Neutropenia causes

Neupogen (filgrastim G-CSF) Neutropenia caused by chemotherapy Bone marrow transplants Amgen Inc. 

Percival, S.S. 1995. Neutropenia caused by copper deficiency possible mechanisms of action. Nutr. Rev. 53(3) 59-66. 

Interleukin-11 is the first growth factor to gain FDA approval for treatment of thrombocytopenia. It is approved for the secondary prevention of thrombocytopenia in patients receiving cytotoxic chemotherapy for treatment of nonmyeloid cancers. Clinical trials show that it reduces the number of platelet transfusions required by patients who experienced severe thrombocytopenia after a previous cycle of chemotherapy. Although IL-11 has broad stimulatory effects on hematopoietic cell lineages in vitro, it does not appear to have significant effects on the leukopenia or neutropenia caused by myelosuppressive chemotherapy. Interleukin-11 is given by subcutaneous injection at a dose of 50 g/kg/d. It is started 6-24 hours after completion of chemotherapy and continued for 14-21 days or until the platelet count passes the nadir and rises to > 50,000 cells/ L. 

MYCOPHENOLATE CO-TRIMOXAZOLE Exacerbates neutropenia caused by mycophenolate Additive effect - For signs and symptoms of neutropenia, see Clinical Features of Some Adverse Drug Interactions, Immunosuppression and blood dyscrasias... 

The oxa2ohdinedione trimethadione [127-48-0] C H NO (50), at one time the dmg of choice for the treatment of absence sei2ures, has been replaced by ethosuximide (41) and valproate (49). (50) has a distinct profile from that of phenytoin but causes photophobia and night blindness in approximately 30% of the patients taking it and has the CNS and sedative properties seen for other anticonvulsants together with moderate neutropenia, hepatitis, and skin rashes (13). Trimethadione does not appear to produce its effects via modulation of GABA-mediated responses. 

Clinically, GM-CSF or G-CSF have been used to accelerate recovery after chemotherapy and total body or extended field irradiation, situations that cause neutropenia and decreased platelets, and possibly lead to fatal septic infection or diffuse hemorrhage, respectively. G-CSF and GM-CSF reproducibly decrease the period of granulocytopenia, the number of infectious episodes, and the length of hospitalization in such patients (152), although it is not clear that dose escalation of the cytotoxic agent and increased cure rate can be rehably achieved. One aspect of the effects of G-CSF and GM-CSF is that these agents can activate mature cells to function more efficiently. This may, however, also lead to the production of cytokines, such as TNF- a, that have some toxic side effects. In general, both cytokines are reasonably well tolerated. The side effect profile of G-CSF is more favorable than that of GM-CSF. Medullary bone pain is the only common toxicity. 

CBC and blood chemistries may be helpful in patients whose symptoms persist. The presence of anemia, leukocytosis, or neutropenia may provide further clues to the underlying cause. 

Adverse Effects Adverse effects are seen regularly in patients given mitoxantrone (see Table 26-3). Patients often experience bluish discoloration of the sclera and the urine for 24 hours after infusion.46 Transient leukopenia and neutropenia are common with a nadir 10 to 14 days after the infusion. Patients should avoid exposure to infectious individuals during this time.46 Patients taking mitoxantrone should not receive live virus vaccines other vaccines should be held for 4 to 6 weeks after a mitoxantrone dose.46 Amenorrhea, caused by a direct toxic effect on the ovary, may be permanent, an important consideration because the MS population includes women of childbearing potential.27... 

Bone marrow suppression ZDV Onset Few weeks to months Symptoms Fatigue, risk of T bacterial infections due to neutropenia anemia, neutropenia 1. Advanced HIV 2. High dose ZDV 3. Preexisting anemia or neutropenia 4. Concomitant use of bone marrow suppressants Avoid in patients with high risk for bone marrow suppression avoid other suppressing agents monitor CBC with differential at least every 3 months Switch to another NRTI D/C concomitant bone marrow suppressant, if possible for anemia Identify and treat other causes consider erythropoietin treatment or blood transfusion, if indicated for neutropenia Identify and treat other causes consider filgrastim treatment, if indicated... 

Infection is a primary cause of death in acute leukemia patients. The majority of chemotherapy used to treat ALL and AML can cause severe myelosupression, placing the patient at risk for sepsis from otherwise normal bacteria. It is important to recognize that symptoms and signs of infection maybe absent in a severely immunosuppressed or neutropenic patient. Fever (greater than 38.3°C, 100.9°F) in a neutropenic patient is a medical emergency. Following chemotherapy, the period of neutropenia usually reaches its nadir approximately 14 days after the... 

Neutropenia is a condition characterized by a decrease in blood neutrophil count below 1.5 X 109 cells per litre a normal blood count is (2.0-7.5) X 109 cells per litre. Its clinical symptoms include the occurrence of frequent and usually serious infections, often requiring hospitalization. Neutropenia may be caused by a number of factors (Table 10.6), at least some of which are responsive to CSF treatment. Particularly noteworthy is neutropenia triggered by administration of chemotherapeutic drugs to cancer patients. Chemotherapeutic agents (e.g. cyclophosphamide, doxorubicin and methotrexate), when administered at therapeutically effective doses, often induce the destruction of stem cells and/or compromise stem cell differentiation. 

Oral colchicine causes dose-dependent GI adverse effects (nausea, vomiting, and diarrhea) in 50% to 80% of patients before relief of the attack. Non-GI adverse effects include neutropenia and axonal neuromyopathy, which may be worsened in patients taking other myopathic drugs (e.g., statins) or in those with renal insufficiency. Colchicine should not be used concurrently with macrolide antibiotics (especially clarithromycin) because reduced biliary excretion may lead to increased plasma colchicine levels and agranulocytosis. 

Many clinicians advocate early institution of empiric IV amphotericin B in patients with neutropenia and persistent fever (more than 5 to 7 days). Suggested criteria for the empiric use of amphotericin B include (1) fever of 5 to 7 days duration that is unresponsive to antibacterial agents, (2) neutropenia of more than 7 days duration, (3) no other obvious cause for fever,... 

Adenopathy can be localized or generalized. Involved nodes are painless, rubbery, and discrete and are usually located in the cervical and supraclavicular regions. Mesenteric or GI involvement can cause nausea, vomiting, obstruction, abdominal pain, palpable abdominal mass, or GI bleeding. Bone marrow involvement can cause symptoms related to anemia, neutropenia, or thrombocytopenia. 

An intravenous infusion of PAF causes rapid (within 60 s) intravascular platelet aggregation, thrombocytopenia and platelet factor 4 release, as well as a profound and reversible neutropenia, due to enhanced aggregation and adherence of these cells. In vitro, PAF effects on neutrophils are dependent upon extracellular Ca2+ and Mg2+ and occur within 60 s of addition. The addition of inhibitors of 5-lipoxygenase activity (e.g. ETYA, 5,8,11,14-eicosatetraenoic acid and NDGA, nordihydroguaiaretic acid) - but not those... 

Infection is the most common cause of morbidity and mortality in MDS patients, accounting for 40-60% of deaths in various studies. The common infections are those normally associated with neutropenias, such as Gramnegative septicaemia and bacterial bronchopneumonias. Indeed, most MDS patients are neutropenic at some stage in their disease. Even those who do not have a neutropenia may have a defect in their neutrophil function. Many patients have clearly-defined defects in T- and B-lymphocyte functions, and variable defects in monocyte numbers or function have been described. Disorders of neutrophil function are common. Many reports indicate that phagocytosis, chemotaxis, respiratory-burst activity and degranulation are defective in some MDS patients, and hypogranulation is often observed. 

Carbimazole tends to cause neutropenia and patients are advised to report any sore throat to the pharmacist for referral. Blood counts would be required. Dry eyes are a consequence of hyperthyroidism and hypromellose eye drops could be recommended as a relief preparation. 

Undesired effects. The magnitude of the antihypertensive effect of ACE inhibitors depends on the functional state of the RAA system. When the latter has been activated by loss of electrolytes and water (resulting from treatment with diuretic drugs), cardiac failure, or renal arterial stenosis, administration of ACE inhibitors may initially cause an excessive fall in blood pressure. In renal arterial stenosis, the RAA system may be needed for maintaining renal function and ACE inhibitors may precipitate renal failure. Dry cough is a fairly frequent side effect, possibly caused by reduced inactivation of kinins in the bronchial mucosa. Rarely, disturbances of taste sensation, exanthema, neutropenia, proteinuria, and angioneurotic edema may occur. In most cases, ACE inhibitors are well tolerated and effective. Newer analogues include lisinopril, perindo-pril, ramipril, quinapril, fosinopril, benazepril, cilazapril, and trandolapril. 

Loss of hair results from injury to hair follicles gastrointestinal disturbances, such as diarrhea, from inadequate replacement of enterocytes whose life span is limited to a few days nausea and vomiting from stimulation of area postrema chemoreceptors (p. 330) and lowered resistance to infection from weakening of the immune system (p. 300). In addition, cytostatics cause bone marrow depression. Resupply of blood cells depends on the mitotic activity of bone marrow stem and daughter cells. When myeloid proliferation is arrested, the short-lived granulocytes are the first to be affected (neutropenia), then blood platelets (thrombopenia) and, finally, Liillmann, Color Atlas of Pharmacology... 

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