Fetal Risk Summary
Telmisartan is a selective angiotensin II receptor antagonist that is used, either alone or in combination with other antihypertensive agents, for the treatment of hypertension. Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by preventing angiotensin II from binding to AT1 receptors.
Reproduction studies have been conducted in pregnant rats and rabbits (1). No teratogenicity was observed in either species at oral doses up to approximately 6.3 and 6.4 times the maximum recommended human dose of 80 mg on a body surface area basis (MRHD), respectively, but embryolethality was noted at the highest dose in rabbits. The highest doses were maternally toxic (reduced body weight gain and food consumption) in both species. In rats, an oral dose approximately 1.9 times the MRHD (also maternal toxic) during late gestation and lactation resulted in neonatal adverse effects, including reduced viability, low birth weight, delayed maturation, and decreased weight gain (1). The no-observed-effect doses for developmental toxicity in rats and rabbits were 0.64 and 3.7 times the MRHD. No adverse effects on reproductive performance were noted in male and female rats at a dose about 13 times the MRHD (1).
It is not known if telmisartan crosses the human placenta to the fetus. The drug is found in rat fetuses in late gestation (1). The molecular weight (about 515) is low enough that passage to the human fetus should be expected.
No reports describing the use of telmisartan during human pregnancy have been located. The antihypertensive mechanisms of action of telmisartan and angiotensin-converting enzyme (ACE) inhibitors are very close. That is, the former selectively blocks the binding of angiotensin II to AT1 receptors, whereas the latter prevents the formation of angiotensin II itself. Therefore, use of this drug during the 2nd and 3rd trimesters may cause teratogenicity and severe fetal and neonatal toxicity that is identical to that seen with ACE inhibitors (e.g., see Captopril or Enalapril). Fetal toxic effects may include anuria, oligohydramnios, fetal hypocalvaria, intrauterine growth retardation, prematurity, and patent ductus arteriosus. Anuria-associated oligohydramnios may produce fetal limb contractures, craniofacial deformation, and pulmonary hypoplasia. Severe anuria and hypotension that are resistant to both pressor agents and volume expansion may occur in the newborn following in utero exposure to telmisartan. Newborn renal function and blood pressure should be closely monitored.
[* Risk Factor DM if used in 2nd or 3rd trimesters.]
Breast Feeding Summary
No reports describing the use of telmisartan during human lactation have been located. The drug is excreted into the milk of lactating rats (1). Because the molecular weight (515) is low enough, excretion into human breast milk should also be expected. The effects of this exposure on a nursing infant are unknown. The American Academy of Pediatrics, however, considers ACE inhibitors, a closely related group of antihypertensive agents, to be compatible with breast feeding (see Captopril or Enalapril).
- Product information. Micardis. Boehringer Ingelheim Pharmaceuticals, 2000.