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Answer to your Health Question

Question (04/30/2013):

Title: ITP and alcohol

I would like to know how severely alcohol affects a person with ITP.

I would have moderate alcohol, and yet behave as though I had been drinking more!

I would be questioned and people would think I was being dishonest about the quantity of alcohol I had consumed. I became very disillusioned and depressed, as I always enjoyed a couple of glasses of wine, but it was thought that through my behavior, I had had much more.

I would like to get clarity on what alcohol does to you if you have ITP.



Dear Celia,

Thank you very much for your question.

According to Cowan DH , ample data exist indicating that alcoholism profoundly affects the hemostatic mechanism.

In alcoholic patients without cirrhosis, the primary effect is on the blood platelet. Both quantitative and qualitative abnormalities appear during ethanol ingestion.

Alcohol-related thrombocytopenia appears to be due to a combination of events: an increased rate of platelet destruction leading to decreased platelet survival and ineffective thrombopoiesis resulting in decreased effective platelet production.

The qualitative abnormalities are also multiple and include decreased platelet aggregation, release, and procoagulant activity and decreased storage pool nucleotides, cyclic AMP, and MAO activity.

The functional and metabolic abnormalities are associated with striking disturbances in ultrastructural morphology.

These defects cause prolongation of the bleeding time and place affected patients at risk for hemorrhagic complications.

The relationship between the quantitative abnormalities and the occurrence of thrombocytopenia is obscure, although their severity appears to increase in parallel.

The various defects are readily corrected after cessation of drinking. Hence, their long-term significance, absent development of cirrhosis, is questionable.

In alcoholic patients with cirrhosis, both platelet abnormalities and coagulation defects may be present. Which predominates in severity varies with each individual.

Due to the chronicity of the underlying clinical state, the duration of the defects is more likely to be prolonged if not permanent.

In addition, owing to the mechanism of their development, treatment or correction of the defects is difficult and of transitory benefit.

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