The Royal National Throat, Nose and Ear Hospital. Screening of 112 consecutive new referrals revealed 32 patients with biochemical abnormalities compatible with vitamin D deficiency. Of these, 26 agreed to serum vitamin D assay and normal values were obtained in all of these cases. This study does not support the claim that vitamin D deficiency is a cause of hearing-loss.

Adult↗
PubMed1983

19-nor-10-ketovitamin D derivatives: unique metabolites of vitamin D3, vitamin D2, and 25-hydroxyvitamin D3.

Three metabolites were isolated after incubation of vitamin D3, vitamin D2, or 25-hydroxyvitamin D3 with bovine rumen microbes. They are identified as 5(E)-19-nor-10-ketovitamin D3, 5(E)-19-nor-10-ketovitamin D2, and 5(E)-19-nor-10-keto-25-hydroxyvitamin D3, respectively. The identifications were based on ultraviolet absorbance, mass spectroscopy, and chemical reactivity. All 5(E)-19-nor-10-ketovitamin D derivatives examined had an absorbance maximum at 312 nm and a characteristic fragment in their mass spectra corresponding to loss of 43 amu from their molecular ions. The vitamin D3 metabolite was identical in all essential spectral and chromatographic aspects with authentic synthetic 5(E)-19-nor-10-ketovitamin D3. These metabolites represent a unique pathway of vitamin D metabolism and the first characterized products of microbial vitamin D metabolism. The conversion of vitamin D and its metabolites to their 19-nor-10-keto forms likely represents a detoxification mechanism.

Animals↗
PubMed1986

Isolation and identification of 1,24,25-trihydroxyvitamin D2, 1,24,25,28-tetrahydroxyvitamin D2, and 1,24,25,26-tetrahydroxyvitamin D2: new metabolites of 1,25-dihydroxyvitamin D2 produced in rat kidney.

Three new metabolites of vitamin D2 were produced in vitro by perfusing isolated rat kidneys with 1,25-dihydroxyvitamin D2. They were isolated and purified from the kidney perfusate by the techniques of methanol-methylene chloride lipid extraction and high-performance liquid chromatography. By means of ultraviolet absorption spectrophotometry, mass spectrometry, and specific chemical reactions, the metabolites were identified as 1,24,25-trihydroxyvitamin D2, 1,24,25,28-tetrahydroxyvitamin D2, and 1,24,25,26-tetrahydroxyvitamin D2. Both 1,24,25,28-tetrahydroxyvitamin D2 and 1,24,25,26-tetrahydroxyvitamin D2 were also produced when a kidney was perfused with 1,24,25-trihydroxyvitamin D2. Thus, it becomes clear that 1,25-dihydroxyvitamin D2 is first hydroxylated at C-24 to form 1,24,25-trihydroxyvitamin D2, which is then further hydroxylated at C-28 and C-26 to form 1,24,25,28-tetrahydroxyvitamin D2 and 1,24,25,26-tetrahydroxyvitamin D2, respectively. From several recent studies, it has been well established that 1,25-dihydroxyvitamin D3 is converted into various further metabolites in the kidney as a result of chemical reactions such as C-23, C-24, and C-26 hydroxylations, C-24 ketonization, and C-23:C-26 lactonization. From our study it is obvious that 1,25-dihydroxyvitamin D2 does not undergo all of the aforementioned chemical reactions except C-24 and C-26 hydroxylations. Also, our study indicates that C-28 hydroxylation plays a significant role in the further metabolism of 1,25-dihydroxyvitamin D2. Thus, for the first time, we describe a novel further metabolic pathway for 1,25-dihydroxyvitamin D2 in a mammalian kidney.

Animals↗
PubMed1988

24,26-Dihydroxyvitamin D2: a unique physiological metabolite of vitamin D2.

A new vitamin D2 metabolite, 24,26-dihydroxyvitamin D2, has been detected in the plasma of rats fed physiologic amounts of vitamin D2. The identity of the new metabolite (isolated from cow plasma) was established by ultraviolet absorbance, mass spectroscopy, chemical reactivity, and NMR spectroscopy. Among these, the mass spectrum was unique for the presence of a peak at M-48 that was attributed to an intramolecular rearrangement involving both the C-24 and C-26 hydroxyl groups. A 300-MHz 1H NMR spectrum of 40 micrograms of metabolite indicated a downfield shift of the C-28 methyl group signal to delta 1.30 and a multiplet at delta 3.66 corresponding to the hydroxylated C-26 methyl group. We determined that the formation of 24,26-dihydroxyvitamin D2 represented a major pathway for further metabolism of 24-hydroxyvitamin D2 in rats, exceeding the formation of 24,25-dihydroxyvitamin D2. Standard bioassays revealed that 24,26-dihydroxyvitamin D2 possessed very little biological activity and most likely represents a deactivation pathway for 24-hydroxyvitamin D2.

Animals↗
PubMed1990

1 alpha-hydroxylation of 24-hydroxyvitamin D2 represents a minor physiological pathway for the activation of vitamin D2 in mammals.

C24-Hydroxylation was evaluated as a possible activation pathway for vitamin D2 and vitamin D3. Routine assays showed that 24-hydroxyvitamin D2 and 1,24-dihydroxyvitamin D2 could be detected in rats receiving physiological doses (100 IU/day) of vitamin D2; however, 24-hydroxyvitamin D3 could not be detected in rats receiving similar doses of vitamin D3. In rats, 24-hydroxyvitamin D2 was very similar to 25-hydroxyvitamin D2 at stimulating intestinal calcium transport and bone calcium resorption. The biological activity of 24-hydroxyvitamin D2 was eliminated by nephrectomy, suggesting that 24-hydroxyvitamin D2 must undergo 1 alpha-hydroxylation to be active at physiological doses. In vivo experiments suggested that when given individually to vitamin D deficient rats, 24-hydroxyvitamin D2, 25-hydroxyvitamin D2, and 25-hydroxyvitamin D3 were 1 alpha-hydroxylated with the same efficiency. However, when presented simultaneously, 24-hydroxyvitamin D2 was less efficiently 1 alpha-hydroxylated than either 25-hydroxyvitamin D3 or 25-hydroxyvitamin D2. 1,24-Dihydroxyvitamin D2 was also approximately 2-fold less competitive than either 1,25-dihydroxyvitamin D2 or 1,25-dihydroxyvitamin D3 for binding sites on the bovine thymus 1,25-dihydroxyvitamin D receptor. These results demonstrate that 24-hydroxylation followed by 1 alpha-hydroxylation of vitamin D2 represents a minor activation pathway for vitamin D2 but not vitamin D3.

Animals↗
PubMed1990

24,25,28-trihydroxyvitamin D2 and 24,25,26-trihydroxyvitamin D2: novel metabolites of vitamin D2.

Understanding of the inactivation pathways of 25-hydroxyvitamin D2 and 24-hydroxyvitamin D2, the two physiologically significant monohydroxylated metabolites of vitamin D2, is of importance, especially during hypervitaminosis D2. In a recent study, it has been demonstrated that the inactivation of 24-hydroxyvitamin D2 occurs through its conversion into 24,26-dihydroxyvitamin D2 [Koszewski, N.J., Reinhardt, T.A., Napoli, J.L., Beitz, C.D., & Horst, R.L. (1988) Biochemistry 27, 5785]. At present, little information is available regarding the inactivation pathway of 25-hydroxyvitamin D2 except its further metabolism into 24,25-dihydroxyvitamin D2 [Jones, G., Rosenthal, A., Segev, D., Mazur, Y., Frolow, F., Halfon, Y., Rabinovich, D., & Shakked, Z. (1979) Biochemistry 18, 1094]. In our present study, we investigated the metabolic fate of 25-hydroxyvitamin D2 in the isolated perfused rat kidney and demonstrated its conversion not only into 24,25-dihydroxyvitamin D2 but also into two other new metabolites, namely, 24,25,28-trihydroxyvitamin D2 and 24,25,26-trihydroxyvitamin D2. The structure identification of the new metabolites was established by the techniques of ultraviolet absorption spectrophotometry and mass spectrometry and by the characteristic nature of each new metabolite's susceptibility to sodium metaperiodate oxidation. In order to demonstrate the physiological significance of the two new trihydroxy metabolites of vitamin D2, we induced hypervitaminosis D2 in a rat using [3 alpha-3H]vitamin D2 and analyzed its plasma for the various [3 alpha-3H]vitamin D2 metabolites on two different high-pressure liquid chromatography systems.(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D 2↗