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  #1  
Old 05-28-2011
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Help Leukocyte Alkaline Phosphatase

Hey Guys!!
I am stuck with this. Not able to find relevant materials to understand this properly.
Wat is LAP? Why is it decreased in Paroxysmal Nocturnal Hematuria?
Can anyone give me some relevant link to find information about this LAP concept?

Thanks in advance....
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Old 05-28-2011
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Cool alp

Quote:
Originally Posted by podebrad View Post
Hey Guys!!
I am stuck with this. Not able to find relevant materials to understand this properly.
Wat is LAP? Why is it decreased in Paroxysmal Nocturnal Hematuria?
Can anyone give me some relevant link to find information about this LAP concept?

Thanks in advance....
  • Leukocyte alkaline phosphatase (LAP) is found within white blood cells. White blood cell levels of LAP can help in the diagnosis of certain conditions.
  • Higher levels are seen in polycythemia vera (PV), essential thrombocytosis (ET), primary myelofibrosis (PM), and the leukemoid reaction.
  • function:still unknown but needs an intact pituitary acess to function
  • in PNH ther is deficit in the anchorage of the protein to the plasma membraneThe defect is a missing glycosyl-phosphatidyl-inositol anchor for membrane proteins caused by an abnormality of the PIG-A gene, which is located on the X chromosome
  • PNH normal or high levels of LAP mRNA are present but defective.therefore even when wbc are broken down.the ALP is lowered instead of high as ALP synthesis was defective..
  • therefore in PNH the rbc break down n release HB .this defect not onyl in rbc but also in other cells like wbc..resulting in pancytopenia and thrombosis (plt dysfunction)
  • in short
  • enzymes deficient :ALP,ACETYL-CHOLINE ESTERASE ,DAF,MIRL
  • ALL OF THESE GLUE CELL MEMBRANE TOGETHER
  • HENCE BREAK DOWN OF CELLS
  • ALP LOW COZ defective synthesis (but not sure of this one )
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  #3  
Old 05-28-2011
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Default

While your questions wasn't specifically on PNH in general, I thought I'd share my notes on it, as I found it really difficult to wrap my head around at first, but once I got it, it didn't feel nearly as complex and elusive, so maybe the notes but be of help.

PNH
-acquired clonal stem-cell disorder
-red cell membrane is abnormally sensitive to lysis by complement (due to deficiency in complement-regulating proteins, CD55 an dCD59)
-screening: flow cytometry to show deficiency of CD59 or CD55
-can progress to aplastic anemia, myelodysplasia, or AML
-intravascular hemolysis leads to urine hemosiderin and serum lactate dehydrogenase
-tx: prednisone is best initial tx
-allogeneic BMT is curative
-eculizumab inactivates C5 in the complement pathway and decreases red cell destruction
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  #4  
Old 05-28-2011
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Default vasculopathy seen in PNH (bonus info)

I think this came up in a practice question or two...

paroxysmal nocturnal hemoglobinuria
-venous thrombosis
--esp hepatic and mesenteric venous thrombosis, also sagittal
-thromboses in the skin resulting in painful purpuric lesions resembling purpura fulminans
-mild thrombocytopenia may also be seen
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