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The Journal of Clinical Endocrinology & Metabolism 88(5):2100 –2105
Copyright © 2003 by The Endocrine Society
doi: 10.1210/jc.2002-021799
Clinical Features and Outcome of Subacute Thyroiditis
in an Incidence Cohort: Olmsted County,
Minnesota, Study
VAHAB FATOURECHI, JAROSLAW P. ANISZEWSKI, GUITI Z. EGHBALI FATOURECHI,
ELIZABETH J. ATKINSON, AND STEVEN J. JACOBSEN
Division of Endocrinology, Diabetes, Metabolism, Nutrition and Internal Medicine (V.F., J.P.A., G.Z.E.F.), Division of
Biostatistics (E.J.A.) and Division of Epidemiology (S.J.J.), Mayo Clinic, Rochester, Minnesota 55905
Subacute thyroiditis (SAT), or granulomatous thyroiditis, is
an inflammatory thyroid condition associated with pain and
systemic symptoms. Few community studies are available. We
studied the 160 patients with SAT in Olmsted County, Minnesota, seen between January 1, 1960, and December 30, 1997.
Subjects were identified through the medical diagnostic index of the Rochester Epidemiology Project. The overall ageand sex-adjusted incidence from 1960 through 1997 was 4.9
cases per 100,000/yr. In the most recent 28-yr period (1970 –
1997), 94 patients were identified. In this group, pain was the
presenting symptom in 96%. SAT recurred in 4% of the patients
6 –21 yr after the initial episode. Corticosteroid therapy was
given to 36%. Early-onset hypothyroidism occurred both in
S
UBACUTE THYROIDITIS (SAT) (also called de Quervain thyroiditis or granulomatous thyroiditis) is a selflimited, possibly viral, inflammatory thyroid disorder usually associated with thyroid pain and systemic symptoms
(1–3). Clinical features of SAT are well known and include
thyroid pain with symptoms of hyperthyroidism, suppressed levels of TSH, low thyroid uptake of radioactive
iodine, and elevated erythrocyte sedimentation rate (4, 5).
Diagnosis is based on clinical and laboratory data. Tissue
diagnosis is rarely needed (4, 6, 7). Although the clinical
features and outcome have been described in many nonpopulation-based studies (8 –11), community and incidence
cohort studies are scarce (12, 13). The epidemiology of SAT
from 1960 –1967 in Olmsted County, Minnesota, was previously reported (13). We used the database of the Rochester
Epidemiology Project to study SAT and its outcome in the
Olmsted County community from 1970 through 1997.
Subjects and Methods
Study setting
This study was carried out within the boundaries of Olmsted County,
Minnesota. Epidemiological research is possible in Olmsted County
because the county is relatively isolated from other urban centers and
because nearly all medical care is delivered to local residents by a small
number of providers. With the exception of a higher proportion of the
working population employed in the health care industry, the characteristics of the population of Olmsted County are similar to those of
United States whites (14). Mayo Clinic provides approximately half of
the primary care and nearly all of the specialty care for the community.
Abbreviations: NSAID, Nonsteroidal anti-inflammatory drug; SAT,
subacute thyroiditis.
patients receiving corticosteroid therapy (29%) and in those
not receiving corticosteroid therapy (37%). At latest follow-up,
significantly more patients who had received corticosteroid
therapy had a diagnosis of hypothyroidism than the group
without corticosteroid therapy (25% vs. 10%, P < 0.05; overall
rate of hypothyroidism, 15%). Early transient hypothyroidism
is common in SAT. Permanent hypothyroidism is less common, and only 15% of the patients are receiving T4 therapy
after 28 yr of follow-up. Symptomatic relief is achieved with
corticosteroid therapy, but such therapy does not prevent
early- and late-onset thyroid dysfunction. (J Clin Endocrinol
Metab 88: 2100 –2105, 2003)
Olmsted Medical Center and its affiliated hospital, along with Mayo
Clinic, provide comprehensive care for the region in every discipline.
The epidemiological potential in the community is enhanced by the
fact that each provider uses a comprehensive medical record system,
whereby all data about an individual are assembled in one place. Thus,
the details of every inpatient and outpatient encounter, including visits
to the emergency department, laboratory results, pathology reports, and
correspondence, can be accessed. Moreover, Mayo Clinic has indexed all
diagnoses and procedures documented in the medical records since the
early 1900s. Since 1966, similar indexes have been developed for nonMayo Clinic providers under the aegis of the Rochester Epidemiology
Project. The result is the linkage of medical records from all sources of
medical care used by the Olmsted County population. This linkage
system, therefore, constitutes a unique opportunity to ensure complete
ascertainment of disease occurrence and clinical outcomes in a geographically defined population.
Study cohort
Data from the medical diagnostic index of Mayo Clinic and the
Rochester Epidemiology Project were used to identify a cohort of patients with SAT, among residents of Olmsted County, during a 38-yr
interval (January 1, 1960, through December 30, 1997). During the study
period, the population of Olmsted County grew from approximately
75,000 to 100,000. The inclusion criteria for diagnosis of SAT were any
one of the following: 1) pathological diagnosis (surgical specimen or
biopsy); 2) painful thyroid and either suppressed uptake of iodine 131
or elevated erythrocyte sedimentation rate, or both; or 3) unilateral
thyroid pain with abnormally low uptake of iodine 131 and elevated
erythrocyte sedimentation rate.
Data were obtained by review of each patient’s medical records and
follow-up information. Inpatient and outpatient records from all providers in the county were included. For the present report, demographic
clinical and laboratory data and information related to treatment patterns and follow-up thyroid function were used. Follow-up was completed in 1997 by review of records and telephone interview when
needed. A total of 160 patients were identified in the community from
1960 through 1997 and 94 patients from 1970 through 1997. The insti-
2100
Fatourechi et al. • Subacute Thyroiditis
J Clin Endocrinol Metab, May 2003, 88(5):2100 –2105 2101
tutional review boards of Mayo Foundation and Olmsted Medical Center approved the protocol.
Laboratory methods
At the beginning of the study period, serum total T4 was measured
with a competitive protein-binding assay; beginning in 1976, an RIA was
used; and beginning in 1990, a commercial chemiluminescence system
was used. Serum TSH was measured initially with a first-generation RIA
and later, starting in 1986, with a third-generation sensitive RIA. In 1989,
a double-antibody chemiluminescent assay was introduced, which used
a modified automated chemiluminescence system (ACS: 180; Bayer
Corp. Diagnostics, Tarrytown, NY) and modified ACS: 180 TSH reagents. Serum total triiodothyronine was measured initially with an RIA
and, in recent years, with an automated chemiluminescent immunoassay (ACS: 180; Bayer Corp. Diagnostics). Serum free T4 was measured
with a dialysis method, using an RIA system, starting in 1974 and, more
recently, with a commercial system (AxSYM analyzer; Abbott Laboratories, Abbott Park, IL). Antimicrosomal antibody was measured with
a microtitration assay based on agglutination of gelatin particles (SeraTek; Fujirebio Inc., Tokyo, Japan). Serum thyroglobulin was measured
with a double-antibody chemiluminescence assay. Other than a change
in the lower limit of detection of serum TSH, despite some changes in
assay methodology, the reference ranges did not change during the
study period (Table 1).
Incidence calculation
In calculating the incidence rates (1960 –1997), the entire population
of Olmsted County was considered to be at risk. Age- and sex-specific
person-year denominators were estimated from decennial census data
for Olmsted County, with linear interpolation between census years (15).
It was assumed that, with a fixed number of person-years, the number
of incidence cases followed a Poisson distribution. This assumption
allowed for the estimation of se and the calculation of confidence intervals for incidence rates. The rates were age- and sex-adjusted to the
distribution of the 1990 United States white population by expressing
adjusted rates as weighted averages of crude rates. The se and confidence intervals of adjusted rates were based on the same assumptions.
The relationships of crude incidence rates to age, sex, seasonality, and
decade of diagnosis were assessed by use of generalized linear models,
assuming a Poisson error structure (16).
Clinical features and outcome
The data from 94 cases seen from January 1, 1970, through December
30, 1997, were evaluated in detail for clinical and laboratory features and
outcomes. Descriptive statistics, the ␹2 test, and the Student t test were
used for comparison of differences between groups and for other analyses of these data.
Results
Incidence
The overall age- and sex-adjusted incidence rate from 1960
through 1997 was 4.9 cases per 100,000/yr (95% confidence
interval, 4.1–5.7). The total age- and sex-adjusted incidence
rate decreased from 8.7 in the 1960s, to 5.6 in the 1970s, to 3.2
in the 1980s (P ⬍ 0.01). In the 1990s, the incidence rate
remained stable at 3.6. The main difference in rates was
between the 1960s and the following years. Differences in
rates among the 1970s, 1980s, and 1990s were only marginally significant (P ⫽ 0.05). Incidence rates for women in the
1960s, 1970s, 1980s, and 1990s were 14.1, 9.0, 4.7, and 4.6,
respectively; for men, 2.8, 2.1, 1.5, and 2.8, respectively. Rates
between the sexes were significantly different (P ⬍ 0.01). The
decrease in the incidence was statistically significant in the
female population between the 1960s and the 1990s (P ⬍ 0.01)
but not in the male population (P ⫽ 0.46). The peak incidence
was in the fifth decade of life for both sexes.
Seasonal variation
Of the 160 patients in 38 yr, 46 were seen in the spring, 45
in the fall, 36 in the summer, and 33 in the winter. In spring
and summer, more patients were seen in May and August
than in any other 2 months (Fig. 1). Although there was a
trend toward more cases in fall and spring, Poisson regression did not show statistical significance (P ⫽ 0.26). There
was no obvious geographic clustering within the county, no
apparent familial aggregation of cases, and no involvement
of more than 1 member in a household.
Clinical features (1970 –1997)
Demographic data. There were 94 patients in the cohort within
the 28-yr period: the female-male ratio was 3.5; mean age was
46 yr (median, 45 yr; range, 14 – 87 yr); 76 patients were
residents of the city of Rochester, and 18 lived in other areas
of the county. Four patients were never seen at Mayo Clinic;
the diagnoses for those 4 were made elsewhere.
Symptoms at onset. A history of upper respiratory tract infection in the 30 d before the onset of SAT was recorded for
20 patients; a history of upper respiratory tract infection in
TABLE 1. Laboratory data at diagnosis for 94 patients with SAT
Laboratory test
n
Reference range
Total T4 (␮g/dl)
Free T4 (ng/dl)b
Total triiodothyronine (ng/dl)c
TSH (␮IU/ml)d
Thyroglobulin (ng/ml)f
Erythrocyte sedimentation rate (mm/h)
78
20
10
44
5
53
Uptake of iodine 131 (%)
79
5.0 –12.5
0.8 –1.8
80 –180
0.30 –5.0
ⱕ59.4
0 –22 (male)
0 –29 (female)
8 –29
a
a
Mean ⫾
SD
Median
12.1 ⫾ 43
2.8 ⫾ 2.0
180 ⫾ 75
0.9 ⫾ 1.6e
383 ⫾ 295
51 ⫾ 26
11.1
2
134
0.05
271
44
3.2 ⫾ 3.5
1.4
To convert to nM, multiply by 12.87.
To convert to pM, multiply by 12.87.
To convert to nM, multiply by 0.0154.
d
To convert to mIU/liter, multiply by 1.0.
e
Mean serum concentration of TSH is higher than expected because, between 1974 and 1986 when the sensitive TSH assay was not available,
the lower limit of detection of serum TSH was higher.
f
To convert to ␮g/liter, multiply by 1.0.
b
c
2102
J Clin Endocrinol Metab, May 2003, 88(5):2100 –2105
Fatourechi et al. • Subacute Thyroiditis
typical of patients with SAT. We excluded from the study 3
patients who had a clinical diagnosis of SAT not confirmed
by fine-needle aspiration biopsy.
FIG. 1. Number of patients with SAT seen in Olmsted County, Minnesota, in different months of the year, from 1960 to 1997.
the 30 –90 d before the onset of SAT was recorded for 4
patients. Mild to severe spontaneous thyroid pain was
present in 90 patients and was absent in 4. Pain was documented in 1 of these 4 patients at a follow-up visit. Radiation
of pain to the jaw was documented in 12 patients and to the
ears in 18 patients. At presentation, dysphagia was present
in 30 patients, arthralgia in 3, myalgia in 12, tremor in 19,
sweating in 22, and weight loss (4.5–18.2 kg) in 15.
Signs. Of 41 patients who had body temperature recorded, 27
had temperatures between 37 C and 38 C, and 7 had temperatures between 38 C and 39.5 C. Only 5 patients did not
have pain on palpation of the thyroid. For cases in which
clinical estimation of goiter weight was recorded, the estimate was between 20 and 70 g in 57 patients and less than
20 g in 19 patients. Tenderness involved the entire gland in
44 patients, the left lobe in 14, and the right lobe in 16.
Localized tenderness of 1 of the lobes was noted in 10 patients; the area of tenderness was not documented in the
remainder. No cases of tracheal compression or deviation
were documented. Palpable nodules were noted in 21 patients, with nodules varying in size between 5 and 30 mm.
Laboratory and imaging data. Initial laboratory data at diagnosis are shown in Table 1. Because the study encompassed
a period when serum TSH or sensitive TSH measurement
was not available, some patients did not have a serum TSH
measurement. Antimicrosomal antibodies were measured
for 14 patients: for 11 patients, they were weakly positive at
a 1:100 dilution; for 3 patients, antimicrosomal antibodies
were highly positive at dilutions of 1:25,600, 1:1,600, and
1:400. Only 2 patients had thyroid-stimulating immunoglobulin measurements, and both were negative.
Technetium 99 thyroid scanning was done in 14 patients;
in each of the 14, the thyroid was not visualized or was
visualized poorly. Thyroid ultrasonography was done in 6
patients; in each, it showed mild thyroid enlargement with
inhomogeneous echo texture and hypoechoic areas consistent with inflammation. Fine-needle aspiration biopsy of the
thyroid was done in 13 patients: results for 11 patients were
typical for SAT; for 1, results were nondiagnostic; and for 1,
results were consistent with Hashimoto thyroiditis. We included these last 2 patients because they were otherwise
Therapy. Table 2 shows the types of therapy for the patients.
Among 94 patients, 34 (36%) received prednisone therapy
(daily starting dose: mean, 40 mg; median, 42 mg). Therapy
with nonsteroidal anti-inflammatory drugs (NSAIDs) was
the only therapy for 39 patients; therapy with NSAIDs and
corticosteroids was given to 18 patients. Acetylsalicylic acid
was given as therapy to 43 patients; 14 received other
NSAIDs. For the group receiving NSAIDs and acetylsalicylic
acid, the mean period from the start of therapy to complete
alleviation of pain was 35 d (median, 21 d; range, 7–150 d).
The duration of therapy with high doses of prednisone
(30 – 40 mg/d) was 3–30 d (median, 7 d; range, 4 – 43 d). After
initial high-dose therapy, prednisone therapy was tapered
and continued for a mean of 34 d (median, 30 d). Five patients
required restarting prednisone therapy because of early recurrence within 2–10 months. Excluding patients who had
early recurrence (within the first 6 –12 months), the median
time to complete resolution of pain, after beginning therapy
with steroids, was 4 d (mean, 8 d). ␤-Blockers were given to
11 patients.
Recurrence. Early initial recurrence resulted in restarting corticosteroid therapy in 10% of the patients who had received
corticosteroid therapy initially. SAT recurred after 6 –21 yr in
4 patients (4% of the patients) (Table 3). A fifth patient had
a clinical diagnosis of recurrence 11 yr after the initial episode, but the data were not adequate for inclusion in this
group. The recurrences were milder than the initial episodes.
One patient had a documented episode of SAT before the
study period and was seen after 6 yr with recurrence. She had
two undocumented episodes before the two documented
episodes. Despite corticosteroid therapy, hypothyroidism
developed in two of the patients who had recurrence.
TABLE 2. Therapy for 94 patients with SAT
Patients
Therapy
NSAIDs alone
NSAIDs alone or NSAIDs ⫹ corticosteroids
Corticosteroids alone
Corticosteroids alone or with other therapy
Acetaminophen
Thyroidectomy
n
%
39
57
15
34
21
1
41
61
16
36
22
1
TABLE 3. Outcome among 94 patients with SATa
Outcome
b
Early recurrence
Early hypothyroidismb
Late recurrencec
Late hypothyroidismc
Nodular goiter
Associated autoimmune disease
Malignancy
Patients (%)
10
34
4
15
5
5
11
a
None had thyroid cancer, Graves’ disease, or Graves’ ophthalmopathy.
b
Early, within the first 6 –12 months.
c
Late, after 1 yr.
Fatourechi et al. • Subacute Thyroiditis
Follow-up of thyroid function. At some time during follow-up,
serum TSH concentrations were more than 5 ␮IU/ml (5
mIU/liter) in 32 patients (34%); in 16 of those patients (17%),
serum TSH was more than 10 ␮IU/ml (10 mIU/liter). Among
the 34 patients who had received corticosteroid therapy, 10
had TSH levels greater than 5 ␮IU/ml (5 mIU/liter) (29%).
Of the 60 patients not receiving corticosteroids, 22 (37%) had
TSH elevation at follow-up; 11 of those (18%) had serum TSH
greater than 10 ␮IU/ml (10 mIU/liter).
TSH elevation was documented in the first year in 27
patients. In 4 patients, TSH elevation persisted after the first
year, and they received T4 therapy. Five patients were treated
within the first year, and treatment was continued long term.
Of the 27 patients with elevated TSH levels in the first year,
only 9 were receiving T4 therapy at latest follow-up; among
the 18 who did not receive therapy, TSH levels normalized
during follow-up. For the 27 patients, mean TSH (⫾sd) was
16 ⫾ 14 ␮IU/ml (16 ⫾ 14 mIU/liter), and median TSH was
9.6 ␮IU/ml (9.6 mIU/liter). For the patients who had TSH
elevation in the first year, the elevation occurred after a mean
of 84 d (median, 68 d). Late-onset hypothyroidism occurred
2–24 yr after SAT in 5 patients.
At latest follow-up, for 14 patients (15%), there was definite previous documentation of hypothyroidism; 3 other
patients were receiving therapy without adequate documentation. With the exclusion of patients with early (in the first
year) TSH elevation, 9 patients (9.5%) were receiving T4
therapy for late (after the first year) hypothyroidism. With
the exclusion of the 3 cases without adequate documentation,
T4 therapy was given to 25% of the group (8 patients) receiving corticosteroid therapy and 10% of the group (6 patients) not receiving corticosteroid therapy. The corticosteroid therapy group had a higher rate of hypothyroidism on
long-term follow-up (P ⬍ 0.05).
No patient had Graves’ disease, Graves’ ophthalmopathy,
or thyroid cancer on follow-up. One patient continued to
have persistent pain beyond 1 yr and had a thyroidectomy.
Five had nodular goiter, and 1 had a subsequent diagnosis
of Hashimoto thyroiditis.
Associated conditions. There was one case of seronegative
rheumatoid arthritis, one case of Sjögren syndrome, one case
of chronic ulcerative colitis, one case of urticaria, one case of
contact dermatitis, and one case of psoriasis. However, nonthyroid malignancies were common (11.4% of patients). Either before or after SAT, three patients had breast cancer and
eight patients had other malignancies (prostate, lung, endometrial, cervical, gastric, and pancreatic cancer; non-Hodgkin
lymphoma; and systemic mastocytosis). It is not clear
whether this rate of malignancy is higher than in the general
population or reflects the long follow-up period of 28 yr.
Discussion
SAT (de Quervain thyroiditis) is a transient, inflammatory
thyroid disease associated with pain and tenderness of the
thyroid as well as with generalized somatic symptoms, causing great discomfort for weeks or months if left untreated.
SAT is most likely the result of a viral infection (17–19). There
is no definitive cure for painful SAT, but there is effective
treatment that will ameliorate the symptoms and allow the
J Clin Endocrinol Metab, May 2003, 88(5):2100 –2105 2103
disease to run its course in an asymptomatic fashion. Diagnosis of SAT excludes forms of infective bacterial and fungal
thyroiditis. The term “SAT” is not usually applied to silent,
painless thyroiditis with lymphocytic pathological features
or to postpartum thyroiditis (6, 20). Salicylates and NSAIDs
can be given to patients with mild and moderate forms of the
disorder (20). In severe forms, therapy with corticosteroids
generally provides rapid relief of symptoms within 24 – 48 h
(20). Prednisone therapy may be initiated in dosages of 40 mg
daily, with a gradual reduction in dosage thereafter over
several weeks (20). Corticosteroid therapy was given to 36%
of our patients; symptoms resolved in a few days. Thyroidectomy should be considered for only a small minority of
patients who have repeated relapses despite appropriate
treatment (21). Only one patient in our series required
thyroidectomy.
Few epidemiological studies of SAT have been reported
(12, 22–26). Only 1 study has attempted to collect and report
all cases seen in a specific community (13). In that report,
from our institution, cases seen between 1960 and 1967 in our
county were studied. The incidence was higher in females
(19.1 per 100,000/yr) than in males (4.4 per 100,000/yr). The
higher incidence in females in the present study is similar to
the findings of previous reports (5). Although the cause is
most likely viral, SAT, like all other thyroid conditions, occurs most commonly (in 80% of cases) in women who are
40 –50 yr old (5). The reason for the reduced incidence after
1970 is not clear. However, the use of more refined laboratory
tests in recent years, resulting in the exclusion of some cases,
may be an explanation. Similar to the results of the previous
Mayo Clinic study, the results of our present study did not
show statistically significant seasonal variation over the extended 38-yr period. However, there was a slight trend toward aggregation of cases in May and August and also in the
fall and spring seasons. Familial or geographic aggregation
of cases was not noted either. In some reports, seasonal
clustering has been reported; but because these were not
community studies, the importance is not clear (12, 25). Other
studies show no seasonal clustering of cases (13, 22). In our
present study, associated autoimmune conditions did not
seem more common than those observed in the general
population.
Transient early hypothyroidism and late-onset (or permanent) hypothyroidism can occur (23, 27–30). Reports indicate
that the hyperthyroid phase is often followed by a transient
phase of hypothyroidism, in which an exaggerated TSH response to TSH-releasing hormone was noted in 56% of the
patients (29). Permanent hypothyroidism is also a known
complication and has been reported in 5% of cases (29).
During the shorter follow-up of the previous Olmsted
County study, only 3 of the 70 patients (4%) required T4
therapy. In the present report with longer follow-up and
more patients, the incidence of hypothyroidism was higher
(9.5% had documented elevated TSH after the first year).
Among our patients, 34% had subsequent abnormal TSH
elevation, the majority occurring within the first year after
onset of SAT symptoms. There was no significant difference
in the overall rate of early-onset hypothyroidism between the
group receiving corticosteroid therapy and the group not
receiving corticosteroid therapy. However, at latest follow-
2104
J Clin Endocrinol Metab, May 2003, 88(5):2100 –2105
up, more patients who had received corticosteroid therapy
were receiving T4 therapy, which indicates that corticosteroid therapy does not prevent development of permanent
hypothyroidism. The reason for the higher degree of permanent hypothyroidism in the corticosteroid-treated group
is not completely clear, but patients with more severe disease
may be more likely to be treated with corticosteroids and
thus be more likely to have hypothyroidism develop. One
study of 29 patients from France reported an incidence of
hypothyroidism of 31% (23). Development of autoimmune
hypothyroidism, initiated by a thyroid-destructive insult,
can explain this finding. One could argue that the hypothyroid cases were transient thyroid failures inappropriately
treated with long-term T4. However, only 5 of the 27 patients
with early TSH elevation received T4 therapy in the first year;
and in the 22 patients who were observed, thyroid function
later normalized in 18 and hypothyroidism persisted in 4,
who required therapy. To determine the actual rate of irreversible hypothyroidism, discontinuation of T4 therapy and
reassessment would be necessary for the early therapy
group, but this was not done for our cohort. In the pathogenesis of late-onset hypothyroidism, autoimmunity and development of antithyroid and blocking antibodies have been
speculated (28, 30 –32). SAT may trigger autoreactive B cells
to produce TSH-receptor antibodies, resulting in TSHreceptor antibody-associated thyroid dysfunction in some
patients (31).
In our community study, we did not see the development
of Graves’ disease and Graves’ ophthalmopathy that have
been reported in isolated cases (33–35); thus, in community
practice, development of subsequent Graves’ disease is unlikely. In a recent report of SAT, 22% of 36 patients had early
recurrence, necessitating restoration of a higher dose of corticosteroids (8). In our study, early recurrence within the
subacute phase occurred in 10% of the group receiving corticosteroid therapy.
SAT, which is considered to be a viral disease (17–19),
rarely recurs after a complete recovery, possibly because of
immunity to the offending virus. However, late recurrence
after several years has been reported (36 –39). In 1 study, 4
recurrent episodes of SAT occurred in 3 of 222 patients
(1.4%). The recurrent episodes were similar to the first episodes of SAT. The titers of various viral antibodies were not
increased during the clinical course of recurrence (39). In a
larger study that evaluated data for 3,344 patients with SAT
between 1970 and 1993, SAT recurred in 48 of 3,344 patients
(1.4%) (mean, 14.5 ⫾ 4.5 yr after the first episode). Five
patients experienced a third episode (mean, 7.6 ⫾ 2.4 yr after
the second episode) (39). Our cohort study showed a 4%
recurrence rate after many years. One patient had 3 recurrences, with several years between episodes. Theoretically,
late recurrence possibly occurs after the disappearance of
immunity to the previous viral infection. Hypothyroidism
developed in 2 of 4 patients with late recurrence; but from
these 2 cases, we cannot conclude that recurrence predisposes to late-onset hypothyroidism.
Our study has some limitations. Data for frequency of
symptoms, in the medical records, may have been incomplete. Diagnostic practices have changed; some of the earlier
cases did not have a sensitive TSH measurement. Not all the
Fatourechi et al. • Subacute Thyroiditis
cases had results for erythrocyte sedimentation rate. Underestimation may have been a problem, and patients with
milder disease may not have sought medical help. Some of
the patients receiving over-the-counter medications may not
have supplied an adequate drug history. There are also some
limitations to the conclusions derived from this retrospective
study. It is probable that patients with severe disease were
more likely to be treated with corticosteroids, and the severity of the thyroid inflammation may have been the cause
of more frequent hypothyroidism in this group. Also, the
greater incidence of hypothyroidism in this cohort could be
an overestimation, because it is not clear whether some patients had temporary disease in the first year and were
treated without a need for lifelong therapy. Our patients
were from a mostly white population, and generalization to
other ethnic groups may not be appropriate. However, a
strong point of our study is that the high quality of primary
care in the community reduces the possibility of missed
cases. In addition, care was given by a limited number of
providers, and the majority of patients were referred to subspecialists for management of thyroid disorder.
In conclusion, our cohort study shows that, in the first year
of onset of SAT, transient hypothyroidism is very common.
There is no significant difference in the incidence of mild
thyroid failure, in this early phase, between patients receiving corticosteroid therapy and those not receiving corticosteroid therapy. In contrast, long-term hypothyroidism requiring T4 therapy is significantly more common in the group
receiving corticosteroid therapy. Therefore, corticosteroid
therapy does not prevent subsequent hypothyroidism. Thus,
we believe that corticosteroid therapy should be given to
improve the symptoms and quality of life without an expectation of reducing long-term thyroid dysfunction. Also,
because of the high incidence of transient hypothyroidism in
the first year, T4 therapy should not be considered lifelong if
started in the first year.
Acknowledgments
Received November 14, 2002. Accepted February 6, 2003.
Address all correspondence and requests for reprints to: Vahab Fatourechi, M.D., Mayo Clinic, 200 First Street SW, Rochester, Minnesota
55905.
This work was supported in part by the Richard Emslander Clinical
Investigator Award and Scholarly Clinician Award of the Mayo Foundation and the U.S. Public Health Service, National Institutes of Health
(AR-30582). These data were presented in part at the 74th Annual Meeting of the American Thyroid Association, November 9, 2001, Washington, D.C., and at the 84th Annual Meeting of The Endocrine Society, June
19, 2002, San Francisco, California.
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