Primary questions Concerned about permanent bone marrow suppression ; : Is this the typical progression you see in patients slowly dropping Neutrophil counts that do not recover ; ? It is common to have delays in chemotherapy because of a low ANC and 1-2 weeks is ok, if it is longer than that I would recommend a bone marrow test to evaluate for bone marrow involvement or signs of suppression from the chemotherapy. Our doctor mentioned permanent suppression; the Cladribine package insert also mentions this along with death from the suppression ; . What is meant by 'permanent' myelosuppression? Is the marrow suppressed forever? If not, for how long? There is a risk of prolonged bone marrow suppression primarily of the platelet precursors which doesn't seem to be the case for Ben ; , and in some cases it lasts for more than 2 years Also in higher doses of 2cda than used for histiocytosis ; . Does 'permanent' suppression equate to death? If the white count does not recover the patient is at risk for infections and that is what is dangerous, patients don't die of low counts but as a consequence. Should he develop a permanent problem, he may need prolonged neupogen shots or a bone marrow transplant but we are nowhere near that at all!!!! ; Is there a way we can more closely monitor to prevent permanent myelosuppression? Checking counts 2X week is the way we monitor for problems. How do you decide how many courses of Cladribine to give a patient if it appears to be working? If the 2cda is working the current thinking is to give a total of 6 courses, there are pts however who have received more. What criteria do you use to decide to continue or not? The criteria are how he is responding- if there is stable disease after 6 or worsening at anytime I would not recommend continuing with 2cda Should we be doing anything differently? So far everything seems appropriate. Secondary questions Concerned that Neupogen could actually speed up the disease, thus artificially counteracting the chemotherapy ; : We are giving Ben Neupogen, which I understand is just actually a recombinantly generated Granulocyte-Macrophage Colony Stimulating Factor. This factor, as I understand it, is partially responsible for the production on monocytes and antigen presenting cells. By giving Neupogen, are we actually 'feeding the flame'? Are we unintentionally supporting production of the lesions? As for the neupogen, it is controversial whether "it feeds the flame" we certainly would not recommend GMCSF granulocyte-macrophage colony stimulating factor not the same as GCSF ; , however in patients who have myelosuppression we are using GCSF Neupogen ; to try to keep the chemotherapy on time and decrease the risk for infection Does blood sample monocyte level somehow correlate or relate to lesion activity? Why or why not? There are no studies that I aware of regarding levels of monocytes in the blood and disease activity, also GCSF will increase the monocyte levels in the blood hope this helps and nitazoxanide.

Pretty scientific again, is it not? The conclusion should never have excluded the ciprofloxacin as a main suspected agent, because it alone causes all the optic pathologies described. Therefore, instead of concluding that linezolid, cipro and the other underlying circumstances caused this severe optic toxicity, cipro emerges unscathed and immaculate once more. The manufacturers of quinolones have done much of the same during the years. First they had to conceive trials that rendered positive results, hiding those that were negative. Then, they limited the doses and the length of the treatments of the trials so that the true toxic profile would not show up clearly. And finally, they never conducted an honest or prolonged post marketing surveillance. They devoted the money that it would have cost for surveillance to spread propaganda and gifts among doctors 1.2 billion dollars per year in gifts and incentives in the U.S. alone ; . Many of us suffer from long debilitating pains in muscles and joints caused by quinolones, with clinical symptoms and laboratory tests that show mild forms of muscle destruction, probably caused by a similar mechanism such as the one used by other drugs like the statins. However nobody in the medical class would ever even consider it as a possibility and norco.
Mak et al Endothelial Antioxidant Effects of Calcium Blockers calcium blockers remain unclear. As reviewed and observed by Dr. Henry4041: these agents do not appear to alter serum lipid levels, and the effects could not be explained entirely by the changes in calcium content in the induced atherosclerotic vessel walls; thus these agents must act through other mechanism s ; . With our findings and those of others at both the membrane and endothelial cell levels, we speculate that the antiperoxidative activities of the calcium blockers may contribute to their beneficial effects in models of atherogenesis and neupogen. In considering this key concept, three tumor categories were defined which depend critically on the availability and appropriate interpretation of high-quality hormone receptor assays and norethindrone Figure 1: Pitch Accent Labelling used in Production Study and Shape Variations Used in Perception Study vertical lines mark segment boundaries, C0 is beg. of first consonant in stressed syllable, V0 is beg. of first vowel in stressed syllable, C1 and V1 are the equivalent in the next syllable, V * is the stressed vowel, T is at the vowel mid-point, B boundary.

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