Doxycycline for Pediatric Infections
The use of tetracycline antibiotics has traditionally been limited in young children because of their ability to cause permanent staining of developing teeth. However, the increasing incidence of tick-borne diseases, such as Rocky Mountain spotted fever (RMSF), ehrlichiosis, and Lyme disease, as well as bioterrorism attacks involving anthrax, has led to a renewed interest in this class. Doxycycline, a synthetic derivative of tetracycline, is now considered the drug of choice in several pediatric infections. It offers a similar antimicrobial spectrum to tetracycline, but has greater bioavailability, a longer half-life, and a more favorable adverse effect profile. This issue of Pediatric Pharmacotherapy will review the basic pharmacology, pharmacokinetics, and dosing of doxycycline in pediatric patients.
Tetracycline antibiotics, including doxycycline, are bacteriostatic. They inhibit protein synthesis by reversibly binding to the 30S ribosomal subunit of susceptible organisms. As a result, they prevent the binding of aminoacyl transfer RNA, thus inhibiting protein synthesis and bacterial cell growth.
The use of tetracycline antibiotics has traditionally been limited in young children because of their ability to cause permanent staining of developing teeth. However, the increasing incidence of tick-borne diseases, such as Rocky Mountain spotted fever (RMSF), ehrlichiosis, and Lyme disease, as well as bioterrorism attacks involving anthrax, has led to a renewed interest in this class. Doxycycline, a synthetic derivative of tetracycline, is now considered the drug of choice in several pediatric infections. It offers a similar antimicrobial spectrum to tetracycline, but has greater bioavailability, a longer half-life, and a more favorable adverse effect profile. This issue of Pediatric Pharmacotherapy will review the basic pharmacology, pharmacokinetics, and dosing of doxycycline in pediatric patients.
Tetracycline antibiotics, including doxycycline, are bacteriostatic. They inhibit protein synthesis by reversibly binding to the 30S ribosomal subunit of susceptible organisms. As a result, they prevent the binding of aminoacyl transfer RNA, thus inhibiting protein synthesis and bacterial cell growth.
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