ACE INHIBITORS REDUCE RISK OF PNEUMONIA IN ASIAN PATIENTS

The literature has suggested that angiotensin-converting enzyme (ACE) inhibitors may confer protection against pneumonia in elderly patients. In a recent study, Ohkubo et al confirmed that ACE inhibitor use reduces the risk of pneumonia in Asian patients, but they were unable to make any clinical recommendations from these findings.

PROGRESS (the Perindopril Protection Against Recurrent Stroke Study) randomized 6,105 patients with a history of stroke from 172 centers in 10 countries. After completing a four- to six-week run-in period, during which they took 2 to 4 mg of perindopril daily, patients either continued receiving perindopril at 4 mg/d or were given an identical placebo. They were evaluated five times during the first year and every six months thereafter. At each visit, patients reported the occurrence of major health-related events, including pneumonia. The cause of death was reviewed for all patients who died during the study. In addition, blood samples were obtained, and genotyping of the ACE insertion/deletion (ACE I/D) polymorphism was done using polymerase chain reaction.

Thirty-nine percent of the patients were Asian, and 61% were non-Asian. The median length of follow-up was 3.9 years. Pneumonia occurred in 3.8% of the treatment group and 4.7% of the placebo group. There was a significant reduction of risk in the subgroup of treated patients who were of Asian ethnicity (the relative risk reduction was 47%), but no significant reduction in risk was seen in the non-Asian patients.

Some of the ACE polymorphisms were more common in the Asian patients than in the other subgroups. However, ACE I/D polymorphisms did not appear to affect either patients’ risk of pneumonia or their likelihood of deriving protection against pneumonia from perindopril.

The authors concluded that ACE inhibitors might protect against pneumonia in some patients, but there was no conclusive evidence that they should be considered a therapeutic option.

Ohkubo T, Chapman N, Neal B, et al. Effects of an angiotensin-converting enzyme inhibitor–based regimen on pneumonia risk. Am J Respir Crit Care Med. 2004;169:1041-1045.

PNEUMOCOCCAL VACCINE NARROWS RACIAL DISPARITY IN DISEASE INCIDENCE

African-Americans have historically had a higher incidence of invasive pneumococcal disease than do white Americans. The widest disparities have been noted among two age-groups: children younger than 2 and adults. A study by Flannery et al evaluated the effects of the pneumococcal conjugate vaccine on disease prevalence for young children. The research team found that use of the childhood pneumococcal vaccine has reduced the racial disparity in disease incidence.

CDC data were used to calculate pneumococcal disease incidence rates for 1998 through 2002. Vaccine coverage rates in children between ages 19 and 35 months were calculated for 2001 (n = 3,576) and 2002 (n = 3,597) using data from the National Immunization Survey.

Incidence rates for pneumococcal disease dropped in all populations after the vaccine was introduced. The differences in incidence between white and African-American children decreased by 60%, from 35.9 cases/100,000 in the prevaccine period to 14.4 in 2002.

By 2002, the incidence of pneumococcal disease caused by the seven vaccine serotypes had decreased by 87% in white children and by 92% in African-American children. The use of the pneumococcal conjugate vaccine contributed to the decrease in disease risk among black children.

Flannery B, Schrag S, Bennett NM, et al. Impact of childhood vaccination on racial disparities in invasive Streptococcus pneumoniae infections. JAMA. 2004;291:2197-2203.

M PNEUMONIAE INFECTION CAN TRIGGER ASTHMA IN CHILDREN

Recent research has suggested a possible role for Mycoplasma pneumoniae in the pathogenesis of asthma. A prospective study by Biscardi et al tested children who visited the emergency department with asthma for acute infections with M pneumoniae or Chlamydia pneumoniae. They found that in children who are predisposed to develop asthma, M pneumoniae infection may trigger its onset.

All children ages 2 to 15 years who were hospitalized for severe acute asthma at one institution between January 1999 and June 2001 were included. Nasopharyngeal samples were taken to test for various respiratory pathogens using polymerase chain reaction. Blood samples were used to test for immunoglobulin (Ig) G and IgM specific for M pneumoniae and C pneumoniae. Two to four weeks later, blood samples were again taken, and testing was repeated.

Patients were divided into two groups according to their asthma history. Group 1 included patients with known asthma; group 2 included children whose initial emergency department visit had been their first asthma attack. Allergic children who were examined as outpatients served as the controls.

Group 1 included 119 children. M pneumoniae was detected in 24 (20%), and four had C pneumoniae infection. Chest radiographs revealed pneumonia in 17 children, four of whom had M pneumoniae infection.

There were 51 children in group 2. Twenty-six children (50%) were diagnosed with M pneumoniae infection—22 had positive IgM in their initial serum sample and four in their second sample. C pneumoniae infection was detected in three children. Chest radiography indicated pneumonia in eight children, five of whom tested positive for M pneumoniae. Fifty-two percent of group 2 children had a family history of asthma or atopy, 27% had a history of atopic dermatitis, and 51% had elevated serum IgE levels.

Only eight (5%) of the 152 controls had evidence of M pneumoniae infection. Testing for C pneumoniae was performed in 120 of the controls; results were positive in three cases.

During the year after hospitalization, asthma recurred in 15 of the 26 group 2 patients diagnosed with M pneumoniae, and in all three who had C pneumoniae infections. Four patients in group 2 did not initially receive macrolide treatment. All four had a severe asthma attack within three weeks of initial hospitalization, and two of these required intensive care. None of the children in the control group had any recurrence of asthma or allergy symptoms resulting in admission to the hospital or emergency department.

Biscardi et al suggest that about one half of first severe asthma attacks in children can occur during an infection with M pneumoniae. In addition, in children with M pneumoniae who are having their first asthma attacks, failure to give macrolides greatly increases the risk of a subsequent severe attack requiring hospitalization or admission to the ICU.

Biscardi S, Lorrot M, Marc E, et al. Mycoplasma pneumoniae and asthma in children. Clin Infect Dis. 2004;38:1341-1346.

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