Methimazole in Pregnancy and Breastfeeding
Fetal Risk Summary
Methimazole, a thiourea antithyroid agent, is used for the treatment of hyperthyroidism. Methimazole readily crosses the placenta to the fetus. Two patients undergoing 2nd trimester therapeutic abortions were given a single 10-mg 35S-labeled oral dose 2 hours before pregnancy termination (1). Fetal:maternal serum ratios were 0.72 and 0.81, representing 0.22% and 0.24% of the administered dose. In the same study, three patients at 14, 14, and 20 weeks' gestation were given an equimolar dose of carbimazole (16.6 mg). Fetal:maternal serum ratios were 0.801.09 with 0.17%0.87% of the total radioactivity in the fetus. The highest serum and tissue levels were found in the 20-week-old fetus (1).
A comparison of the placental transfer of methimazole and propylthiouracil (PTU) in the perfused human term placental lobule was reported in 1997 (2). There were no significant differences between the drugs, and the investigators concluded that the drugs have similar placental transfer kinetics (2).
Early References reported 11 cases of scalp defects (aplasia cutis congenita) in newborns exposed in utero to methimazole or carbimazole (converted in vivo to methimazole) (3,4,5,6 and 7). In two of the 11 infants, umbilical defects (patent urachus in one; patent vitelline duct in another) were also observed, suggesting to one investigator, because of the rarity of these defects, that the combination of anomalies represented a possible malformation syndrome (5). In one the above cases, a-fetoprotein was elevated in both the maternal serum (318 standard deviations [SD] above normal) and the amniotic fluid (2.44 SD above normal) (7). The 6-cm scalp defect was the only defect found in the newborn who had been exposed during the 1st trimester to methimazole (10 mg/day).
In contrast, a 1987 study examined the records of 49,091 live births for cases of congenital skin defects (8). Twenty-five (0.05%) such cases were identified, 13 (0.03%) of which were confined to the scalp. In the sample of 48,057 women, 24 were treated with methimazole or carbimazole during the 1st trimester, but none of these mothers produced children with the skin defects. The authors concluded that they could not exclude an association between the therapy and scalp defects, but if it existed, it was a weak association (8).
Defects observed in two infants exposed to the antithyroid agents in two other reports were imperforate anus (4) and transposition of the great arteries (died at 3 days of age) (9). In a large prospective study, 25 patients were exposed to one or more noniodide thyroid suppressants during the 1st trimester, 9 of whom took methimazole (10). From the total group, four children with nonspecified malformations were found, suggesting that the drugs may be teratogenic. However, since 16 of the group took other antithyroid drugs, the relationship between methimazole and the anomalies cannot be determined. In a study of 25 infants exposed to carbimazole, 2 were found to have defects: bilateral congenital cataracts, and partial adactyly of the right foot (11). Because no pattern of malformations has emerged from these reports, it appears that these malformations were not associated with the drug therapy. In addition, other reports have described the use of methimazole and carbimazole during pregnancy without fetal anomalies (12,13,14,15,16,17,18,19,20,21,22,23,24,25 and 26).
In a surveillance study of Michigan Medicaid recipients involving 229,101 completed pregnancies conducted between 1985 and 1992, 5 newborns had been exposed to methimazole during the 1st trimester (F. Rosa, personal communication, FDA, 1993). One (20.0%) major birth defect was observed (none expected), a hypospadias.
A 1984 report described the relationship between maternal Graves' disease and major structural malformations of external organs, including the oral cavity, in 643 newborns (27). Of 167 newborns delivered from mothers who were hyperthyroid during gestation, 117 were exposed in utero to methimazole. In 50 newborns, the mothers received no treatment, other than subtotal thyroidectomy before or during pregnancy. The incidences of anomalies in these two groups were 1.7% (2 of 117) and 6.0% (3 of 50), respectively. For 476 neonates the mothers were euthyroid during gestation, with 126 receiving treatment with methimazole and 350 receiving no treatment (other than surgery). No malformations were observed in the methimazole-exposed infants and only 1 (0.3%) occurred in the patients not receiving drug therapy. The difference in malformation rates between the nonexposed neonates in the hyperthyroid and euthyroid groups was significant (6% vs. 0.3%, p<0.01). Similarly, the difference between the two groups in total malformations, 3% (5 of 167) vs. 0.2% (1 of 476) was also significant (p<0.01). The defects observed were malformation of the earlobe (methimazole-exposed, hyperthyroid), omphalocele (methimazole-exposed, hyperthyroid), imperforate anus (hyperthyroid), anencephaly (hyperthyroid), harelip (hyperthyroid), and polydactyly (euthyroid). The authors concluded that the disease itself causes congenital malformations and that the use of methimazole lessened the risk for adverse outcome (27).
A 1987 case report described a female infant (46,XX) who had been exposed throughout gestation to methimazole and propranolol given for maternal hyperthyroidism (28). Choanal atresia was noted at birth and treated surgically. At 6 months of age, she was noted to be developmentally delayed, especially in gross motor development, and had mild neurosensory hearing loss bilaterally and recurrent dacryocystitis. By 3.5 years, her development continued to be markedly delayed. Her height and weight were below the 3rd percentile and a small area of alopecia was noted in the parietal region close to the midline on the otherwise normal scalp. Although the chest was symmetrical, both nipples were absent (athelia). Other abnormalities noted at this time were upper slanting palpebral fissures and epicanthal folds, a broad nasal bridge with slightly anteverted nostrils, and a tented upper lip with a short philtrum (28).
Two cases of esophageal atresia and tracheoesophageal fistula in newborn infants exposed throughout gestation to methimazole (30 mg/day) were reported in 1992 (29). The mothers were euthyroid during pregnancy. Both newborns were small for gestational age and had palpable goiters with laboratory evidence of hypothyroidism. Surgical correction of the defects was attempted but the infants died from postoperative sepsis and renal failure. At autopsy, in addition to the defects noted above, one infant had a ventricular septal defect and a Meckel diverticulum, and both had diffuse goiters. Because of the relatively low frequency of esophageal atresia and tracheoesophageal fistula (1:3,0001:4,500), the authors attributed the defects to methimazole (29).
A 1992 study reported no difference in the intellectual capacity of offspring of 31 mothers with Graves disease who were treated during gestation with either methimazole (N=15) or propylthiouracil (PTU) (N=16) when compared with nonexposed controls (30). The ages of the subjects ranged from 4 to 23 years. None were hypothyroid or had goiter at birth. There were no differences between the antithyroid drugs, and there was no correlation between dosage used and intelligence (30).
Two reports, one in 1994 and the other in 1995, described aplasia cutis in two newborns exposed during pregnancy to methimazole (31,32). In reviewing their case and previously published cases, the authors of the 1994 publication were uncertain of a causal association between the drug and the scalp defect (31). The other group of authors concluded that the evidence indicated a strong association between the drug and aplasia cutis (32). Both groups concluded, because no such cases had been reported with PTU, that this drug was preferred for the treatment of hyperthyroidism during pregnancy (31,32).
A female infant exposed in utero to methimazole during the first 2 months of pregnancy and then to PTU until term was described in a 1997 abstract (33). Birth weight and length were normal, as was the chromosomal analysis (46,XX). Malformations observed in the infant were choanal atresia, right iris/retinal coloboma, right renal pelvis ectasia, and minor facial anomalies.
A brief 1996 report described multiple malformations in a newborn of a woman who was treated with methimazole (34). Metoprolol (150 mg/day) and methimazole (30 mg/day) were taken throughout most of the 1st trimester. Levothyroxine was also administered during most of the pregnancy. Metoprolol was discontinued at about 9 weeks' gestation and the methimazole dose was gradually tapered until a subtotal thyroidectomy was performed at 18 weeks. Premature labor could not be arrested and a 750-g, male infant was delivered at 27 weeks with Apgar scores of 1, 0, and 3 at 1, 5, and 10 minutes, respectively. Major malformations evident were choanal atresia, esophageal atresia with tracheoesophageal fistula, omphaloenteric connection, and multiple ventricular septal defects. The infant died at 6 weeks of age secondary to complications arising from corrective surgery (34).
A 1998 case report described a 3-year-old boy with choanal atresia (surgically corrected shortly after birth), hypoplastic nipples (hypothelia; see also Reference #28 above for a case of athelia), and developmental delay (35). He had been exposed throughout a 34-week gestation to carbimazole, but was euthyroid at birth. He was hypotonic at birth and remained so at 3 years of age. He had mild global, but predominantly motor, developmental delay. His height and weight were at the 10th percentile or less. Other features noted were short upslanting palpebral fissures (length <3rd percentile), small nose and mouth, and a short philtrum. The nipples were hypoplastic and inverted. The mother had a normal, healthy child before and after the subject case. The authors suggested that the combination of malformations represented a rare but distinct syndrome of methimazole teratogenicity (35).
A case of multiple defects in an newborn infant exposed in utero to methimazole (20 mg/day) was reported in 1999 (36). The mother, who was euthyroid on therapy, had taken methimazole for 9 years prior to conception and was continued on the drug during the first 7 gestational weeks (i.e., 9 weeks after the first day of the last menstrual period [LMP]). At that time she was changed to PTU for the remainder of her pregnancy. A 1475-g (25th50th percentile) male preterm infant was delivered at 31 gestational weeks because of premature rupture of the membranes. The Apgar scores, length, and head circumference were not recorded, but severe respiratory distress required assisted ventilation. Anomalies observed in the infant were bilateral choanal atresia, esophageal atresia and tracheoesophageal fistula, patent ductus arteriosus (closed spontaneously at 2 months), and periventricular leukomalacia with bilateral parieto-occipital cavitations. The latter defect was confirmed by magnetic resonance imaging (MRI) at age 2 years and was thought to be of possible hypoxic-ischemic origin and related to prematurity. At 7 months of age, abdominal sonography, chromosomal analysis, and brain-stem auditory evoked responses were normal. An eye examination revealed bilateral convergent strabismus, mildly pale papillae, and diffuse depigmentation of the fundi. Severe psychomotor retardation with mixed tetraparesis was evident. At 4.25 years, the weight and height were both below the 3rd percentile for age, he was unable to walk or sit without support, and language was absent. Physical examination noted dolichocephaly, bilateral ptosis of the eyelid with inner epicanthal fold, convergent squint, mild malar hypoplasia, small nose with moderately anteverted nostrils, long and flat philtrum, a highly arched palate, bilateral bridged palmar creases, axial hypotonia and limb hypertonia, poor head control, Moro-like reflexes, and bilateral talipes varus. A localized (6 6 cm) patchy defect consisting of short, sparse, kinky, and hypopigmented hair in the occipital region was also noted. Based on previously reported cases, the defects suggested to the authors that they represented a specific teratogenic malformation syndrome (36).
A 2000 report described various congenital abnormalities observed in a term female infant of a woman who was kept euthyroid throughout pregnancy with methimazole 30 mg/day (37). Aplasia cutis congenita was noted at birth. Seizures were noted at 18 months of age. At 3 years of age, her height, weight, and head circumference were normal (75th80th percentile) as was her psychomotor development. Minor facial abnormalities consisted of hypertrichosis of the eyelashes and synophrys. There were areas of hyperpigmented skin on the back; two supernumerary nipples; bilateral syndactylies between the third and fourth fingers and between the second and third toes; dystrophic, small, and shortened fingernails; and longitudinal ridges on a finger of each hand. A brain MRI, electroencephalogram, and karyotyping were normal. The authors considered this case to represent a new combination of signs, including abnormalities of various tissues of ectodermal origin (fingernails and skin anomalies) and epilepsy, that were associated with in utero exposure to methimazole (37).
Several reports have studied pregnancies complicated by hyperthyroidism and the effects of methimazole and carbimazole on maternal and fetal thyroid indexes (23,38,39,40 and 41). In separate pregnancies in a mother with Graves' disease, fetal thyrotoxicosis was treated with 2040 mg/day of carbimazole with successful resolution of fetal tachycardia in both cases and disappearance of fetal goiter in the first infant (23). A woman with hyperthyroidism was treated with a partial thyroidectomy before pregnancy (39). She subsequently had four pregnancies, all of which were complicated by fetal hyperthyroidism. No antithyroid therapy was administered during her first two pregnancies. The first ended in a late stillbirth, and the second resulted in a child with skull deformities. Both adverse outcomes were compatible with fetal hyperthyroidism. Carbimazole was administered in the next two pregnancies and both resulted in normal infants (39).
A 1992 abstract and a later full report described a retrospective evaluation of hyperthyroid pregnancy outcomes treated with either methimazole (N=36) or PTU (N=99) (42,43). One newborn (2.8%) in the methimazole group had a birth defect (inguinal hernia), whereas three (3.0%) defects were observed in those exposed to PTU (ventricular septal defect; pulmonary stenosis; patent ductus arteriosus in a term infant). No scalp defects were observed.
Treatment of maternal hyperthyroidism may result in mild fetal hypothyroidism because of increased levels of fetal pituitary thyrotropin (17,20,40,44). This usually resolves within a few days without treatment (20). An exception to this occurred in one newborn exposed to 30 mg of carbimazole daily to term who appeared normal at birth but who developed hypothyroidism evident at 2 months of age with subsequent mental retardation (12).
A brief 1992 report from Spain examined the relationship between the illicit and uncontrolled use of methimazole in cattle feed as a weight enhancer and the appearance of congenital scalp aplasia cutis in humans (45). Seven cases of the rare malformation were observed in 19901991 in regions thought to have used methimazole in cattle food. The investigators speculated that pregnant women eating the meat of methimazole-exposed cattle would expose their fetuses to the drug (45).
Small, usually nonobstructing goiters in the newborn have been reported frequently with PTU (see Propylthiouracil). Only two goiters have been reported in carbimazole-exposed newborns and none with methimazole (9). Long-term follow-up of 25 children exposed in utero to carbimazole has shown normal growth and development (11).
Combination therapy with thyroid-antithyroid drugs was advocated at one time but is now considered inappropriate (see also Propylthiouracil) (18,22,44,46,47). Two reasons contributed to this change: (a) use of thyroid hormones may require higher doses of the antithyroid drug to be used, and (b) placental transfer of levothyroxine and liothyronine is minimal and not sufficient to reverse fetal hypothyroidism (see also Levothyroxine and Liothyronine) (20).
In summary, because of the possible association with aplasia cutis and other malformations, and the passage of methimazole into breast milk, many investigators, including two in 1984 (48), consider PTU to be the drug of choice for the medical treatment of hyperthyroidism during pregnancy. However, this opinion is not universal (47). A specific pattern of rare congenital malformations secondary to exposure to methimazole during the first 7 weeks of gestation (9 weeks after the LMP) has been suggested that consists of some or all of the following: scalp or patchy hair defects, choanal atresia, esophageal atresia with tracheoesophageal fistula, minor facial anomalies, hypoplastic or absent nipples, and psychomotor delay. These defects may indicate a phenotype for methimazole embryopathy (35,36), but the complete spectrum of anomalies may still need further definition (37). If methimazole or carbimazole is used, the lowest possible dose to control the maternal disease should be given (9,44). One review recommended that the dosage should be adjusted to maintain the maternal free thyroxine levels in a mildly thyrotoxic range (41).
Breast Feeding Summary
Methimazole is excreted into breast milk (49,50,51,52 and 53). In a patient given 10 mg of radiolabeled carbimazole (converted in vivo to methimazole), the milk:plasma ratio was a fairly constant 1.05 over 24 hours (38). This represented about 0.47% of the given radioactive dose. In a second study, a patient was administered 2.5 mg of methimazole every 12 hours (50). The mean milk:plasma ratio was 1.16, representing 1639 g of methimazole in the daily milk supply. Extrapolation of these results to a daily dose of 20 mg indicated that approximately 3 mg/day would be excreted into the milk (50). Five lactating women were given 40 mg of carbimazole, producing a mean milk:plasma ratio at 1 hour of 0.72 (51). For the 8-hour period after dosing, the milk:plasma ratio was 0.98. A new radioimmunoassay was used to measure methimazole milk levels after a single 40-mg oral dose in four lactating women. The mean milk:plasma ratio during the first 8 hours was 0.97, with 70 g excreted in the milk (51).
A 1987 publication described the results of carbimazole therapy in a woman breast-feeding twins (53). Two months after delivery, the mother was started on carbimazole, 30 mg/day. The dose was decreased as she became euthyroid. Three paired milk:plasma levels revealed ratios of 0.300.70. The mean free methimazole concentration in milk, determined between 2 and 16 weeks of therapy, was 43 ng/mL (range 092 ng/mL). Peak milk levels occurred 24 hours after a dose. Mean plasma levels in the twins were 45 ng/mL (range 0105 ng/mL) and 52 ng/mL (range 0156 ng/mL), with the highest concentrations occurring while the mother was taking 30 mg/day. No evidence of thyroid suppression was found clinically or after thyroid function tests in the nursing twins (53).
Two other studies also found no effect on clinical status or thyroid function in nursing infants of mothers taking carbimazole or methimazole (54,55). In one report, no adverse effects were observed during a 3-week study of 11 infants whose mothers were taking carbimazole 515 mg/day (54). In the other study, normal thyroid function in 35 nursing infants, whose mothers were taking methimazole, was documented over periods ranging from 1 to 6 months (55). Most mothers were taking 510 mg/day, but six received 20 mg/day for 1 month and then tapered to 5 mg/day.
Because the amounts found in some studies may cause thyroid dysfunction in the nursing infant, methimazole and carbimazole have, in the past, been considered contraindicated during lactation. If antithyroid drug therapy was required, PTU was considered the treatment of choice, partially because PTU is ionized at physiologic pH and because 80% of the drug is protein bound (56). Methimazole is neither ionized nor protein bound, but small doses of methimazole (e.g., 1020 mg/day or less) do not appear to pose a major risk to the nursing infant if thyroid function is monitored at frequent (e.g., weekly or biweekly) intervals (54,55 and 56).
In 2000, a long-term study confirmed the lack of toxicity in infants of mothers being treated with methimazole (57). A total of 139 thyrotoxic lactating mothers and their nursing infants were studied, 51 of whom were treated with methimazole during pregnancy and continued their treatment during lactation. The other 89 women started methimazole therapy during lactation with 1020 mg/day for 1 month, 10 mg/day during the second month, then 510 mg/day thereafter. Methimazole serum levels in six infants whose mothers were taking 20 mg/day were <0.03 g/mL, 2 hours after breast feeding. No effects on infant thyroid function were detected at various times up to 12 months. In a blinded assessment, the total IQ scores, including verbal and performance IQ, of 14 children (age 4874 months) exposed to methimazole in milk did not differ from 17 nonexposed controls (57).
The American Academy of Pediatrics considers methimazole and carbimazole to be compatible with breast feeding (58).
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Questions and Answers
Can my thryoid levels be affected from cutting and handling my cat's methimazole?, For several years I've been cutting up the cat's methimazole on the kitchen counter and I'm showing signs of low thryoid myself. Is it possible I've gotten enough into my system to lower my levels?
Can being taken off of methimazole cause rashes on your body?, Since my doctor has taken me off of methimazole for my thyroid I have broken out in a rash between my breasts. They are small itchy bumps that look like a pimple. I don't have acne on my face I never have. I have gone to the doctor but they said that it looks like a viral infection and to put a cream on it. I have been putting a hydrocortisone cream on it but it doesn't help. What could it be and how can I possibly stop it from spreading?
That area of reaction is a very unusal area to react from medication. I would question if it is not just a heat rash? Mosby's Drug reference 1999 makes no mention of a rash except for during overdose/hypersensitivity. One may have a reaction to medication, several weeks after they have stopped taking medication.
what is the prescription drug methimazole?, I have recently been diagnosed with hyperthyroidism, t3 toxicosis and grave's disease. The symptoms that I have experienced over the last few months are not normal for these diseases. I have gained 30 lbs, my body has been swollen like a sausage (from my feet to my wrists), I am unable to concentrate, and from time to time I slur my words. Along with behumidine (to control the water retention) I have been prescribed this medicine: methimazole to help reduce the effects of these diseases. However, I have never heard of or taken this before. Is there anyone who knows anything about this medication or has taken it? Any bit of information will be greatly appreciated.
Your thyroid is producing too much thyroid hormone. Methimizole is an anti-thyroid drug. It prevents your thyroid from producing so much thyroid hormone.
How do I get my cat to take his medication ( methimazole) a very bitter drug?, My cat foams at the mouth when I give him his anti-Thyroid medication.
The portion of the pill you give is a very tiny amount. (Normally, cats start out with only a part of a pill). It is possible to find a formulation pharmacist who will do it in the form of a transdermal gel, and you rub in on his ears. I have posted a link on one such place, but there are others.
Also, pet stores usually sell items called pill pockets, that are flavored, and you hide the pill inside. As the pill is so small, it should be very easy.
Can I get in Australia Methimazole treat ( chicken flavour) for my cat ? I plan to move there with my cat?, My cat has hyperthyroidism and takes Methimazole treat ( chicken flavour). No need to force the pill into her throat, she eats this medication as a treat, and loves it.
Does somebody know if Methimazole is sold like a treat at any veterinarian hospital in MELBOURNE ?.
Thanks for help !!
Your best bet is going to be getting in contact with a vet in Melbourne and explaining the situation and asking them if they have something of the same sort for hyperthyroidism in cats. They might, they might not. If possible get someone already living there to do it for you (the reasons for that are obvious).
how long does it take to get methimazole out of your system?, My endo thinks i had an allergic reaction to it and so i stopped taking it completely on friday. I only took it a month 30mg a day then i ended up in the ER two weeks ago so i stopped taking it then for three days then started taking 10mg a day till Friday. I still don't feel much better.
Apparently, the half-life of methimazole is 5-6 hours when taken orally ( http://www.ithyroid.com/graves_treatment... )
So, taking 30mg a day, you will be down to 3.75mg 24 hours later. After three days you will be down to 2mg (if taking 30mg each day still) - not much. So, it will be almost completely out of your system by day three. If you stopped taking it on Friday, after taking 10mg a day, it again will be completely out by now.
Hope that helps
Can I get in Australia METHIMAZOLE treat ( chicken flavor) for my cat who has hyperthyroidism ?, I live in USA and I give my cat METHIMAZOLE as a treat ( chicken flavor) for hyperthyroidism twice a day, she loves to eat her pill, she thinks I'm giving her chicken. The veterinarian hospital makes this medication as if it is a treat. I plan to go to live in Australia but I'd be concerned if I wouldn't get this medication as a treat from a veterinarian hospital ( my cat won't swallow any pill ) .
Thanks for your kind help
If you can't get it made into a pill, check with a vet down there to see if it can be made into a transdermal gel - this is what we use on hypyerthyroid kitties that the owners can't or won't pill. It is applied to the skin inside the ears, and they absorb it through the skin. (it is something you have to wear gloves for, or you will absorb some too)
My doctor just prescribed methimazole for my thyroid. I have already had radiation to "kill" my thyroid. Why?, Why would my doctor prescribe a thyroid decreasing medicine when my thyroid is "dead"? I noticed when looking at the uses for this medicine that is is used for preparing people for thyroid removal surgery and radiation therapy. Since I already had radiation I dont understand the purpose for prescribing this.
After I-131 radioablative therapy for a thyroid pathology, if serologic levels indicate that their is some functional tissue, your physician may opt to place you on methimazole instead of subjecting you to more I-131 therapy.