Autoimmune hemolytic anemia

[aspiringmd1015]

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Hey guys, really would appreciate if someone could clear my concept about this. My question is, for those drugs that cause side effects related to anemia's thrombocytopenias leukopenia's etc. are these due to a hapten sort of reaction? where the drug when binding to the membranes of these blood cells allows the immune system to recognize them(due to the hapen response) and then initiate destruction? and if so, how does this relate to immune hemolytic anemia, concept is really unclear about all of this. Someone help, please!

 

[scoKraz4]

There 2 main mechanisms by which drugs can cause an autoimmune hemolytic anemia. Drug-DEpendent and drug-INdependent.
In drug-dependent there are 2 different ways: 1) Hapten-drug adsorption and 2) Immune complex.
1) In hapten-drug, the classic examples are penicillins/cephalosporins. The drug will then form a complex with proteins on the surface of the RBC and cause lysis via a complement mediated pathway (minor) or extravascular hemolysis (major). This is a Type II hypersensitivity reaction.
2) In the immune complex pathway the class examples are quinidine/quinine. Anti-drug antibodies bind the free floating drug to make a floating immune complex that can then deposit in tissues and RBC's. Complement is activated and lysis occurs. This is a Type III hypersensitivity reaction and is primarily intravascular hemolysis

The classic drug-independent example is alpha-methyldopa. The reason why it is called drug-independent is because the autoimmune reaction occurs even after withdrawing the drug. This is a warm (IgG) hemolytic anemia. Introduction of the drug stimulates auto-antibodies against Rh blood group antigens on RBC's causing lysis. This is a Type II hypersensitivity.

Hope this helps.

 

[aspiringmd1015]

so the classic drug independent example would be an exmaple of molecular mimicry? thanks for the help man

 

[scoKraz4]

I'm not sure if it is molecular mimicry or if the drugs are modifying surface proteins to appear foreign.