Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
SODIUM P.A.S. vs CAPREOMYCIN SULFATE
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Sodium P. A. S. (para-aminosalicylate) inhibits folic acid synthesis in Mycobacterium tuberculosis by competing with para-aminobenzoic acid, thereby suppressing bacterial growth.
Inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of m RNA and inhibiting translation initiation. Also alters membrane permeability.
Treatment of tuberculosis as part of a multi-drug regimen (FDA-approved),Off-label: treatment of inflammatory bowel disease (ulcerative colitis, Crohn's disease) and other mycobacterial infections
Treatment of pulmonary tuberculosis as part of combination therapy,Salvage therapy for multidrug-resistant tuberculosis
4 g orally three times daily (total 12 g/day). For intravenous administration, 4 g (10 m L of 40% solution) diluted in 250 m L of 5% dextrose or normal saline infused over 2-3 hours three times daily.
15 mg/kg (up to 1 g) intramuscularly or intravenously once daily for 60 days, then 15 mg/kg (up to 1 g) 2-3 times weekly for 12-18 months in combination with other antituberculosis agents.
0.5–1 hour (normal renal function); prolonged to ≥10 hours in renal impairment (requires dose adjustment).
Terminal elimination half-life: 24-40 hours (prolonged in renal impairment; anuria may extend to 96-120 hours).
Hepatic acetylation via N-acetyltransferase (NAT2); undergoes conjugation with glycine and glucuronic acid.
Not significantly metabolized; primarily excreted unchanged in urine via glomerular filtration.
Primarily renal (80-90% as unchanged drug) via glomerular filtration and tubular secretion; biliary/fecal ≤10%.
Primarily renal (80-90% as unchanged drug via glomerular filtration). Biliary/fecal elimination: <1%.
50–60% bound to serum albumin.
Approximately 30% bound to serum proteins (albumin).
0.2–0.4 L/kg (suggests low tissue penetration, primarily extracellular).
0.4-0.6 L/kg (suggests distribution primarily into extracellular fluid; poor CNS penetration unless meninges inflamed).
Oral: ~80–90%. IV: 100%.
IM: 100% (only IM route available; no oral formulation).
GFR 30-50 m L/min: administer every 12 hours. GFR 10-30 m L/min: administer every 24 hours. GFR <10 m L/min: administer every 48 hours or avoid use.
Cr Cl 50-80 m L/min: 15 mg/kg every 24-36 hours; Cr Cl 30-50 m L/min: 15 mg/kg every 48 hours; Cr Cl 10-30 m L/min: 15 mg/kg every 72 hours; Cr Cl <10 m L/min: 15 mg/kg every 96-120 hours.
Child-Pugh Class A: no adjustment. Child-Pugh Class B: reduce dose by 50%. Child-Pugh Class C: avoid use due to risk of hepatotoxicity.
No dose adjustment required for hepatic impairment; monitor for hepatotoxicity.
Children: 150-300 mg/kg/day orally in 3-4 divided doses, maximum 12 g/day. Intravenous: 150-300 mg/kg/day in divided doses every 6-8 hours.
15-30 mg/kg intramuscularly or intravenously once daily (maximum 1 g) for 60 days, then 15-30 mg/kg 2-3 times weekly (maximum 1 g).
Start at lower end of dosing range (e.g., 4 g orally twice daily) and titrate based on renal function. Monitor for electrolyte disturbances and hepatotoxicity.
Initiate at lower end of dosing range; adjust based on renal function due to age-related decline in glomerular filtration rate.
No FDA black box warning.
None officially listed by FDA; however, use with caution due to potential nephrotoxicity and ototoxicity.
Hepatotoxicity, including hepatic necrosis and jaundice,Hypersensitivity reactions (drug rash, fever, eosinophilia),Gastrointestinal intolerance (nausea, vomiting, diarrhea),Renal impairment may require dose adjustment,Monitor liver function tests, blood counts, and renal function
Nephrotoxicity: Monitor renal function; risk increases with cumulative dose and concomitant nephrotoxic drugs.,Ototoxicity: Can cause vestibular and cochlear damage, especially in patients with renal impairment.,Neuromuscular blockade: May exacerbate weakness in patients with myasthenia gravis or other neuromuscular disorders.,Electrolyte disturbances: Hypokalemia, hypocalcemia, and hypomagnesemia due to renal tubular effects.
Hypersensitivity to para-aminosalicylate or any component,Severe hepatic impairment,Severe renal impairment (Cr Cl < 30 m L/min)
Hypersensitivity to capreomycin or any component,Pre-existing severe renal impairment (Cr Cl < 30 m L/min) unless benefit outweighs risk,Pre-existing hearing loss
Take with food to minimize gastrointestinal irritation. Avoid alcohol due to hepatotoxicity risk. No significant food-drug interactions except for potential interference with vitamin B12 absorption; consider monitoring B12 levels with prolonged use.
No specific food interactions. However, maintain adequate hydration and electrolyte-rich diet (bananas, potatoes) to mitigate hypokalemia.
PAS is not associated with major congenital malformations. First trimester: no significant increase in defect risk. Second/third trimester: may increase risk of maternal hemolysis in G6PD deficiency; no direct fetal toxicity reported. Limited human data.
Animal studies suggest embryotoxicity and teratogenicity; human data limited. Avoid in first trimester; use in second and third trimesters only if clearly needed. Risk of ototoxicity and nephrotoxicity to fetus.
PAS enters breast milk in low concentrations; M/P ratio unknown. Considered compatible with breastfeeding by American Academy of Pediatrics, but monitor infant for gastrointestinal disturbances or allergic reactions.
Small amounts excreted in breast milk; not expected to cause adverse effects in infants due to poor oral absorption. M/P ratio unknown.
Pregnancy may decrease serum concentrations due to increased renal clearance. Monitor therapeutic levels if available; consider increasing dose if subtherapeutic. No standard dose adjustment, but individual titration based on clinical response and serum levels recommended.
No dose adjustment recommended for pregnancy alone; however, concurrent use may require monitoring and adjustment. No pharmacokinetic changes reported.
Sodium P. A. S. (para-aminosalicylic acid) is a second-line antitubercular agent used in combination therapy for multidrug-resistant tuberculosis (MDR-TB). Administer with food to reduce gastrointestinal irritation. Monitor liver function tests due to hepatotoxicity risk. May cause hypothyroidism; monitor thyroid function. Avoid in patients with severe renal impairment (Cr Cl <30 m L/min).
Capreomycin is a second-line injectable agent for multidrug-resistant tuberculosis (MDR-TB). Monitor for nephrotoxicity (creatinine, BUN) and ototoxicity (audiometry, vestibular testing). Electrolyte disturbances (hypokalemia, hypomagnesemia) are common; replace aggressively. Administer deep IM injection; rotate sites. Contraindicated in pregnancy (teratogenic). Synergistic with other antituberculars; never use as monotherapy.
Take with food to reduce stomach upset.,Complete full course of therapy as prescribed, even if you feel better.,Report any signs of liver problems: yellowing of skin/eyes, dark urine, severe nausea/vomiting.,May cause hypothyroidism; report fatigue, weight gain, or cold intolerance.,Avoid alcohol due to increased risk of liver damage.
Take exactly as prescribed; do not skip doses to prevent resistance.,Report hearing loss, ringing in ears, or dizziness immediately.,Report decreased urine output, swelling, or unusual fatigue.,You will need regular blood tests (kidney function, electrolyte levels).,Avoid alcohol and excessive salt intake.,Contact your doctor if you develop severe injection site pain or fever.
No interactions on record
"Decamethonium, a depolarizing neuromuscular blocker, and capreomycin, an aminoglycoside antibiotic, synergistically prolong neuromuscular blockade. Capreomycin decreases acetylcholine release at the motor endplate, while decamethonium persistently depolarizes the postsynaptic membrane, leading to enhanced and prolonged muscle relaxation. This interaction can result in extended respiratory depression and apnea, particularly during anesthesia or in critically ill patients."
"Streptozocin, a nitrosourea alkylating agent, may potentiate the neuromuscular blocking effects of capreomycin, a cyclic polypeptide antibiotic that inhibits neuromuscular transmission by reducing acetylcholine release at the motor endplate. This interaction can lead to prolonged or enhanced muscle weakness, including respiratory depression, particularly in patients with underlying neuromuscular disorders (e.g., myasthenia gravis) or those receiving other neuromuscular blocking agents. The clinical outcome may range from mild skeletal muscle weakness to severe respiratory compromise requiring mechanical ventilation."
"Paromomycin, an aminoglycoside antibiotic, and capreomycin, a polypeptide antibiotic, both possess neuromuscular blocking properties. Their co-administration can result in additive or synergistic neuromuscular blockade, potentially leading to prolonged or enhanced muscle relaxation, respiratory depression, or apnea. This interaction is particularly dangerous in patients receiving general anesthetics, neuromuscular blocking agents, or those with underlying neuromuscular disorders such as myasthenia gravis."
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about SODIUM P.A.S. vs CAPREOMYCIN SULFATE, answered by our medical review team.
SODIUM P.A.S. is a Antitubercular Agent that works by Sodium P. A. S. (para-aminosalicylate) inhibits folic acid synthesis in Mycobacterium tuberculosis by competing with para-aminobenzoic acid, thereby suppressing bacterial growth.. CAPREOMYCIN SULFATE is a Antitubercular Agent that works by Inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of m RNA and inhibiting translation initiation. Also alters membrane permeability.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between SODIUM P.A.S. and CAPREOMYCIN SULFATE depend on the specific clinical indication. These are both Antitubercular Agent agents and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of SODIUM P.A.S. is: 4 g orally three times daily (total 12 g/day). For intravenous administration, 4 g (10 m L of 40% solution) diluted in 250 m L of 5% dextrose or normal saline infused over 2-3 hours three times daily.. The standard adult dose of CAPREOMYCIN SULFATE is: 15 mg/kg (up to 1 g) intramuscularly or intravenously once daily for 60 days, then 15 mg/kg (up to 1 g) 2-3 times weekly for 12-18 months in combination with other antituberculosis agents.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between SODIUM P.A.S. and CAPREOMYCIN SULFATE in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. SODIUM P.A.S. is classified as Category C. PAS is not associated with major congenital malformations. First trimester: no significant increase in defect risk. Second/third trimester: may increase risk of maternal hemolysis . CAPREOMYCIN SULFATE is classified as Category C. Animal studies suggest embryotoxicity and teratogenicity; human data limited. Avoid in first trimester; use in second and third trimesters only if clearly needed. Risk of ototoxici. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.