Questions about acute megakaroblastic leukemia...?

---

1. Is AML chemorisistant like acute promyelocytic leukemia? I think I remember reading somewhere that it is, but I'm not sure.

2. According to Wikipedia, pancytopenia (the reduction of red and white blood cells as well as platelets) was a side-effect of AML. Now, in most leukemia patients, pancytopenia is caused by chemo, not the disease itself. Could someone please explain the relationship between AML and pancytopenia to me in more detail?

Thanks in advance!
-Elly :-)
Be careful with the term AML for this. "AML" usually refers to Acute Myelogenous leukemia also known as Acute Myeloblastic or Myelocytic Leukemia for which there are at least 7 types. Acute megakaryoblastic leukemia (AMKL) is classified as "M7" type in the FAB (French-American-British) classification. You can get a simple review via Wiki - which you have already done. http://en.wikipedia.org/wiki/Acute_megakaryoblastic_leukemia

Acute Promyelocytic Leukemias (FAB M3 type) are responding very well to treatment today. From http://asheducationbook.hematologylibrary.org/cgi/content/full/2006/1/147 "Cure of acute promyelocytic leukemia (APL) is now a possibility for most patients through the use of state-of-the-art treatments, which include simultaneous administration of all-trans retinoic acid (ATRA) and anthracycline-based chemotherapy for induction and consolidation, as well as ATRA-based maintenance."
Also - http://www.cancer.org/docroot/CRI/content/CRI_2_4_4x_Treatment_of_Acute_Promyelocytic_M3_Leukemia_AML.asp

Pancytopenia is a common presentation of AMKL rather than a side effect. The reason is that there is often fibrosis in the marrow space. The marrow is often "packed" with large numbers of blasts such that the production of normal red cells, white cells, and platelets is severely impeded. We see this in some cases of other AML subtypes and call this aleukemic leukemia because there is not a high white cell count in the peripheral blood. There are variations in responsiveness from one case of AMKL to another since each case has different chromosomal abnormalities, levels of fibrosis, and other characteristics which we do not completely understand at this time. Responses in all types of AML depend on a complex array of factors not all of which have been completely identified. We still have much to learn, but the bottom line is that no two patients are identical with any type or subtype of malignancy - including the many leukemias.

"MDgreg" I would expect to see reduced platelets, aberrant platelet morphology, and RBC poikilocytosis (with an elevated automated RDW) on a personal peripheral blood smear examination - which is the only way a real hematologist should evaluate someone with a blood disorder. Does anyone look at blood smears anymore? We never charged for this and it is time consuming, so maybe it's not "cost effective."  (+ info)

MDS, is there a type that is heritray?

---

Is there any type of MDS that is hereditary, my father finally got a diagnosis of MDS this week, after having pancytopenia for at least 5 years. He also has/had 2 sisters both with pancytopenia. 1 that after having low counts for years, with no sign of cancer with multiple bone marrow biopsy's, developed AML and passed 2 years ago, just 2 weeks after her cancer diagnosis. My father had 3 bone marrow biopsy's and seen 3 other hematologist before seeing a new hematologist a couple weeks ago, that did yet another biopsy. And finally was given a diagnosis yesterday, I told him 2 years ago to ask about MDS, and told him to ask this new doctor about it, but he didn't have to since he actually said this what is wrong with him.
Neither of his sisters have ever been given a diagnosis of MDS either. But look how long it took my dad to get one.
  (+ info)

is there any physician or clinical pharmacist to suggest right drugs for the case below:?

---

25 years, obese male presented to the emergency room after a sudden change in the mental status he was previously well but history of hypertention, in emergency room he show respiratory distress and increase in oxygen demand.
Previously he was afebrile(36.8c), B.P:120/60 respiratory rate of 18 breaths/min and 89%oxygen saturation after nasal canolaton-98%.
After physical examination .Left bronchi: Inflamation-rhonchi.

Assisments:
chest x-ray right mid zone and left mid zone show bilateral pneumonia
ECG findings - sinus tachycardia
rectal body temprature - 41c.
Tachypanic (High respiration)
40 breaths/min
b.p-60/40
Prescribe any antibiotic-?

blood test:
W.B.C count-17,000/dl
HB level-15.39/dl
Pletlet count-129000
Differential count-28%N
48%L
Chemistry:

Glucose-137/dl
Creatinine level-3.1mg/dl
PO2=53m/hg
Bicarbonates-15mg/dl

MRSA-Methecilin resistance staphylococcus aureus

If during this period "pancytopenia" occur
i.e,All blood cell count decreases.
What is the complication in your opinion?

if the antibiotic sugested was vancomycin...should we continue it or replace it?after having pancytopenia
which antibiotic is suitable for prophylaxis of pancytopenia induced infections?
If he was previously well x hypertension, his current main problem is the bilat pneumonia. it's probably viral pneumonia and not bacterial pneumonia so no antibiotics, treat his symptoms in the ER and have him follow up with his doc in a few days.
Not sure what you mean with the MRSA line, are you suggesting he has MRSA? Vancomycin and teicoplanin are glycopeptide antibiotics used to treat MRSA infections but several newly discovered strains of MRSA show antibiotic resistance even to vancomycin and teicoplanin. These new evolutions of the MRSA bacterium have been dubbed Vancomycin intermediate-resistant Staphylococcus aureus (VISA). Linezolid, quinupristin/dalfopristin, daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.

Good question  (+ info)

---

---

• Home
• Our method
• Usage examples
• Index

• Statistics
• Contact

---