Goljan vs Robbins

[FutureDoc4]

Conflicting info, and I find it extremely irritating.

Cold (IgM) hemolytic anemia:

Goljan--IgM binds to surface, activates complement through the MAC--destruction (intravascular)

New Robbins--IgM at cold temperatures fixates C3b to cell surface, but does not actually cause cell destruction. Afterwards, cells are taken up in the spleen (extravascular).

This is not in the errata for Goljan's 3rd edition. Honestly, Goljans mechanism is more intuitive. However, the Robbins mechanism explains splenomegaly and susceptiblity to rupture better with a Mycoplasma infection. Thoughts?

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[ELS Marketer]

Conflicting info, and I find it extremely irritating.

Cold (IgM) hemolytic anemia:

Goljan--IgM binds to surface, activates complement through the MAC--destruction (intravascular)

New Robbins--IgM at cold temperatures fixates C3b to cell surface, but does not actually cause cell destruction. Afterwards, cells are taken up in the spleen (extravascular).

This is not in the errata for Goljan's 3rd edition. Honestly, Goljans mechanism is more intuitive. However, the Robbins mechanism explains splenomegaly and susceptiblity to rupture better with a Mycoplasma infection. Thoughts?

Hi FutureDoc4,

I work for the company that publishes both Goljan and Robbins. When I came across your post, I asked if either Drs Goljan or Kumar had any comments that could help you out. When I receive their responses, I'll post them for you.

-Lisa (Elsevier Marketing)

 

[FutureDoc4]

bump

 

[ELS Marketer]

According to both Drs Goljan and Aster, authors of the two books you referenced, the answer to your question is simple.


According to Dr Goljan, "f. you read the section on IgM-hemolysis, page 219, you can see that it can be intravascular or extravascular depending on the degree of activation of the complement system. It is usually intravascular." .


In Robbins, the relevant section in Chapter 14 is correct. It says, "IgM binding agglutinates red cells and fixes complement rapidly. As the blood recirculates and warms, IgM is released, usually before complement-mediated hemolysis can occur. However, transient with IgM is sufficient to deposit sublytic quantities of C3b, and excellent opsonin, which leads to removal of affected red cells...."


According to Dr Aster, "The key word is 'usually'. Most patients do not have evidence of substantial intravascular hemolysis, with its attendant hemoglobinemia and hemoglobinuria, and in these patients it is believed that most of the hemolysis is extravascular, due to removal of complement-coated red cells by phagocytes. As the reader points out, this is the explanation for the splenomegaly, which can be striking in some patients."


Hope that helps!
-Lisa

 

[MDpride]

does STUDENT CONSULT has exact copy of goljan?


I am thinking of using online version so that i don't have to carry around book.

Some people say HY stuff in margin is not on online version.