Haematinics II: Clinical Pharmacological and Therapeutic Aspects

Summary

The treatment of choice for iron deficiency is iron, and it can and should be given orally in sufficient quantities to restore the body’s stores to normal levels, in addition to achieving the desired elevation of the haemoglobin level. As a therapeutic agent, iron has the combined virtues of simplicity and inexpensiveness, and is most effective in producing the desired result. The simplest and most useful form of iron is ferrous sulphate, taken orally. Iron is one of the few therapeutic agents where oral therapy is more predictable and more effective than the systematically administered form. Many oral iron preparations exist, but they are no more efficient in producing an optimal haemoglobin response than ferrous sulphate. There may however, be a need in some instances to use preparations other than ferrous sulphate in an endeavour to minimise symptoms of gastro-intestinal intolerance, an aspect which has been unduly emphasised in the past. The principal benefit of slow or sustained release preparations appears to be the convenience of once-daily administration and their palatability; they do not appear to be any more efficient in delivering the desired amounts of iron to the body.

Intravenous and intramuscular iron are indicated rarely, in such instances as profound iron deficiency in a pregnant patient (to increase iron stores rapidly), where self-medication is unreliable, where there is genuine and severe gastro-intestinal intolerance, or where there is a clearly demonstratable gastro-intestinal absorbtive defect. Parenteral iron is probably mandatory where blood loss is chronic and of major proportions. Blood transfusion is seldom if ever indicated in the treatment of iron deficiency.

Iron poisoning may result from the ingestion of large quantities of iron, particularly in children for whom a fatal dose may be as little as 1 g ferrous sulphate. The treatment of iron poisoning is now well defined and includes use of the chelating agent desferrioxamine to assist in the removal of excessive amounts of the ingested iron.

Hydroxocobalamin is to be preferred to cyanocobalamin or long acting dosage forms of cyanocobalamin in the treatment of vitamin B₁₂ deficiency. The aim is to achieve a haematological remission and to replace the body stores of vitamin B₁₂. Oral vitamin B₁₂ is indicated only in the patient in whom injections are undesirable (e.g. bleeding disorder). If the response to vitamin B₁₂ therapy is poor or absent, it is likely that the megaloblastic anaemia is due to folate deficiency.

Oral administration of 5 mg folic acid is more than adequate in treating a deficiency state, even in the patient with intestinal malabsorption. Long-term folate therapy is probably required only in older people who have a nutritional deficiency which is not likely to be remedied by improvement in their dietetic habits. Prophylactic folate is probably desirable in pregnancy, given together with an iron supplement.

Because the blood volume is usually normal or increased in megaloblastic anaemia, blood transfusion is seldon if ever indicated, except in the most unusual circumstances.