Neuraminidase inhibitors in patients with underlying airways disease.
Influenza virus infection accounts for significant morbidity, mortality, and healthcare expenditures among persons worldwide. Approximately 20,000 to 40,000 people in the US die each year as a result of influenza. Individuals most susceptible to adverse outcomes include the elderly and those with asthma, chronic obstructive pulmonary disease (COPD), heart disease, renal failure, malignancy, or immunosuppression. Prior to the AIDS epidemic, underlying respiratory disease was the greatest risk factor for influenza-related hospitalization ranking third to heart disease and malignancy for risk of mortality. Although the influenza vaccine can help prevent pneumonia and hospitalization, it is limited by less than ideal immunization rates and the possibility of viral antigenic shifts that render the vaccine ineffective. Pharmacologic interventions play an important role in the management of influenza virus infection by shortening the duration of symptoms. The advent of the neuraminidase inhibitors (NAIs) zanamivir and oseltamivir has significantly affected the treatment of influenza. Unlike NAIs, the older therapeutic options amantadine and rimantadine may cause significant central nervous system adverse effects. In addition, amantadine and rimantadine are not active against influenza B viruses, whereas NAIs are active against both influenza A and B. Post-marketing surveillance of the NAIs has revealed that bronchospasm may occur in patients with underlying respiratory disease treated with the NAI zanamivir. Recent data suggest zanamivir is effective in patients with underlying respiratory disease, but the data are insufficient to elucidate the true risk of bronchospasm. Based on post-marketing reports, zanamivir should be used with caution in patients with asthma or COPD. Although oseltamivir has not been associated with any significant respiratory adverse effects, no data exist on the safety and efficacy of this NAI in patients with underlying respiratory disease.
Williamson
John C
JC
Department of Pharmacy, Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina 27157, USA. johnwill@wfubmc.edu
Pegram
P Samuel
PS
D000081:Acetamides / Q000494:pharmacology / Q000627:therapeutic use*; D000547:Amantadine / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D000998:Antiviral Agents / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use*; D001249:Asthma / Q000150:complications*; D001986:Bronchial Spasm / Q000139:chemically induced*; D015897:Comorbidity; D006146:Guanidines; D006801:Humans; D007251:Influenza, Human / Q000188:drug therapy*; D009439:Neuraminidase / Q000037:antagonists & inhibitors*; D053139:Oseltamivir; D011358:Product Surveillance, Postmarketing; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications*; D011714:Pyrans; D012299:Rimantadine / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D012307:Risk Factors; D012794:Sialic Acids / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use*; D053243:Zanamivir
D000081:Acetamides; D000998:Antiviral Agents; D006146:Guanidines; D011714:Pyrans; D012794:Sialic Acids; D012299:Rimantadine; D053139:Oseltamivir; D000547:Amantadine; D009439:Neuraminidase; D053243:Zanamivir