Chronic Bacterial Prostatitis Medication
- Author: Sunil K Ahuja, MD; Chief Editor: Edward David Kim, MD, FACS more...
Medication Summary
As previously mentioned, the mainstay in the treatment of chronic bacterial prostatitis (CBP) is the use of oral antimicrobial agents, with the most effective medications being fluoroquinolones and TMP-SMZ. Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Alpha blockers, which relax smooth muscle in the bladder neck, can help to decrease recurrences of CBP by diminishing urinary obstruction due to prostate enlargement or congestion secondary to inflammation.
Antibiotics
Class Summary
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Fluoroquinolones are frequently used because they are able to concentrate in the prostate and are lipid soluble. Sulfonamides are also used, because they are lipid soluble.
Since 2008 the FDA has issued a Black Box warning regarding the long-term use of fluoroquinolones. There is a risk of tendonitis and tendon rupture that may cause long-term and possibly permanent damage. The occurence is about 1 in 100,000, about 4 times the normal risk. The risk is greatest for the Achilles tendons, but shoulder and hand tendon ruptures also have been reported.
Moxifloxacin (Avelox)
Moxifloxacin is a quinolone that has antimicrobial activity based on its ability to inhibit bacterial deoxyribonucleic acid (DNA) gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Differences in chemical structure between quinolones have resulted in altered levels of activity against different bacteria. Altered chemistry in quinolones results in toxicity differences.
Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)
TMP-SMZ inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid.
Ciprofloxacin (Cipro)
Ciprofloxacin is a fluoroquinolone with activity against pseudomonas, streptococci, MRSA, Streptococcus epidermidis, and most gram-negative organisms, but with no activity against anaerobes. It inhibits bacterial DNA synthesis and, consequently, growth.
Ofloxacin
Ofloxacin penetrates the prostate well and is effective against Neisseria gonorrhea and C trachomatis. It is a derivative of pyridine carboxylic acid with broad-spectrum bactericidal effects.
Doxycycline (Doryx, Periostat, Adoxa, Vibramycin, Oraxyl)
Doxycycline inhibits protein synthesis and, thus, bacterial growth by binding to 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.
Gentamicin
Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. It is used in combination with an agent against gram-positive organisms and one that covers anaerobes. It is not the drug of choice, but consider its use if other, less toxic drugs are contraindicated, when it is clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.
Levofloxacin (Levaquin)
Levofloxacin is indicated for pseudomonal infections and for infections that are due to multidrug-resistant, gram-negative organisms.
Alpha-Adrenergic Blocking Agents
Class Summary
These agents relax the smooth muscle to the bladder neck, thus reducing bladder outlet obstruction.
Terazosin
Terazosin is a quinazoline compound that counteracts alpha1-induced adrenergic contractions of the bladder neck, facilitating urinary flow in the presence of prostate inflammation.
Doxazosin (Cardura, Cardura XL)
Doxazosin counteracts alpha1-induced adrenergic contractions of the bladder neck, facilitating urinary flow in the presence of prostate inflammation.
5-Alpha-Reductase Inhibitors
Class Summary
These agents inhibit the conversion of testosterone to dihydrotestosterone (DHT).
Finasteride (Proscar)
Finasteride inhibits the steroid 5-alpha-reductase, which converts testosterone into 5-alpha-DHT, causing serum DHT levels to decrease.
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