Pulmonary Eosinophilia Medication
- Author: Jussi J Saukkonen, MD; Chief Editor: Zab Mosenifar, MD more...
Medication Summary
For extrinsic diseases, remove any offending agent. Treat parasitic infections with the appropriate antibiotics. ABPA and other diseases with prominent wheezing are managed with bronchodilators, inhaled corticosteroids, and, for exacerbations, systemic corticosteroids. Use systemic corticosteroids judiciously in individuals with parasitic infection.
Intrinsic diseases are generally managed with oral or intravenous corticosteroids. CSS is also occasionally treated with cyclophosphamide or azathioprine. IHES is usually initially treated with systemic corticosteroids, with half the patients responding. Other treatments for IHES include cyclophosphamide, azathioprine, busulfan, and others.
Take care to establish a diagnosis or to at least rule out parasitic or cryptococcal infection before treating the patient with steroids because of the risk of dissemination.
Corticosteroids
Class Summary
Eosinophils are exquisitely sensitive to steroids. These medications inhibit eosinophil egress from the vascular compartment, inhibit their chemotaxis, and decrease eosinophil survival.
Prednisone (Sterapred)
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. May be used in both extrinsic diseases (eg, ABPA, trichinosis, TPE, toxocariasis) and intrinsic diseases. Doses vary depending on disease and severity. Low-dose suppression may be needed in some cases.
Methylprednisolone (Solu-Medrol, Medrol)
Decreases inflammation by suppressing migration of PMN leukocytes and reversing increased capillary permeability. Administered IV for severe disease. Doses vary depending on disease and severity.
Bronchodilators
Class Summary
Provide symptomatic relief of dyspnea from bronchospasm. Do not use as sole management of these diseases.
Albuterol (Proventil, Ventolin)
Relaxes bronchial smooth muscle by action on beta-2 receptors, with little effect on cardiac muscle contractility.
Antifungals
Class Summary
Most of the fungal diseases discussed do not require specific antifungal treatment. For disseminated, severe, or invasive fungal infection, amphotericin B is administered IV. Short-term itraconazole can improve symptoms in ABPA and may have a steroid-sparing effect. Itraconazole is generally reserved for steroid-refractory cases.[25] Fluconazole and other azoles have been used in the treatment of patients who are stabilized with progressive or disseminated coccidioidomycosis. Various agents are available for treatment of P carinii pneumonia.
Coccidioidomycosis does not usually require treatment, but treatment is required for immunocompromise or progressive or disseminated disease. Itraconazole can be used for mild-to-moderate disease, and it is also used for treatment of blastomycosis.
Itraconazole (Sporanox)
Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes. Used anecdotally, with steroid-sparing effects, in several patients with ABPA or aspergilloma, but benefit has not been proven.
Available as tab, PO, and IV solutions. Duration of therapy depends on disease and clinical response, but is generally months.
If patient has invasive Aspergillus infection, is eating well, has good GI function, and is not on medication that reduces gastric acidity or induces cytochrome P-450, can use as alternative to amphotericin B.
Highly protein–bound with poor CSF penetration. Should not be used to treat primary meningitis.
Fluconazole (Diflucan)
Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. Used as first-line treatment of progressive or disseminated coccidioidomycosis or in host who is immunocompromised.
Also used in candidal and cryptococcal infections.
Dosage, dose intervals, and duration of therapy vary with age and illness.
Amphotericin B (Fungizone)
Produced by a strain of Streptomyces nodosus. Can be fungistatic or fungicidal. Binds to sterols, such as ergosterol, in the fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death.
Used for severe or life-threatening fungal infections (eg, invasive aspergillosis, blastomycosis, candidiasis, disseminated histoplasmosis, zygomycoses, penicilliosis, sporotrichosis, progressive or disseminated coccidioidomycosis).
No benefit demonstrated in aspergilloma.
Available as nonlipid form, which is less expensive. Also available as lipid, liposomal, or cholesteryl complexes, which achieve higher tissue levels, are cleared more rapidly, and have larger volumes of distribution. The latter forms are used in individuals intolerant of or refractory to nonlipid therapy. Liposomal form is used in patients who are refractory, those with renal insufficiency, or those intolerant of nonlipid form. Lipid forms have less toxicity than nonlipid form.
Antiparasitic agents
Class Summary
Several of the azoles inhibit microtubule assembly and, in some instances, glucose uptake. Albendazole is a preferred agent because of the low incidence of adverse effects, in contrast to thiabendazole.
Albendazole (Albenza)
Decreases ATP production in worm, causing energy depletion, immobilization, and finally death. First-line agent for ascariasis, hookworm, strongyloidiasis, and C sinensis infection. Alternative agent for visceral larva migrans.
Efficacy in echinococcal disease not demonstrated but is used in conjunction with surgery.
Mebendazole (Vermox)
Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell. For treatment of ascariasis, hookworm infection, and toxocariasis. Alternative agent for visceral larva migrans and trichinosis.
Thiabendazole (Mintezol)
Inhibits helminth-specific mitochondrial fumarate reductase. Alleviates symptoms of trichinosis during invasive phase. Little value in disease that spreads beyond lumen of intestines because absorption from GI tract is poor. Alternative agent for treatment of strongyloidiasis, toxocariasis, and hookworm infection (eg, Necator species, Ancylostoma species).
Ivermectin (Mectizan)
First-line therapy for strongyloidiasis and filariasis (W bancrofti or B malayi). Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death.
Praziquantel (Biltricide)
DOC in most infections and active against all schistosomal species. Increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. In addition, produces vacuolization and disintegration of schistosome tegument. This is followed by attachment of phagocytes to parasite and death.
Tabs should be swallowed completely with some liquid during meals. Keeping tabs in mouth may reveal bitter taste, which can produce nausea or vomiting.
Diethylcarbamazine (Hetrazan)
First-line therapy for visceral larval migrans. Alternative therapy for filariasis. Not generally available in United States but possible through Wyeth-Ayerst or Parasite Disease Service of CDC.
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