Piroxicam Pregnancy and Breastfeeding Warnings

Brand names: Feldene

Medically reviewed by Drugs.com. Last updated on May 13, 2024.

Piroxicam Pregnancy Warnings

Use should be limited between about 20 and 30 weeks gestation; use should be avoided at about 30 weeks gestation and later in pregnancy.
-According to some authorities: Use is not recommended during the first 2 trimesters of pregnancy unless the benefit outweighs the risk to the fetus; use is contraindicated during the third trimester of pregnancy.

AU TGA pregnancy category: C
US FDA pregnancy category: Not assigned

Risk summary: Study data on the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in pregnant women during the first or second trimester were inconclusive to inform potential embryofetal risks. NSAID use in pregnant women at about 20 weeks gestation or later has been associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, impaired neonatal renal function, and at about 30 weeks gestation or later increases the risk of premature closure of the fetal ductus arteriosus.

Comments:
-If an NSAID is required at about 20 weeks gestation or later in pregnancy, use should be limited to the lowest effective dose and shortest duration possible.
---If use of this drug extends beyond 48 hours, monitoring with ultrasound for oligohydramnios should be considered.
---If oligohydramnios occurs, it is recommended to discontinue this drug and follow up according to clinical practice.
-Patients of childbearing potential who desire pregnancy should be advised that NSAIDs (including this drug) may be associated with a reversible delay in ovulation.
---According to some authorities: This drug is not recommended in women attempting to conceive.

Animal studies have revealed evidence of fetotoxicity (postimplantation loss), delayed parturition, and increased incidence of stillbirth; studies in rats and rabbits failed to reveal evidence of teratogenicity at exposures up to 5 and 10 times the maximum recommended human dose (MRHD), respectively. After dosing pregnant rats during organogenesis, increased postimplantation losses were observed at exposures up to 5 times the MRHD (of 20 mg) based on mg/m2 body surface area (BSA); pregnant rats in the last trimester had increased gastrointestinal tract toxicity compared to those in earlier trimesters or nonpregnant rats. In pregnant rats, reduced weight gain and death were observed at doses 5 times the MRHD (based on mg/m2 BSA); treated dams revealed peritonitis, adhesions, gastric bleeding, hemorrhagic enteritis and dead fetuses in utero. In rats, delayed parturition and increased incidence of stillbirth were seen at doses equivalent to the MRHD; there are no human studies on the effects of this drug during labor or delivery. In animal studies, use of prostaglandin synthesis inhibitors (such as this drug) led to increased pre- and postimplantation loss; at clinically relevant doses, these agents have been reported to impair kidney development. There are no controlled data in human pregnancy.

In published studies and postmarketing reports, maternal NSAID use at about 20 weeks gestation or later in pregnancy has been associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, impaired neonatal renal function. In general, these adverse reactions occurred after days to weeks of therapy, but infrequently, oligohydramnios has been reported as soon as 48 hours after starting an NSAID. In most cases, decreased amniotic fluid was transient and reversible upon stopping the drug. Few cases of maternal NSAID use and neonatal renal dysfunction without oligohydramnios have been reported; some were irreversible. Some cases of neonatal renal dysfunction required invasive procedures (e.g., exchange transfusion, dialysis). These postmarketing studies and reports had methodological limitations which preclude a reliable estimation of the risk of adverse fetal and neonatal outcomes with maternal NSAID use. Published safety data on neonatal outcomes included mostly preterm infants; therefore, it is unclear whether certain reported risks can be generalized for full-term infants exposed to NSAIDs via maternal use.

Based on mechanism of action, the use of prostaglandin-mediated NSAIDs (including this drug) may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. Small studies in women treated with NSAIDs have shown a reversible delay in ovulation. Withdrawal of NSAIDs (including this drug) should be considered in women who have difficulties conceiving or who are undergoing investigation of infertility.

AU TGA pregnancy category C: Drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible. Accompanying texts should be consulted for further details.

US FDA pregnancy category Not Assigned: The US FDA has amended the pregnancy labeling rule for prescription drug products to require labeling that includes a summary of risk, a discussion of the data supporting that summary, and relevant information to help health care providers make prescribing decisions and counsel women about the use of drugs during pregnancy. Pregnancy categories A, B, C, D, and X are being phased out.

See references

Piroxicam Breastfeeding Warnings

Shorter-acting agents may be preferred while breastfeeding newborn or preterm infants.
-According to some authorities: Use is contraindicated or not recommended.

Excreted into human milk: Yes (low amounts)

Comments:
-There is no published experience with this drug during breastfeeding in the newborn period.
-According to some authorities: Developmental and health benefits of breastfeeding should be considered as well as the mother's clinical need for this drug. The effects in the nursing infant are unknown; potential adverse effects in the breastfed child due to this drug or the mother's underlying condition should be considered.

Limited data from 2 reports that included 6 breastfeeding women and 2 infants showed this drug is excreted into human milk at about 1% to 3% of the maternal plasma concentration. No drug accumulation occurred in milk relative to that in maternal plasma during therapy.

This drug would not be expected to produce harmful effects in older breastfed infants due to low amounts in milk and failure to detect this drug or its metabolites in the urine of 2 older infants.

Milk was collected from 2 women receiving 20 and 40 mg per day; peak milk levels were 170 and 220 mcg/L, respectively. No drug was detected in the serum of the 13-month-old infant whose mother was taking 20 mg/day for 4 months starting the ninth month postpartum; no adverse effects occurred in this breastfed infant.

In 3 women, peak milk levels averaged 40 mcg/L during the first week of therapy (20 mg orally per day). After steady-state was attained in these 3 women (plus an additional woman), milk levels averaged 102 mcg/L within 12 hours of dosing and 73 mcg/L during the 13 to 24 hours after dosing; a breastfed infant would receive an estimated average 3.5% and maximum 6.3% of the weight-adjusted maternal dosage. Neither this drug nor its metabolites were detected (less than 15 mcg/L) in the urine of 1 infant after 52 days of maternal therapy with 20 mg/day, and 4 infants (aged 3 to 4.5 months) remained healthy during long-term maternal therapy at 20 mg/day.

See references

Further information

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