Re: Zidovudine and Anaemia: Imp Observations

[Guest guest]

Dear Forum,

Dr. Diwakar Tejaswi has pointed an important issue but I think we need to do

little more work up before blaming our Iron reserve /generics.

It accepeted that Zidovudine indused anemia is much more common in advanced

disease compared to early disease(1% vs 7%). This can be either Bone marrow

suppression or Megaloblastic change. Also, if an individual with advanced

disease gets anemia we should also look into other possibilities like TB of bone

marrow, parvo virus infection, immune reconstitution syndrome and his/her food

habits and gastric intolerance to drugs which leads to decreased food intake.

If the no of patients remain high even after ruling out all these causes we

should be worried.

There are reports of side effects of ZDV indused anemia and Stavudine induced

toxicities from various parts of the country and it is likely that we will start

seeing more ZDV induced problems in the near future following a shift in NACO

policy to start more patients on ZDV based regimen –a positive shift from

Stavudine based regimen .

This is not to underestimate the possibility of a real problem. I am happy to

see some posting on the problems of ART program from clinicians in this forum.

Dr. Ajithkumar.K

Medical college, Trichur, Kerala.

e-mail: <trc_ajisudha@...>

[Guest guest]

Dear FORUM,

Re: Dr. Diwakar Tejaswi's correspondence on Zidovudine and Anaemia: Imporatant

Observations.

Dr. Diwakar Tejaswi is right in being concerned about anemia in patients taking

AZT.

But reports show that only about 1% of patients (in contrast to your group 12%!)

on AZT develop severe anemia and need to switch the drug. These reports are

mostly from developed countries and as you said better nutrition also decreases

the risk of anemia. But, there are also other risk factors for anemia in

patients taking AZT some of which should explain your problems;

-Preexisting anemia

-Advanced stage disease ( your cases were 'full blown AIDS')

-High viral load

-Some opportunistic infections like disseminatedTB /MAC coinfections

-Other heamatotxic drugs - Cotrimoxazole, Acyclovir,..

Normally upto 25% of patients may show decrease in heamoglobin level in the

first few weeks which stabilizes in most after the first three months. So the

danger of AZT is in the first few critical weeks and not later.

D4T is nowadays being left out of the recommendations for Firstline ART (see new

WHO 2006 guideline) the preferred drugs now are if available TDF and ABC

otherwise AZT.

To conclude, for everyone concerned with this toxicity there may be one way out.

This is starting patients with D4T based regimen and after six months when

patients have good health and stabilized heamoglobin switch them to AZT based

regimen. D4T toxicities like neuropathy and lipodystrophies, lactic acidosis are

more common in the long term after six months of therapy.

For your second question I don't have much to say as you have answered it well.

The magnitude of new infections happening does not correspond with the

theoretical transmission risks definately and the reason is that there are

multiple factors that can amplify transmission by increasing the viral load in

the transmitted fluid or increasing the entry points. The main factors

implicated are STDs, early and late HIV.

Other febrile illnesses also amplify viral replication and presence in the

transmitted fluid. Contraceptives like Spermicides and oral contraceptives have

also been implicated in increasing risk of transmission by causing inflammatory

changes in the female genitaltract.

I hope I helped! pls report what happened to your anemic cohort inlong term

Good luck

Dr. Tewodros Woldemariam Teketel

e-mail: twoldema@...