Corticosteroids antineoplastic

Vaccinations containing live organisms are not administered within 3 months of immune globulin administration because antibodies in the globulin preparation may interfere with the immune response to the vaccination. Corticosteroids, antineoplastic dru, and radiation therapy depress the immune system to such a degree that insufficient numbers of antibodies are produced to prevent the disease. When the salicylates are administered with the varicella vaccination, there is an increased risk of Reye s syndrome developing. 

Although not readily quantifiable, abnormalities may exist in granulocyte function, as well as in cell numbers. Defects in phagocyte function may be caused by underlying disease (e.g., leukemia) or its treatment (e.g., corticosteroids, antineoplastic agents, and radiation). ... 

In general, hospital patients have an increased susceptibility to infection [7]. Common chemotherapeutic treatments (e.g., corticosteroids, antineoplastic agents, and antibiotics) individually and synergistically contribute to increased susceptibility [8]. This is due mainly to immune system suppression and/or altering the patient s normal flora, often with replacement by antibiotic-resistant hospital microorganisms, as previously discussed. 

Treatment Discontinue or minimize immunosuppressants Surgical, radiologic, or antineoplastic therapy Do not abruptly withdraw corticosteroids... 

Uses Severe, systemic fungal Infxns oral cutaneous candidiasis Action Binds ergosterol in the fungal membrane to alter permeability Dose Adults Peds. Test dose 1 mg IV adults or 0.1 mg/kg to 1 mg IV in children then 0.25—1.5 mg/kg/24 h IV over 2-6 h (range 25—50 mg/d or qod). Total dose varies w/ indication PO 1 mL qid Caution [B, ] Disp Inj SE -l K+/Mg2+ from renal wasting anaphylaxis reported, HA, fever, chills, nephrotox, X BP, anemia, rigors Notes X In renal impair pre-Tx w/ APAP antihistamines (Benadryl) X SE Interactions T Nephrotoxic effects W/ antineoplastics, cyclosporine, furosemide, vancomycin, aminoglycosides, T hypokalemia W/ corticosteroids, skeletal muscle relaxants EMS May cause electrolyte imbalances, monitor ECG OD May effect CV and resp Fxn symptomatic and supportive... 

Whereas idiopathic OM often resolves, spontaneously or after administration of intravenous immunoglobuline or corticosteroids [58], the outcome of paraneoplastic OM is more variable and depends on the tumor response to therapy. Children with paraneoplastic OM frequently respond to chemotherapy, adrenocorticotropic hormone, or immunomodulation [223], The response to immune therapy in adults with paraneoplastic OM is very modest, but prompt tumor therapy, immunomodulation, and depletion of IgG may be of some benefit [62, 224], Without antineoplastic therapy, the prognosis is usually poor, and symptoms often progress, ultimately causing death [62],... 

Clinically important, potentially hazardous interactions with altretamine, amikacin, aminoglycosides, antineoplastics, bleomycin, busulfan, carboplatin, carmustine, chlorambucil, cisplatin, corticosteroids, cyclophosphamide, cytarabine, dacarbazine, dactinomycin, daunorubicin, docetaxel, doxorubicin, estramustine, etoposide, fludarabine, fluorouracil, gemcitabine, gentamicin, hydroxyurea, idarubicin, ifosfamide, indomethacin, kanamycin, levamisole, lomustine, mechlorethamine, melphalan, mercaptopurine, methotrexate, mitomycin, mitotane, mitoxantrone, neomycin, pentostatin, plicamycin, procarbazine, streptomycin, streptozocin, thioguanine, thiotepa, tobramycin, tretinoin, uracil, vinblastine, vincristine, vinorelbine... 

Immunodeficiency diseases High-dose corticosteroids Immunosuppressants Antineoplastic agents Central venous catheters Total parenteral nutrition (TPN)... 

Mitotane is an antineoplastic agent. The primary action is on the adrenal cortex. The production of adrenal steroids is reduced. The biochemical mechanism of action is nnknown. Data suggest that the drug modifies the peripheral metabolism of steroids and directly suppresses the adrenal cortex. Use of mitotane alters the peripheral metabolism of cortisol, even though plasma levels of corticosteroids do not fall. The drug causes increased formation of 6-beta-hydroxycortisol. Mitotane, a chlorophenothane (DDT) analog with antineoplastic properties (1 to 6 g p.o. daily in divided doses), is used in the treatment of inoperable adrenocortical cancer. 

These interaetions are not firmly established, but good pulmonary function monitoring appears to be advisable when colony-stimulating factors are used with antineoplastics causing pulmonary toxicity, such as bleomycin. If interstitial pneumonia occurs, the drugs should be discontinued and high-dose corticosteroids started immediately. More study is needed. Consider also Cyclophosphamide + Colony-shmulating factors , p.625. 

There seems to be little clinical confirmation that the potential interactions with the drugs listed above, other than corticosteroids (which found the opposite of the predicted effect) have clinical relevance, but good monitoring would be a prudent precaution. See also Antineoplastics -i-Protease inhibitors , p.615. 

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