Why Has Cyanocobalamin Not Been Withdrawn?

Freeman, A. G.; Wilson, John; Foulds, W.S.; Phillips, C I

doi:10.1016/s0140-6736(78)90900-5

Cited by 11 publications

(2 citation statements)

References 8 publications

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“…If injected, cyanocobalamin is poorly retained and some patients may fail to respond or even have side effects such as muscular pains, possibly due to inability to process cyanide. There is thus a case for withdrawal of this drug [ 34 ]. Oral treatment is based on the finding that when large doses of vitamin B 12 are given orally, sufficient amounts are absorbed, even in the absence of intrinsic factor.…”

Section: Treatmentmentioning

confidence: 99%

Imerslund-Gräsbeck syndrome (selective vitamin B12 malabsorption with proteinuria)

Gräsbeck

2006

Orphanet J Rare Dis

141

163

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Imerslund-Gräsbeck syndrome (IGS) or selective vitamin B 12 (cobalamin) malabsorption with proteinuria is a rare autosomal recessive disorder characterized by vitamin B 12 deficiency commonly resulting in megaloblastic anemia, which is responsive to parenteral vitamin B 12 therapy and appears in childhood. Other manifestations include failure to thrive and grow, infections and neurological damage. Mild proteinuria (with no signs of kidney disease) is present in about half of the patients. Anatomical anomalies in the urinary tract were observed in some Norwegian patients. Vitamin B 12 absorption tests show low absorption, not corrected by administration of intrinsic factor. The symptoms appear from 4 months (not immediately after birth as in transcobalamin deficiency) up to several years after birth. The syndrome was first described in Finland and Norway where the prevalence is about 1:200,000. The cause is a defect in the receptor of the vitamin B 12 -intrinsic factor complex of the ileal enterocyte. In most cases, the molecular basis of the selective malabsorption and proteinuria involves a mutation in one of two genes, cubilin (CUBN) on chromosome 10 or amnionless (AMN) on chromosome 14. Both proteins are components of the intestinal receptor for the vitamin B 12 -intrinsic factor complex and the receptor mediating the tubular reabsorption of protein from the primary urine. Management includes life-long vitamin B 12 injections, and with this regimen, the patients stay healthy for decades. However, the proteinuria persists. In diagnosing this disease, it is important to be aware that cobalamin deficiency affects enterocyte function; therefore, all tests suggesting general and cobalamin malabsorption should be repeated after abolishment of the deficiency.

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Section: Treatmentmentioning

confidence: 99%

Imerslund-Gräsbeck syndrome (selective vitamin B12 malabsorption with proteinuria)

Gräsbeck

2006

Orphanet J Rare Dis

141

163

View full text Add to dashboard Cite

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“…It would seem that nifedipine merits some consideration as an alternative to vasodilators when third-line antihypertensive therapy is required, since it may be better tolerated than the other preparations currently available. Both hydrallazine and prazosin may produce serious but usually reversible dosedependent side effects1 2-for example, 10 Hypernephroma SIR,-I have read with profit your leading article (14 March, p 844) entitled "Hypernephroma," which summarised the many pathological, clinical, and therapeutic facets of this interesting neoplasm. May I, however, add another clinical pointer to your conspectus ?…”

Section: S S Chatterjeementioning

confidence: 99%