VINOSIN 500MG

Indications

• Complicated skin and soft tissue infections
• Bone infections
• Joint infections
• Community-acquired pneumonia
• Hospital-acquired pneumonia, including ventilator-associated pneumonia
• Infective endocarditis
• Acute bacterial meningitis
• Bacteraemia
• Surgical prophylaxis for patients at high risk of bacterial endocarditis

Mechanism of action

Vancomycin exerts its bactericidal action by inhibiting cell wall biosynthesis. It specifically binds to the terminal D-alanyl-D-alanine residues of the peptidoglycan precursors, preventing their incorporation into the peptidoglycan matrix, which is vital for the structural integrity of Gram-positive bacteria. This leads to cell lysis and death. Additionally, vancomycin alters bacterial cell membrane permeability and affects RNA synthesis, contributing to its antimicrobial effects.

Pharmacodynamics

As a nonribosomal peptide antibiotic, vancomycin is often considered a drug of last resort and is used when other treatments have failed. It demonstrates activity against several significant pathogens, including Listeria monocytogenes, Streptococcus pneumoniae (including penicillin-resistant strains), and various enterococci. Vancomycin can synergistically enhance the effects of aminoglycosides against certain strains, leading to improved clinical outcomes in specific infections.

Pharmacokinetics

Vancomycin is administered intravenously or intramuscularly, with its pharmacokinetics influenced by renal function. The drug is distributed widely in body tissues and fluids, with a volume of distribution of approximately 0.4 to 1 L/kg. It is primarily eliminated via the kidneys, necessitating dosage adjustments in patients with renal impairment. Trough concentrations should be monitored to ensure efficacy while preventing toxicity, especially during prolonged therapy.

Contra-indications

• Previous hearing loss
• Hypersensitivity to vancomycin or any component of the formulation

Adverse effects

• Nephrotoxicity
• Ototoxicity
• Red man syndrome
• Thrombophlebitis
• Hypersensitivity reactions
• Skin rash

Interactions

• Increased risk of nephrotoxicity when used with other nephrotoxic drugs (e.g., aminoglycosides, nonsteroidal anti-inflammatory drugs)
• Potential interactions with muscle relaxants and anesthetics

Precautions

• Monitor renal function and auditory function during prolonged treatment
• Use with caution in patients with renal impairment
• Assess for potential allergic reactions prior to administration

Pregnancy

Vancomycin is classified as category B. It should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Vancomycin is excreted in breast milk. Caution should be exercised when administering to nursing mothers.

Storage

Store in a cool, dry place. Protect from light. Do not freeze.

Formulations

• Solution for injection
• Powder and solvent for solution for injection

Mechanism of action

The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix, which forms the major structural component of Gram-positive cell walls. Vancomycin forms hydrogen bonds with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides, preventing the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi. Vancomycin is bactericidal and appears to bind to the bacterial cell wall causing blockage of glycopeptide polymerization. This effect, which occurs at a site different from that affected by the penicillins, produces immediate inhibition of cell wall synthesis and secondary damage to the cytoplasmic membrane. Magnesium, manganese, calcium, and ferrous ions reduce the degree of adsorption of vancomycin to the cell wall, but the in vivo importance of this interaction is unknown. The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis.

Pharmacodynamics

Vancomycin is a branched tricyclic glycosylated nonribosomal peptide often reserved as the "drug of last resort", used only after treatment with other antibiotics has failed. Vancomycin has been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections: <i>Listeria monocytogenes</i>, <i>Streptococcus pyogenes</i>, <i>Streptococcus pneumoniae</i> (including penicillin-resistant strains), <i>Streptococcus agalactiae</i>, <i>Actinomyces</i> species, and <i>Lactobacillus</i> species. The combination of vancomycin and an aminoglycoside acts synergistically in vitro against many strains of Staphylococcus aureus, Streptococcus bovis, enterococci, and the viridans group streptococci.