Etoposide phosphate, the water soluble prodrug of etoposide

  title={Etoposide phosphate, the water soluble prodrug of etoposide},
  author={Remko Bakker and Dees P. M. Brandjes},
  journal={Pharmacy World and Science},
An elevated plasma homocysteine level may result from various enviromental and genetic factors. Hereditary causes of severe hyperhomo-cysteinaemia are very rare and usually lead to disease in childhood or adolescence. Common pathology consists of early atherosclerotic vascular changes, arterioocclusive complications and venous thrombosis. Mildly elevated genetically determined plasma homocysteine levels are observed in 5% of the general population. In the last two decades research has shown… 


Hyperhomocysteinaemia: a newly recognized risk factor for vascular disease.
  • G. Boers
  • Medicine, Biology
    The Netherlands journal of medicine
  • 1994
Mild hyperhomocysteinaemia can be reduced to normal in virtually all cases by simple and safe treatment with vitamin B6, folic acid, and betaine, each of which is involved in methionine metabolism, which could make large-scale screening mandatory for this risk factor.
Prevalence of Moderate Hyperhomocysteinemia in Patients with Early-Onset Venous and Arterial Occlusive Disease
The aim of this study was to evaluate the prevalence of moderate hyperhomocysteinemia and of established disorders of inherited thrombophilia in a series of consecutive patients with early-onset venous or arterial occlusive disease.
Homocystinuria: what about mild hyperhomocysteinaemia?
Pooled data from a large number of studies demonstrate that mild hyperhomocysteinaemia after a standard methionine load is present in 21% of young patients with coronary artery disease, in 24% of patients with cerebrovascular disease, and in 32% of Patients with peripheral vascular disease.
The natural history of homocystinuria due to cystathionine beta-synthase deficiency.
An international questionnaire survey has been conducted to define better the natural history of homocystinuria due to cystathionine beta-synthase deficiency and permit evaluation of treatment. Data
Hyperhomocysteinaemia and endothelial dysfunction in young patients with peripheral arterial occlusive disease
Pyridoxine plus folic acid treatment normalizes homocysteine metabolism in virtually all patients, and appears to ameliorate endothelial dysfunction.
A new inborn error of metabolism was found in two mentally retarded children. The excretion of homocystine was accompanied in one boy by ectopia lentis, failure to thrive, poor developmental
High prevalence of hyperhomocyst(e)inemia in patients with juvenile venous thrombosis.
It is indicated that moderate hyperhomocyst(e)inemia is associated with an increased risk of developing venous thromboembolism at a young age and that measurements of fasting and postmethionine plasma homocyst (e)ine levels may be useful in the evaluation of patients with juvenile venous Thrombosis, particularly if their family history suggests the presence of an inherited abnormality.
Intermediate homocysteinemia: a thermolabile variant of methylenetetrahydrofolate reductase.
Evidence of a hitherto undescribed mutant MTHF reductase is provided in two patients with intermediate homocysteinemia, suggesting that a moderate deficiency of MTHf reduct enzyme might be associated with vascular disorders in adult life.