Eithne01,
The treatment of chronic myeloid leukemia (CML) has changed significantly since the late 1990s, with the development and subsequent approval by the Food and Drug Administration of imatinib (in 2001), the first of a class of medications called tyrosine kinase inhibitors, which target the specific abnormality that causes CML.
Before that time, patients were treated with other therapy, including interferon and bone marrow transplant, and had very poor outcomes.
Are you currently on any medication like imatinib? The neutropenia can be due to your current medication. You can ask your hematologist for G-CSF injection if you have persistent neutropenia. Patients with CML are immunocompromised and can easily acquire infections. Neutropenia also puts a patient in an immunocompromised state.
For now, it is very important to prevent acquiring any infection. You should avoid crowded places and persons with ongoing infection.
Good luck.
Hi.
Chronic Myelogenous Leukemia (CML) is a blood disorder caused by an acquired genetic defect in the pleripotent stem cell. It has several phases: indolent chronic or stable phase, aggressive or advanced phase, and accelerated and blastic phase. The transition between phases may take years (on the average, 4 to 6 years from the stable phase to aggressive phase).
The LDH is high and now he wants us to do FISH BCR-ABL test. We were worried and we took some second opinions to find out the the WBC count is High in Pregnancy and LDH count can also go high. Now we are not sure if we should do this test or not. Can any one help in this please...
A definite diagnosis of chronic myelogenous leukemia (CML) is made by demonstrating the existence of the Philadelphia chromosome on cytogenetic studies of the bone marrow cells (harvested by bone marrow biopsy) or by detecting the bcr-abl gene (this is the defective gene responsible for the CML) by means of a test called polymerase chain reaction or PCR. If these two tests were not done, I can't see how a diagnosis of CML can be made.
Average survival rates are generalizations, not applicable to a particular patient. The prognosis is relatively good. Newer techniques are being tried, including imatinib and stem cell transplantation.
All the best, and God Bless!
I tried to weigh more than my hubby, didn't work.
There are no non-mecdication ways that have worked for me, and I've tried pretty much everything. I could "survive", but I wouldn't b abl to get anything done.Many alternative treatments require an investment of either time or money that I don't have. I can't rally just kind of "talk to my doctor": since the most likely rsponse I'd get is that I shouldn't be having a kid now anyway, plus I'm uninsured, making it an expensive hassle . .
TY for the reply. Yes I was told and am thinking that its parasitc or allergy. I went to aruba in June but that wouldn't have an affect on me now, would it?
Therapy with corticosteroids is used for the treatment of most and additional therapy is available and dependent upon the type of HS. Newer medicines such as imatinib and mepolizumab are said to be promising. So, should your son have HS, there is reason to be optimistic regarding a positive response to currently available therapy.
You should request, of his doctor, an additional explanation for the tentative diagnosis of pre-hypertension.
Good luck.
I am in the same boat as yall. I have a 6, 5 and 18 month old. I will be having my baby in march and we are looking at suburbans with 3rd row seat. I drive a 4 door chevy truck right now and it is hard with 3 car seats in the back.
i never had sex with any body, I started masturbation from 17 age, from that day i masturbating daily twice, 2 to 3 years back i abl to do 2 times per week now i able to do only twice a month. now i feeling very bad what i did, i am going to marry in 6 months as per my mother saying i am avoiding marriage because, i think i not able satisfy my wife daily, disturbed too much, some times i loose memory, no concentration on my work. & feel what peoples thinking on me. i feel bad.
The ensuing chronic inflammation leads to local pathologic anatomic changes, namely, periodontal pocket formation, clinical attachment loss (CAL), and alveolar bone loss (ABL) [20]. As the disease progresses and more bone is lost, junctional epithelium at the bottom of the periodontal pocket migrates apically along the root surface and the pocket depth increases. Untreated periodontitis eventually leads to tooth loss.
Recommended
