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Thionamides: Side effects and toxicities

Author: Douglas S Ross, MD
Section Editor: David S Cooper, MD
Deputy Editor: Jean E Mulder, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Sep 2019. | This topic last updated: Aug 31, 2018.

INTRODUCTION

Thionamide compounds were found in 1943 to inhibit thyroid hormone synthesis. They are actively
transported into the thyroid gland where they inhibit both the organification of iodine to tyrosine
residues in thyroglobulin and the coupling of iodotyrosines (figure 1) [1]. Adverse effects of
thionamides include common, minor side effects (eg, rash) and rare but serious adverse effects,
such as agranulocytosis and hepatotoxicity. Patients should be made aware of side effects at the
time of drug initiation, preferably in writing, and at subsequent visits.

The adverse effects of propylthiouracil (PTU) and methimazole and their management will be
reviewed here. Specific issues related to their use in the treatment of Graves' disease are
discussed separately. (See "Thionamides in the treatment of Graves' disease".)

PHARMACOKINETICS

Propylthiouracil (PTU) and methimazole are the thionamide drugs available in the United States.
Carbimazole is a third option available in many countries, but not in North America. Methimazole
and carbimazole are interchangeable because carbimazole is completely metabolized to
methimazole. The carbimazole dose required to yield an equivalent dose of methimazole is
approximately 40 percent higher.

PTU, but not methimazole, inhibits the 5'-monodeiodinase that converts thyroxine (T4) to
triiodothyronine (T3) in extrathyroidal tissue. However, methimazole has several important
pharmacokinetic advantages over PTU:

● The serum half-life of methimazole is four to six hours, whereas that of PTU is 75 minutes.

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● The intrathyroidal methimazole concentration, which can reach a thyroid-to-serum ratio of

100:1, remains high for up to 20 hours, considerably longer than that of PTU.

● Perchlorate discharge tests, which are a measure of inhibition of iodine organification,

demonstrate the superiority of methimazole over PTU. In one study, perchlorate discharged
37 percent of the radioiodine tracer 24 hours after a single 15 mg dose of methimazole versus
only 8.6 percent after a 300 mg dose of PTU [2].

COMMON, MINOR SIDE EFFECTS

Both methimazole and propylthiouracil (PTU) can cause pruritus, rash, urticaria, arthralgias,
arthritis, fever, abnormal taste sensation, nausea, or vomiting in up to 13 percent of patients [3]. In
one trial, the percentage of patients who discontinued antithyroid drugs due to adverse reactions
was 17, 29, and 34 percent for 15 or 30 mg of methimazole or PTU, respectively [4].

Mild skin reactions can be treated with antihistamine therapy without stopping methimazole or
PTU [5], with the caveat that some skin reactions from PTU may be indicative of vasculitis. If one
drug is not tolerated, the other drug can be substituted, but up to 50 percent of patients have
cross-sensitivity. For patients with serious allergic reactions, prescribing the alternative drug is not
recommended and the patient should be managed with radioiodine or surgery.

The gastrointestinal side effects are dose dependent. Thus, we prefer to use divided doses in
patients taking higher doses of methimazole (≥20 mg) and then change to single daily dosing if
tolerated and as the dose is reduced. (See "Thionamides in the treatment of Graves' disease",
section on 'Dosing'.)

RARE BUT SERIOUS ADVERSE EFFECTS

Potential teratogenicity — Thionamides have been associated with possible teratogenic effects,
but teratogenic effects are more severe with methimazole and carbimazole compared with
propylthiouracil (PTU). This topic is discussed in greater detail separately. (See "Hyperthyroidism
during pregnancy: Treatment", section on 'Choice of thionamide'.)

Agranulocytosis — Agranulocytosis is a rare but serious complication of thionamide therapy with

a prevalence of 0.1 to 0.5 percent. The risk of agranulocytosis is higher for thionamides than for
20 other classes of drugs associated with this rare complication [6]. If a patient develops
agranulocytosis with either PTU or methimazole, use of the other drug is contraindicated due to
risk of cross-reactivity.

Agranulocytosis usually occurs within the first two to three months of treatment [7-10]. In one
study from Japan, the average time to onset of agranulocytosis was 69 days (range 11 to 233

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days) [8].

The risk of agranulocytosis from methimazole (but not PTU) appears to be dose related.
Compared with low doses of methimazole, PTU (any dose) appears more likely to cause
agranulocytosis [10]. In one study, agranulocytosis was more frequent in older patients taking
methimazole in doses higher than 40 mg/day [11], while in two other studies, agranulocytosis was
more common with doses >20 mg daily versus 5 to 15 mg daily [6,12], and in a third study, no
cases were seen with methimazole doses under 30 mg and the prevalence of agranulocytosis with
PTU was dose independent [11]. However, a Japanese study found that the development of
agranulocytosis from methimazole was independent of dose, age, duration of treatment, or second
exposure to the thionamide [13].

In the United Kingdom, reports of agranulocytosis are more common with PTU than carbimazole
[14]. Most cases occur within three months after treatment is begun.

● White blood cell (WBC) assessment – We advise patients taking a thionamide to have an
immediate white cell count with differential at the earliest sign of a fever, sore throat, or other
infection and to discontinue the drug until the result is available.

Controversy exists as to the value of monitoring WBC counts. Most clinicians in the United
States do not perform periodic monitoring, and the American Thyroid Association (ATA)
guidelines do not recommend monitoring [5]. However, a study from Japan was able to
identify 78 percent of cases of granulocytopenia before the development of agranulocytosis or
the onset of symptoms by checking blood counts every two weeks for the first two months of
therapy [15]. (See "Thionamides in the treatment of Graves' disease", section on 'Monitoring'.)

● Prognosis – Recovery from agranulocytosis usually takes a few days but can be prolonged,
and morbidity and death from serious infections can occur. In a Japanese registry, 30 of 754
cases (4 percent) were fatal [9]. Granulocyte colony-stimulating factor (G-CSF) has been
used as adjunctive therapy in severe cases [16], but its efficacy was called into question in an
older, randomized, prospective, controlled trial of 24 patients with a thionamide-induced
neutrophil count of less than 500/microL, showing no difference in the time to neutrophil
recovery between those who received G-CSF versus those who did not [17]. However, this
study has been criticized because of its small sample size (n = 24) and the use of a likely
inadequate dose of G-CSF (100 to 250 mcg/day). Subsequent nonrandomized studies have
documented the effectiveness of hematopoietic growth factors to decrease the time to WBC
normalization and the length of hospital stay [18]. However, there is no firm evidence that
such therapy impacts mortality from antithyroid drug-induced agranulocytosis [19].
Glucocorticoid therapy is ineffective. (See "Drug-induced neutropenia and agranulocytosis".)

Hepatotoxicity — Hepatotoxicity is a rare complication of thionamide therapy. Patients taking

PTU or methimazole who develop jaundice, dark urine, light stools, abdominal pain, anorexia,

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nausea, or other evidence of hepatic dysfunction should be told to discontinue the drug
immediately and to contact the clinician for assessment of liver function (transaminases, bilirubin)
[5]. PTU should not be used if transaminases reach three times the upper limit of normal and fail
to improve on repeat testing one week later. After discontinuation, liver function tests should be
monitored weekly until normalization. If they do not normalize, immediate referral to a hepatologist
or gastroenterologist may be necessary.

Serum transaminase concentrations increase transiently in up to one-third of patients taking PTU;

this abnormality may be associated with focal hepatic necrosis on liver biopsy [20]. A literature
survey published in 1997 reported 49 cases of hepatotoxicity, 28 associated with PTU (including
seven deaths) and 21 associated with methimazole (including three deaths) [21]. There was no
relationship between a fatal outcome and either the dose or duration of thionamide treatment.

Although methimazole has been associated with liver disease, reports from the United States had
suggested it is typically due to cholestatic dysfunction not hepatocellular inflammation [22]. In
contrast, studies from Taiwan and China suggest similar [23] or higher rates of hepatitis with
methimazole than PTU when the dose exceeded 13 mg/day [24], although the risk of liver failure
was less [24]; almost all cases occurred within the first 180 days of treatment [24].

PTU, on the other hand, can cause fulminant hepatic necrosis [25,26]. Over the past 20 years, 22
cases of severe hepatotoxicity in adults in the United States resulted in nine deaths and five liver
transplants. Over the same period, 12 children developed liver failure resulting in three deaths and
six liver transplants. It was estimated that this complication occurs in 1 in 10,000 adults taking
PTU, with an even greater risk in children (1 in 2000) [25,27,28]. PTU-related hepatotoxicity
typically occurs within 90 days of starting the medication (although cases occurring up to one year
have been reported), and it is not dose related.

Accumulating evidence on PTU-associated hepatotoxicity, particularly in children [27], led to

changes in recommendations for the use of thionamides. At a 2009 joint meeting of the ATA and
US Food and Drug Administration (FDA), it was recommended that PTU not be prescribed as a
first-line drug in children or adults [25,28]. PTU has a "boxed warning" because of the risk of liver
failure. (See "Thionamides in the treatment of Graves' disease", section on 'Choice of drug'.)

ANCA-positive vasculitis — An antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis

has been reported in association with PTU use [29]. There is also a possible association between
methimazole and ANCA-positive vasculitis, but the number of cases is too small to establish a
cause-and-effect relationship. This is one of several reasons why we strongly prefer the use of
methimazole or carbimazole rather than PTU.

In a review of studies of patients with thionamide-induced ANCA-positive vasculitis, ANCA were

present in 4 to 64 percent of patients taking PTU and 0 to 16 percent of patients taking
methimazole; however, only approximately 15 percent (1 in 6) of ANCA-positive patients develop

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clinical evidence of vasculitis [29]. In a subsequent prospective study from Brazil, 21 percent of
patients taking methimazole had ANCA, but none developed vasculitis [30]. Approximately one-
third of the studies showed an association between duration of thionamide therapy and onset of
ANCA positivity. In a retrospective report of 16 cases from China, median time of onset of PTU-
induced ANCA-associated vasculitis was 36 months (range 1 to 193 months) [31]. (See "Clinical
spectrum of antineutrophil cytoplasmic autoantibodies", section on 'Drug-induced ANCA-
associated vasculitis'.)

Clinical symptoms of ANCA-positive vasculitis may include fever; joint pain; weight loss; myalgia;
ocular signs (eg, uveitis, scleritis); painful, necrotic, purpuric skin lesions, often affecting the ears
and nose; hematuria, reflecting glomerular injury; hemoptysis; and central nervous system
involvement. Since the majority of ANCA-positive patients have no clinical symptoms of vasculitis,
we only assess ANCA levels in those patients who have symptoms consistent with possible
vasculitis.

Treatment involves discontinuation of the offending drug and immunosuppressive therapy with
glucocorticoids and other agents like cyclophosphamide. (See "Clinical spectrum of antineutrophil
cytoplasmic autoantibodies", section on 'Management'.)

Other — Other rare but serious side effects of thionamides include aplastic anemia [32],
pancreatitis (methimazole) [33], and insulin autoimmune syndrome with hypoglycemia
(methimazole) [34]. (See "Hypoglycemia in adults without diabetes mellitus: Diagnostic approach",
section on 'Determining the cause of hypoglycemia'.)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Hyperthyroidism".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short, easy-to-
read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and
more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
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subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Hyperthyroidism (overactive thyroid) (The Basics)")

● Beyond the Basics topics (see "Patient education: Hyperthyroidism (overactive thyroid)
(Beyond the Basics)" and "Patient education: Antithyroid drugs (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Propylthiouracil (PTU) and methimazole are the thionamide drugs available in the United
States. Carbimazole is a third option available in many countries, but not in North America.
Methimazole and carbimazole are interchangeable because carbimazole is completely
metabolized to methimazole. The carbimazole dose required to yield an equivalent dose of
methimazole is approximately 40 percent higher. (See 'Pharmacokinetics' above.)

● Methimazole has clinical advantages and less severe toxicity when compared with PTU, and
it is usually preferred to PTU (except during the first trimester of pregnancy or during the initial
treatment of thyroid storm). (See "Thionamides in the treatment of Graves' disease", section
on 'Choice of drug'.)

● Both methimazole and PTU can cause pruritus, rash, urticaria, arthralgias, arthritis, fever,
abnormal taste sensation, nausea, or vomiting in up to 13 percent of patients [3]. (See
'Common, minor side effects' above.)

● Agranulocytosis is a rare but serious complication of thionamide therapy, with a prevalence of

0.1 to 0.5 percent. We advise patients taking a thionamide to have a white blood cell (WBC)
count with differential at the earliest sign of a fever, sore throat, or other infection and to
discontinue the drug until the result is available. (See 'Agranulocytosis' above.)

● Patients taking PTU or methimazole who develop jaundice, dark urine, light stools, or other
evidence of hepatic dysfunction should be told to discontinue the drug immediately and to
contact the clinician for assessment of liver function. (See 'Hepatotoxicity' above.)

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REFERENCES

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28. Bahn RS, Burch HS, Cooper DS, et al. The Role of Propylthiouracil in the Management of
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29. Balavoine AS, Glinoer D, Dubucquoi S, Wémeau JL. Antineutrophil Cytoplasmic Antibody-
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31. Yang J, Yao LP, Dong MJ, et al. Clinical Characteristics and Outcomes of Propylthiouracil-
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Topic 7875 Version 20.0

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GRAPHICS

Thyroid hormone biosynthesis

Thyroid hormone synthesis includes the following steps: (1) iodide (I -) trapped by the
thyroid follicular cells; (2) diffusion of iodide to the apex of the cells; (3) transport of
iodide into the colloid; (4) oxidation of inorganic iodide to iodine and incorporation of
iodine into tyrosine residues within thyroglobulin molecules in the colloid; (5)
combination of two DIT molecules to form tetraiodothyronine (T4) or of MIT with DIT to
form T3; (6) uptake of thyroglobulin from the colloid into the follicular cell by
endocytosis, fusion of the thyroglobulin with a lysosome, and proteolysis and release of
T4, T3, DIT, and MIT; (7) release of T4 and T3 into the circulation; and (8) deiodination
of DIT and MIT to yield tyrosine. T3 is also formed from monodeiodination of T4 in the
thyroid and in peripheral tissues.

T4: thyroxine; T3: triiodothyronine; DIT: diiodotyrosine; MIT: monoiodotyrosine.

Modified from: Scientific American Medicine, Scientific American, New York, 1995.

Graphic 76931 Version 5.0

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Contributor Disclosures
Douglas S Ross, MD Consultant/Advisory Board: Medullary Thyroid Cancer Registry Consortium [Thyroid
cancer]; Shire [Hypoparathyroidism (Parathyroid hormone for injection)]; Spectrix Therapeutics, LLC
[Hypothyroidism (Thyroid hormone)]; IBSA Pharma Inc [Hypothyroidism (Levothyroxine sodium)]. Other
Financial Interests: Abbott India (honorarium) [Hyperthyroidism (carbimazole, levothyroxine)]; Quest
Diagnostics (honorarium) [Hyperthyroidism]. David S Cooper, MD Nothing to disclose Jean E Mulder,
MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.

Conflict of interest policy

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