Indications
Cefdinir is recognized for its effectiveness in treating a variety of bacterial infections in both children and adults. It is prescribed for acute bacterial otitis media, acute maxillary sinusitis, and community-acquired pneumonia. Additionally, cefdinir is used to manage acute bacterial exacerbations of chronic bronchitis, pharyngitis/tonsillitis, as well as uncomplicated skin and skin structure infections. The drug is effective against organisms such as Haemophilus influenzae, Haemophilus parainfluenzae, Streptococcus pneumoniae (penicillin-susceptible), Moraxella catarrhalis, Streptococcus pyogenes, Staphylococcus aureus, and various beta-lactamase producing bacteria, which are susceptible to its action.
Pharmacodynamics
Cefdinir functions as a bactericidal agent by inhibiting bacterial cell wall synthesis, which leads to the elimination of the bacterial infection. It demonstrates broad-spectrum activity against numerous gram-positive and gram-negative bacteria, including strains that produce beta-lactamase enzymes. This attribute allows cefdinir to be effective against certain bacterial strains that show resistance to other cephalosporins.
Absorption
The absorption of cefdinir reaches its peak plasma concentration approximately 2 to 4 hours following oral administration. The bioavailability of cefdinir varies with its formulation; for instance, when taken as a capsule, its bioavailability ranges from 16% to 21%, while the suspension form has an absolute bioavailability of 25%. Consumption of high-fat meals can reduce absorption by up to 15%, although this reduction is not clinically significant, allowing cefdinir to be administered with or without food. However, concurrent intake with antacids containing aluminum or magnesium, or with iron supplements, can reduce its absorption. It is advisable to separate the administration of cefdinir and these agents by at least 2 hours.
Metabolism
Cefdinir underdoes minimal metabolism in the body, with its therapeutic effects primarily attributed to the parent drug itself. The limited metabolism supports its efficacy in clearing infections, as it maintains its active form for a longer duration in the systemic circulation.
Mechanism of Action
Cefdinir, a cephalosporin antibiotic, exhibits enhanced bactericidal activity due to its structural composition, which includes a six-member dihydrothiazine ring rather than the five-member thiazolidine ring found in penicillins. This structural feature enables cefdinir to resist inactivation by certain bacterial enzymes. The antimicrobial efficacy of cefdinir is primarily achieved through the inhibition of bacterial cell wall synthesis by binding to specific penicillin-binding proteins (PBPs). Similar to other beta-lactam antibiotics, cefdinir penetrates the bacterial cell wall and effectively counters the actions of beta-lactamase enzymes, resulting in the inactivation of PBPs. This inhibition disrupts the transpeptidation process essential for cell wall integrity, ultimately causing cell lysis and the demise of susceptible bacteria. Cefdinir specifically targets penicillin-binding proteins 2 and 3 and has demonstrated the ability to inhibit transpeptidase enzymes across various bacterial strains, contributing to its bactericidal properties. Additionally, an in vitro study has indicated that cefdinir may inhibit the extracellular release of myeloperoxidase, though the significance of this potential interaction in its mechanism of action remains unclear.
