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gungho49

Clozapine and Infection

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Sorry if I am sounding daft.

We all know that for someone on Clozapine we shud lookout for any developing infection like sorethroat etc the logic being the agranulocytosis and neutropenia caused by clozapine.

my query is what happens when clozapine causes agranulocytosis and this then leads to infection.In this case from what I understand the WCC and the neutrophil count will remain low.

So does that mean that with someone on clozapine with a clear clinical infection sorethroat, chest infection et al and their WCC and neutrophils are normal or raised then that means we dont have to get concerned about the fact of them being on clozapine. and treat it like any other infection. The only instance to get worried is if there are clinical signs of infection but WCC are low. Did I get it right :-/

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[highlight]clinical signs of infection but WCC are low. Did I get it right [/highlight]

yeah

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Sorry if I am sounding daft.

   We all know that for someone on Clozapine we shud lookout for any developing infection like sorethroat etc the logic being the agranulocytosis and neutropenia caused by clozapine.

my query is what happens when clozapine causes agranulocytosis and this then leads to infection.In this case from what I understand the WCC and the neutrophil count will remain low.

So does that mean that with someone on clozapine with a clear clinical infection sorethroat, chest infection et al and their WCC and neutrophils are normal or raised then that means we dont have to get concerned about the fact of them being on clozapine. and treat it like any other infection. The only instance to get worried is if there are clinical signs of infection but WCC are low. Did I get it right  :-/

Even if WCC count remained normal I would keep an eye, as by logic the expected increase in the count wouldnt happen if the WCC are affected.

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Recent studies reveal increased intracellular superoxide anion production and enhanced expression of pro-apoptotic genes in leukocytes of clozapine-treated patients who develop leukopenia. This suggests that oxidative stress by a chemically reactive metabolite of clozapine initiates the intrinsic apoptotic pathway leading to agranulocytosis. Clozapine and its pharmacologically active major metabolite desmethyl-clozapine do not directly produce oxidative stress in leukocytes in vitro at therapeutic concentrations. Despite a better understanding of the hematologic effects of clozapine treatment, it remains unclear why only a small percentage of clozapine-treated patients develop leukopenia and progress to agranulocytosis. Until clinical predictors of clozapine agranulocytosis can be identified, patients should continue to be intensively monitored during treatment, particularly during the initial 4–6 months of therapy when susceptibility to this blood dyscrasia appears greatest

Psychopharmacology Research Tutorial for Practitioners - Clozapine Agranulocytosis: Mechanism of Drug Toxicity

Donald S. Robinson, MD

Primary Psychiatry. 2006;13(3):27-29

http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=422

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