Similarly, prematurity was more common in groups 2 and 3 [OR in group 2, 2. Eclampsia was also more common in group 3 women OR 4. In this study there was no increase in the frequency of infants who were small for gestational age, although Mitsuda et al.
Davis, et al. Interestingly, another study found that the altered hemodynamics seen in pregnant hyperthyroid women with congestive heart failure improved but did not normalize with restoration of a euthyroid state This may be one explanation for the development of preeclampsia even in women whose hyperthyroidism is controlled during pregnancy 8. Mitsuda et al. In a report from the U.
These data suggest that there may be a small increase in the rate of congenital anomalies in women with untreated or incompletely treated hyperthyroidism in the first trimester, but more information is clearly needed. ATD therapy is obviously indicated for hyperthyroidism when it is moderate or severe. Although there is no generally accepted definition of moderate or severe hyperthyroidism, it would be reasonable to treat women whose free T 4 levels are more than 2. However, for an asymptomatic woman whose pregnancy is progressing satisfactorily and whose serum free T 4 is minimally above 2.
It should be noted that all prior studies linking hyperthryoidism to adverse pregnancy outcomes have reported a correlation with elevations of maternal thyroid hormone levels rather than the presence or absence of maternal symptomatology. It might also be reasonable to measure free T 4 by equilibrium dialysis in borderline cases, because some free T 4 assays may report erroneously high free T 4 levels in situations of increased T 4 binding such as pregnancy Both propylthiouracil PTU and methimazole MMI have been used in pregnancy and are equally effective in the management of hyperthyroidism in this setting 12 , 13 , In the U.
However, MMI or its precursor carbimazole are used widely throughout the world to treat pregnant women. Transplacental passage. In the only in vivo human study to formally examine the possible placental transfer PTU and MMI, 9 pregnant women ingested 35 S-labeled compounds 2 h before the elective termination of pregnancies that ranged in gestational age from 8 to 20 weeks Only seven of the nine women had complete data.
For PTU, the ratio ranged from 0. These investigators also obtained drug transfer data from pregnant rats that supported these observations. More recently, a study using isolated perfused human placentae found no difference in the rate or extent of transplacental passage between PTU and MMI Failure to achieve a steady-state with a single dose of drug was offered as the likely explanation for the differences that were observed between this study and the earlier report by Marchant et al.
Although it is uncertain whether this in vitro model is completely representative of in vivo events, a lack of a difference in placental transfer of PTU and MMI is consistent with clinical observations showing similar fetal outcomes with either drug, in terms of thyroid function and congenital anomalies 12 , 15 , and with data showing that cord blood PTU levels were similar to or higher than simultaneously obtained maternal serum PTU levels Possible drug-related congenital anomalies.
Aplasia cutis is a congenital localized absence of skin, typically present as a 0. The lesions may close spontaneously or skin grafting may be required in more severe cases.
It occurs spontaneously in approximately 1 in births 20 , is often familial, and can occur alone or in association with other anomalies.
In , Milham and Elledge 21 reported that of 12 cases of aplasia cutis that occurred in Washington state in a 6-month period, 2 mothers had taken MMI. Subsequently, additional cases were reported in association with MMI 20 , Although Van Dijke et al. Furthermore, Martinez-Frias et al. Perhaps of greater concern than aplasia cutis are recent descriptions of a MMI embryopathy 8 cases , which includes aplasia cutis, choanal atresia, tracheal-esophageal fistulae, hypoplastic nipples, facial anomalies, and psychomotor delay reviewed in Refs.
When considering the significance of all of these reports, it must be emphasized that there are no case reports of aplasia cutis or other congenital anomalies in association with PTU exposure. This is particularly significant because PTU is the preferred drug therapy of hyperthyroidism in pregnancy in the U.
On the other hand, the rare but probable real association between MMI usage and fetal anomalies makes MMI a less attractive first line alternative. All things being equal, PTU is probably still the first choice for the treatment of hyperthyroidism in pregnancy, although MMI remains a reasonable second-line agent in the case of an allergic reaction, intolerance, or poor response to PTU.
When the diagnosis of moderate to severe hyperthyroidism is made, therapy with mg PTU every 8 h should be initiated. Lower doses should be used in milder cases, because baseline thyroid function is a major factor in the rate of drug response. If the patient has been taking MMI before she becomes pregnant, switching to PTU would be reasonable before a planned conception or if the pregnancy is diagnosed in the first trimester during the period of organogenesis.
On the other hand, if the severe hyperthyroidism persists, there should be no hesitation to increase the dose in an effort to control the hyperthyroidism to the appropriate pregnancy target. Limited data for MMI in pregnancy also suggest that drug clearance may be more rapid than in nonpregnant women Despite these caveats, Wing et al. However, if the requirement for high doses of PTU or MMI persists during pregnancy, thyroidectomy may be warranted 1 — 6.
As thyroid function improves, the dose of PTU may be gradually tapered, and when it is in the range of 50— mg daily, it is often possible to discontinue the drug altogether. As alluded to above, and as proposed by Daniels 2 low doses of ATDs should be discontinued if serum TSH levels become normal 2 , given the relationship between maternal and fetal thyroid function noted above. In one retrospective report of 30 PTU-treated women, 10 were able to discontinue it before the end of pregnancy It is clear that overzealous treatment of maternal hyperthyroidism can lead to fetal hypothyroidism 37 and goiter 38 , 39 , although most cases of hypothyroidism are really transient episodes of subclinical hypothyroidism, with mild hyperthyrotropinemia and normal serum free T 4 and T 3 levels 13 , 15 , Momotani et al.
In one report 13 , no cases of neonatal hypothyroxinemia or elevated serum TSH were seen in the offspring of treated women whose serum free T 4 levels remained elevated. This latter observation and the close relationship between maternal and fetal thyroid function might be explained by the possibility that fetal thyroid function may be under the influence of maternal thyroid stimulating immunoglobulins, as suggested by Mortimer et al.
This may also provide a rationale for using higher ATD doses to control maternal thyroid function, if need be, rather than fail to control the disease for fear of inducing fetal hypothyroidism. On the other hand, data from Haddow et al. However, it does not appear that any of the women in the study by Haddow et al. Follow-up data from infants exposed to either PTU or MMI in utero have not revealed any differences in intelligence quotient IQ when compared with age-matched controls 43 or unexposed siblings 44 , but since maternal thyroid function during the index pregnancy is not reported in these studies, it is difficult to know whether any of the children were born to mothers who were hypothyroid during gestation.
Is there a role for combined thyroxine and ATD therapy to prevent maternal hypothyroidism or fetal complications of maternal ATD exposure? This small study showed that combined therapy does not necessarily prevent neonatal hypothyroxinemia, but also showed that PTU doses are not necessarily higher when adjunctive thyroid hormone therapy is used. ATD and thyroxine therapy in pregnancy is currently anathema because it could lead to inadvertent overdosing of ATDs 6.
However, this notion might need reassessment if it could be shown that maternal hypothyroidism, a strong predictor of fetal hypothyroxinemia 13 , could be prevented. In women with either overt hyperthyroidism or such mild disease that ATDs could be discontinued, adding thyroxine to their ATD therapy would not be sensible. However, in women who require drug doses above the minimum e.
However, only prospective studies with long-term follow up data would be able to address this question. The question of the safety of lactation during ATD therapy arises in several clinical situations. Others may have previously stopped ATD therapy late in pregnancy and are currently nursing, but subsequently experience an exacerbation of hyperthyroidism requiring ATD initiation; however, they wish to continue breast-feeding.
Again, if such women are currently nursing, they often desire to continue even if ATD therapy is required. This recommendation derives from studies of thiouracil, one of the first thiourea compounds used for treatment of thyrotoxicosis. In , Williams et al. Although thiouracil treatment of hyperthyroidism was soon discontinued for other reasons, no studies of the currently used ATD drugs were published until 20 yr ago. In , Kampmann et al. The mean total amount of PTU excreted in breast milk over that period was 0.
Subsequent studies on the transfer of MMI or cabimazole CM into milk have shown that a higher proportion of an orally administered dose of these drugs to the mother appears in the milk. The mean milk to serum ratio of MMI concentration is 1.
Remember me. Log in. Forgot password or user name? Hyperthyroidism medication PTU and breastfeeding. Posts Latest Activity Photos. Page of 3. Filtered by:. Previous 1 2 3 template Next. Hi all, My name is Vasudha and I have 4 and half months baby girl.
I am just diagnosed for hyperthyroidism T4 - 20 and TSH - 0. Doctor has put me on PTU medicine mg two times a day. My doctor does not have a definite answer when I ask him can I breast feed my baby. He says we need to monitor her closely. I am dead scared thinking what if it affects my baby.
I have stopped feeding her my milk and giving her formula and she is really really fussy and cranky. She just doesn't like it. My supply was quite low before I started taking medication.
Since I express and give her milk i know this. I have already started on PTU and my supply all of a sudden increased just after one dosage. My heart pops out when throw the expressed milk in the sink.
It is very traumatic for my little girl and baby to have formula. Is it absolutely safe to breastfeed while on PTU medication for hyperthyroidism? Or is there any other alternative. One more thing. I was diagnosed for hypothyroidism when I was just pregnant. My doctor says it was due to pregnancy and I was on 75micrograms of thyroxine supplement throughout pregnancy. After delivery I took 25 micrograms but I did not realize when it became hyper.
Now my TSH level is 0. My baby is starving! Tags: None. Vasudha: We have good data on the transfer of PTU propylthiouracil and methimazole into human milk and both are generally considered safe to use in breastfeeding mothers.
We've used both of these medications for years without any problem in breastfed infants. I'd suggest you restart breastfeeding immediately. If you worry about this drug and breastfeeding, simply have your pediatrician do a T4 level on your infant after a month or so.
I'm sure it will be normal. Comment Post Cancel. Thanks a lot for the information. I am getting her back to breastfeeding from today. I will be on 50mg two times a day. To be safe I am going to express the milk 3 hrs after I take the medicine and discard the same. I will feed her later on. I am hoping for the best. Thanks Vasudha. Further query about PTU Hi, I need more information with respect to hyperthyroid medication and breastfeeding. Is methimazole better than PTU for breastfeeding?
Currently I am on 50mg ptu , two times a day 2. I am not feeding her the milk that I express 3 hours later I take the medicine. I am discarding that milk. I feed her then onwards. Does that decrease the affects of ptu or is it just mere waste of my milk? My supply is quite low already because of my thyroid condition and my little girl has growing demands.
Or should I just feed her around 4 hours later I take the medicine. Talk with your healthcare provider s before making any changes to this medication. It is important to make sure any medical conditions you have are treated appropriately, especially during pregnancy. Hyperthyroidism can increase the chance of poor outcomes for the pregnancy including miscarriage, preterm delivery, low birth weight, thyroid storm life-threatening overactive thyroid , and maternal congestive heart failure.
Miscarriage can occur in any pregnancy. Two studies did not find a higher chance of miscarriage when using PTU during pregnancy. Hyperthyroidism has been associated with an increase in the chance for miscarriage. This is called the background risk. Studies do not agree if hyperthyroidism itself can increase birth defects. Studies also do not agree if PTU alone can increase birth defects.
There has not been a confirmed pattern of birth defects to more strongly suggest cause from PTU exposure alone. Additionally, other studies show no increased chance for birth defects. In summary, although studies do not agree, there is not strong evidence to say PTU clearly increases birth defects. You and your healthcare team will decide what is best for your specific situation. Hyperthyroidism has been found to increase the chance for pregnancy complications like preterm delivery delivery before week 37 and low birth weight less than 2lb 3oz.
One study did not find a higher chance of preterm delivery when PTU was used during pregnancy. It is not clear if PTU is associated with low birth weight because studies do not agree.
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