Graves' disease is an autoimmune disorder in which antibodies (TRAK / TRAb / TSI) bind to the TSH receptor and
drive the thyroid into overdrive β too much T3 and T4. It is the most common cause of hyperthyroidism, and it overwhelmingly affects women.
A woman's lifetime risk is roughly 3%, versus about 0.5% for men β a 5β8Γ imbalance driven by
estrogen effects on the immune system, X-chromosome genetics, and reproductive transitions (pregnancy, postpartum, menopause).
In plain terms. The thyroid is a small butterfly-shaped gland in the front of the neck. It acts like the body's
thermostat β it sets how fast everything runs: heart rate, body temperature, energy use, mood, digestion. In Graves', the immune
system makes a mistake and produces an antibody that latches onto the thyroid and jams the accelerator down. The thyroid can't tell
the difference, so it keeps pumping out hormone. The body runs hot and fast: racing heart, weight loss without trying, trembling
hands, feeling warm when others feel cold, trouble sleeping, anxiety, tired-but-wired. It's not caused by stress, diet, or anything
the person did β it's the immune system misfiring. It's also the most common cause of an overactive thyroid, well understood, and
treatable: medication (which calms the thyroid down while the immune system settles), radioactive iodine, or surgery. Most people
get back to a normal life; many go into long-term remission.
TRHTSHIodine (Iβ»)T3 / T4 (and TRAK in Graves')Negative feedback
Want the prevalence numbers, age-of-onset curves, and women-vs-men comparisons? Head over to the Statistics tab.
Graves' by the numbers
Who gets Graves', when, and how often β the headline epidemiology.
~3%Lifetime risk in womenvs ~0.5% in men
5β8ΓMore common in women than mendriven by estrogen, X-chromosome, reproductive transitions
37.9Annual incidence per 100,000 women
20β50Peak age of onset (years)
1β4 / 1,000Pregnancies affected (US)
~40%Postpartum relapse within 1 yr
Compare your labs to the dataset
Enter your thyroid panel and see where it lands against ~9,100 patients in the UCI reference dataset. Saved locally in your browser β nothing uploaded.
Not a diagnostic tool. The UCI data is from one institution in the 1980s β useful as a reference distribution,
not a clinical decision aid. Reference ranges shown are typical lab ranges; your own lab's ranges may differ.
Your entry
Your saved entries
No entries yet β fill in the form to log your first.
Date
TSH
T3
TT4
FTI
Where you land
Each chart shows the dataset distribution as bars; your value is the pink line. The percentile is "how many people in the cohort are below your value." For TSH, low percentiles (suppressed TSH) suggest hyperthyroid; for T3/TT4/FTI, high percentiles do.
TRAK statistics
How well TRAK performs as a diagnostic, and how its level predicts relapse after antithyroid drugs.
Tip: The last column actually looks like negative.|3733 β the part after | is the record ID, useful for joining
across the Garavan files but not for analysis.
Causes β why me?
Graves' isn't caused by any single thing. It's a perfect storm: a genetic predisposition that primes the immune system, plus a trigger that
tips it into producing the TRAK antibody. Most of the predisposition is unchangeable. Some of the triggers are.
Predisposition (unchangeable)
+
Trigger (sometimes modifiable)
β
Immune system makes TRAK antibody β Graves'
Predisposition β can't change
βοΈ
Female sex
5β8Γ higher lifetime risk than men β estrogen effects on immunity + X-chromosome genetics.
π§¬
Family history
Graves', Hashimoto's, T1D, vitiligo, or other autoimmune disease in close relatives raises risk substantially.
π¬
Specific gene variants
HLA-DR3, CTLA-4, CD40, PTPN22 β none deterministic, but they shift the baseline.
π
Existing autoimmune disease
If you have T1D, celiac, vitiligo, or RA β your immune system has already shown it can misfire.
Triggers β sometimes modifiable
π€±
Postpartum (0β12 months)
The single biggest hormonal trigger in women. Immune rebound after the pregnancy "tolerance" state.
π¬
Smoking
~2Γ the risk of Graves' overall, and the strongest modifiable risk for the eye disease (orbitopathy).
π°
Severe stress / major life events
Bereavement, divorce, severe illness β implicated in ~30% of new diagnoses and relapses.
π¦
Viral infections
EBV, retroviruses, and now SARS-CoV-2 have been linked to triggering autoimmune thyroid disease.
π§
Excess iodine
Kelp, iodine supplements, iodinated contrast can unmask Graves' in a predisposed person.
βοΈ
Vitamin D deficiency
Low D is more common in Graves' patients; whether it's cause or consequence isn't fully settled.
It is not your fault. No diet, lifestyle choice, or "thing you should have done differently" causes Graves' on its own. The autoimmune
misfire is the core problem; triggers just decide when a predisposed immune system tips over.
The female life course
Graves' interacts with every major reproductive transition. The shape below is the relative incidence across a woman's life β a peak in the reproductive years, a second peak around menopause. Hover or tap any pin to see what changes at that stage.
1
Puberty / teens
Rare but possible. Easily mistaken for anxiety, eating disorder, or stress.
2
Reproductive years
Peak onset window. Anovulatory cycles, subfertility. Treatment usually restores cycles.
3
Pregnancy β 1st trimester
hCG may unmask Graves'. PTU preferred over methimazole.
4
Pregnancy β 2nd / 3rd
TRAK often falls. Switch from PTU to methimazole after week 16. RAI contraindicated.
5
Postpartum (0β12 mo)
~40% of women in remission relapse here. Differentiate from postpartum thyroiditis.
6
Perimenopause / menopause
Second peak. Hot flashes & palpitations can mask Graves' β check TSH if atypical.
Symptoms women notice first
Graves' touches almost every system in the body. Symptoms below are ranked by how common they are in women with active disease (approximate, from clinical literature β varies by age and severity). Hover any bar to see more detail.
1
π Racing heart / palpitations
~85%
Tachycardia, palpitations, A-fib
2
π₯΅ Heat intolerance
~80%
Sweating, flushing β mimics perimenopause
3
βοΈ Weight loss
~75%
Despite increased appetite
4
π° Anxiety / insomnia
~72%
Often the presenting complaint in young women
5
π¬ Hand tremor
~70%
Fine tremor visible with arms extended
6
π Irregular periods
~65%
Light, infrequent, or absent menstruation
7
π Hair thinning
~50%
Diffuse hair loss, brittle nails
8
πͺ Muscle weakness
~45%
Stairs, getting up from chairs
9
π¦ Visible goiter
~40%
Front-of-neck swelling
10
ποΈ Eye changes
25β50%
Bulging, dryness, double vision (orbitopathy)
11
π€° Difficulty conceiving
~25%
Anovulation; miscarriage risk
12
𦴠Bone loss
~20%
Accelerated osteoporosis β esp. post-menopause
How it's diagnosed
Diagnosis follows a defined sequence: confirm hyperthyroidism with thyroid hormone labs, then confirm Graves' as the cause (rather than a toxic nodule
or thyroiditis) with antibodies and/or imaging.
1
Suspect from symptoms
Racing heart, weight loss, heat intolerance, anxiety, tremor, irregular periods. Often picked up by a GP first.
βΌ
2
TSH β the first screening test
Very sensitive. Low (often < 0.01 mIU/L) suggests hyperthyroidism. Normal TSH essentially rules it out.
βΌ
3
FT4 and FT3 β confirm hyperthyroidism
Both elevated β overt hyperthyroidism. FT4 normal but FT3 elevated β "T3 toxicosis," common early in Graves'.
βΌ
4
TRAK / TRAb β confirms Graves' specifically
Positive in ~97% of Graves' cases. Specificity ~99%. A positive TRAK with low TSH and high FT4 is essentially diagnostic β no imaging needed.
βΌ
5
Imaging β only if TRAK negative or borderline
Thyroid ultrasound (preferred in pregnancy / women planning to conceive) shows diffuse enlargement and increased vascularity.
Radioactive iodine uptake (RAIU) shows high diffuse uptake in Graves' vs focal hot spot in toxic nodule vs low in thyroiditis. Contraindicated in pregnancy.
Differential diagnosis β Graves' vs other causes of hyperthyroidism
Cause
TRAK
RAIU pattern
Course
Graves' disease
Positive
High, diffuse
Persistent without treatment
Toxic nodular goiter
Negative
Focal hot spot(s)
Persistent; surgery / RAI
Subacute thyroiditis (de Quervain's)
Negative
Low
Painful neck; self-limited (weeks)
Postpartum thyroiditis
Negative
Low
Self-limited (months)
Factitious (exogenous T4)
Negative
Low
History of thyroid hormone intake
If you're newly diagnosed. Ask for your actual numbers β TSH, FT4, FT3, TRAK. Knowing where you started is the only way to track whether
treatment is working. The TRAK section on the Treatment tab explains how to interpret your level.
Course over time β what to expect
Graves' is a chronic condition with several possible long-term paths. The trajectory depends mostly on which treatment is chosen and how the immune system
behaves after β relapse is common in the first 5 years, and a subset of people eventually drift into hypothyroidism even without RAI or surgery.
Preferred if planning pregnancy soon, severe eye disease, or large goiter
Common long-term patterns
The relapse window
After an ATD course, relapse risk is highest in the first year and decreases over time. Most relapses happen within 5 years; after 10 years of remission, relapse becomes uncommon. Postpartum is its own distinct relapse window β see the Pregnancy tab.
"Burnout" to hypothyroidism
A subset of people on ATD eventually drift into hypothyroidism as the gland fibroses from chronic autoimmune attack. This isn't a treatment failure β it's natural history. They transition to levothyroxine, the same endpoint as RAI or surgery but slower.
Pregnancy & Graves'
Roughly 1β4 in 1,000 pregnancies are complicated by Graves'. Untreated, maternal hyperthyroidism raises the risk of miscarriage,
pre-eclampsia, preterm birth, low birth weight, stillbirth, and fetal/neonatal thyroid problems. Treated well, outcomes are close to normal.
For drug choices and trimester-by-trimester management, see the
Treatment in pregnancy section on the Treatment tab.
This page focuses on what to watch for β fetal/neonatal effects, the thyroid-storm emergency, and the postpartum relapse window.
Risk timeline β what to watch for, when
Fetal & neonatal effects
Four possible problems β two driven by maternal TRAK crossing the placenta, two driven by maternal antithyroid drugs crossing the placenta.
Watch for: newborn TSH screen catches it; usually self-resolves in days
Thyroid storm in pregnancy
25%mortality if untreated
A true obstetric emergency. Most often triggered by labor itself, infection, surgery, or abrupt drug stop. Treat fast; deliver if mother becomes unstable.
β Signs
High fever
Severe tachycardia (> 140)
Agitation / altered mental status
Heart failure
π₯ Triggers
Labor & delivery
Infection
Surgery
Abrupt antithyroid drug stop
π Treatment
PTU / methimazoleIodineBeta-blockerSteroidSupportive care
Deliver if mother is unstable.
Postpartum β the relapse window
New hyperthyroid symptoms in the first 12 months postpartum are common and split into two very different conditions β they look similar but the treatment and prognosis diverge sharply.
Postpartum thyroiditisSelf-limited
TRAKNegative
RAIU uptakeLow
CourseResolves in months
TreatmentBeta-blocker only
vs
Graves' relapsePersistent
TRAKPositive
RAIU uptakeHigh, diffuse
CoursePersistent without Rx
TreatmentATD or definitive (RAI / surgery)
Cumulative postpartum relapse risk over 24 months is plotted on the
Statistics tab.
Where to start
Pick the situation that fits β it'll take you to the section you need first.
Three disease-modifying options. None is best for everyone β the choice depends on age, pregnancy plans, severity, eye involvement, and your own preference.
Beta-blockers control symptoms but don't treat the disease.
π
Acronyms used in this section.
ATD β antithyroid drug. The drug class that blocks the thyroid from making new hormone. In Graves' management this means one of two drugs: MMI or PTU. "ATD therapy" = the drug route, as opposed to RAI (radioactive iodine) or surgery.
MMI β methimazole (also called thiamazole; brand names Tapazole, Thacapzol). The default ATD outside pregnancy: more potent than PTU, once-daily dosing, lower liver-injury risk. Carbimazole (used in Europe/UK) is a prodrug the body converts to methimazole β same drug for clinical purposes.
PTU β propylthiouracil. The other ATD. Preferred in the first trimester of pregnancy (lower embryopathy risk than methimazole) and in thyroid storm. Carries an FDA black-box warning for rare severe liver injury, so it's not first-line outside those situations.
RAI β radioactive iodine (I-131). A definitive treatment that destroys overactive thyroid tissue.
FT4 / TSH / TRAK β the lab values that drive every treatment decision; see the Labs & monitoring section.
π
Antithyroid drugs (ATD)
~40β50% remission
How it worksMethimazole (or PTU) blocks the thyroid from making T3/T4
Time to effectSymptoms improve in 2β6 weeks; FT4 normalizes in weeks; TSH lags 6β8 weeks
Duration12β18 month course, then attempt stop
Reversible?Yes β preserves thyroid
Main risksRash (~5%), liver injury, agranulocytosis (rare but serious)
Best forMildβmoderate disease, planning pregnancy, eye disease, first-line in most women
β’οΈ
Radioactive iodine (RAI)
~90β95% cure
How it worksOral I-131 capsule destroys overactive thyroid cells
Time to effectWeeks to months; most become hypothyroid within 6β12 months
DurationSingle dose (sometimes repeat); lifelong levothyroxine after
Reversible?No β permanent
Main risksCan worsen eye disease (esp. in smokers); permanent hypothyroidism
Female notesContraindicated in pregnancy & breastfeeding. Wait β₯ 6 months before conceiving.
πͺ
Thyroidectomy (surgery)
~99% definitive
How it worksTotal or near-total surgical removal of the thyroid
Time to effectHypothyroid immediately; start levothyroxine the next day
DurationOne-time procedure; lifelong levothyroxine after
Reversible?No β permanent
Main risksHypoparathyroidism (~1β2%), nerve injury (~1%), surgical risks
Best forLarge goiter, severe eye disease, drug-intolerant, planning pregnancy soon
β€οΈ
Beta-blockers (propranolol, atenolol) β supportive only. Bring down heart rate, tremor, anxiety while disease-modifying treatment kicks in.
Propranolol is safe at low doses in pregnancy. Not a treatment for Graves' itself.
Success rates at a glance
TRAK β your lab result
The single most useful number for predicting how the disease will behave and when you can stop antithyroid drugs.
TRAK (German TSH-Rezeptor-AntikΓΆrper; English TRAb / TSI) is the autoantibody that drives Graves' β it
activates the TSH receptor on the thyroid and causes the disease.
What your band predicts
Approximate relapse risk after a standard 12β18 month antithyroid drug course, based on TRAK level at the end of treatment.
Negative / Low+
~20β30%
Best prognosis. Often the green light to taper or stop antithyroid drugs.
Moderate
~50%
Coin-flip relapse risk. Most endocrinologists continue ATD or consider definitive treatment.
High
~70β80%
High relapse risk. Often steers the decision toward surgery or RAI rather than another ATD course.
Pregnancy threshold. TRAK is IgG and crosses the placenta β even a mother who's euthyroid after RAI or surgery can cause
fetal or neonatal hyperthyroidism. Values above 3Γ the upper limit of normal in pregnancy trigger fetal monitoring (heart rate, growth ultrasound, TRAK at 18β22 weeks).
When to re-check. At diagnosis Β· before stopping antithyroid drugs Β· early pregnancy and again at 18β22 weeks if elevated Β· if relapse is suspected.
Don't re-check more often than every 6β8 weeks during a drug change β antibody levels move slowly.
Treatment in pregnancy & breastfeeding
Pregnancy changes almost every treatment decision. Methimazole becomes risky in the first trimester; radioactive iodine is off the table entirely; some supplements need to be re-thought.
The full epidemiology, fetal/neonatal considerations, and postpartum relapse window live on the
Pregnancy tab β this section focuses on what to do.
Pre-conception planning
Ideally, achieve a stable euthyroid state before conception. Choices:
On antithyroid drugs, controlled? Two accepted paths β decide with the endocrinologist before stopping contraception:
Pre-conception switch to PTU. Safest if conception may happen quickly β no window where an unrecognized early pregnancy (weeks 4β6) gets methimazole.
Stay on methimazole, switch at first positive test. Limits PTU liver exposure, but only works if she tests early and the switch happens within days β the teratogenic window (weeks 6β10) comes up fast.
In remission, off drugs for β₯ 1 year? No PTU needed β but remission β cure. TRAK antibodies can persist and cross the placenta regardless of maternal thyroid status. Required:
TRAK measured pre-conception and again at 18β22 weeks. If > 3Γ ULN, fetal monitoring (heart rate, growth, goiter on US) is indicated even if mom is euthyroid.
TSH / FT4 through pregnancy β relapse risk is elevated, especially postpartum (up to ~50% in the first year).
TRAK very high (>5Γ ULN) or large goiter? Consider definitive therapy (surgery preferred over RAI if planning pregnancy soon) 6+ months before trying β removes the drug question entirely.
If RAI: wait at least 6 months and confirm euthyroid before trying.
Already pregnant on methimazole? Switch to PTU urgently in 1st trimester (lower teratogenic risk).
Trimester-by-trimester management
Stage
Preferred drug
Monitoring
Avoid
1st trimester (0β13w)
PTU 50β300 mg/day
FT4 every 2β4 weeks; aim for upper third of normal
Methimazole (aplasia cutis, choanal atresia), RAI
2nd trimester (14β27w)
Switch to methimazole 5β15 mg/day (lower liver risk)
FT4 every 4 weeks; TRAK at 18β22w if previously high
RAI
3rd trimester (28β40w)
Methimazole, often at lowest effective dose
FT4; fetal heart rate, growth ultrasounds; TRAK
RAI; high-dose ATDs (fetal hypothyroidism)
Labor & delivery
Continue ATD; watch for thyroid storm trigger (infection, stress)
Maternal HR, BP, T; cord blood TSH/FT4 + TRAK
Iodinated contrast unless absolutely needed
Breastfeeding
Methimazole ≤ 20 mg/day or PTU ≤ 450 mg/day
Take dose after feeds; monitor infant TSH if mom on high dose
RAI scanning/treatment
Off the table during pregnancy
β Radioactive iodine
Crosses the placenta, destroys fetal thyroid. Wait β₯ 6 months after RAI before conceiving.
β High-dose iodine / contrast
Iodinated CT contrast and high-iodine supplements can cause fetal hypothyroidism & goiter.
β High-dose ATD
Crosses the placenta β use lowest effective dose, aim for upper-third FT4 to protect the fetus from over-treatment.
β Abrupt drug stop
Risks thyroid storm at labor β an obstetric emergency with up to 25% mortality untreated.
Natural / lifestyle during pregnancy β what stays safe & what to re-think
What stays safe
βοΈ
Vitamin D
Keep at > 30 ng/mL through pregnancy & nursing β standard prenatal guidance.
π
Omega-3 (DHA)
Good for fetal brain development; choose low-mercury sources or purified supplements.
π§
Stress reduction
Postpartum is a major relapse window β yoga, breathwork, CBT, social support all matter.
π΄
Sleep
Hard with a newborn, but protected sleep windows blunt the postpartum relapse risk.
π
No smoking
Strongest modifiable risk for Graves' eye disease β and obvious fetal harm.
πΆ
Gentle exercise
Walking, prenatal yoga, swimming β once heart rate is controlled.
What to re-think
Item
Reason to pause
Selenium supplements
Helpful for mild eye disease outside pregnancy β but doses > 200 Β΅g/day not well-studied in pregnancy. Discuss with your endocrinologist.
L-carnitine
Limited pregnancy safety data. Skip unless your doctor specifically recommends it.
High-iodine kelp/seaweed
Excess iodine can flip the fetal thyroid into hypothyroidism. Keep iodine to the prenatal RDA (~220 Β΅g).
"Thyroid support" herbal blends
Often contain undeclared iodine, ashwagandha, or thyroid extract. Avoid entirely.
High caffeine
Compounds tachycardia & insomnia; also limited per general pregnancy guidance (< 200 mg/day).
Strict elimination diets
Risk of under-nutrition during pregnancy. Only restrict with a clear medical reason (e.g., confirmed celiac).
If you're planning pregnancy: get to a stable euthyroid state first, choose a treatment path with your endocrinologist that
accounts for the next 12β18 months (ATDs vs. definitive treatment with surgery), and confirm baseline TRAK β high TRAK predicts fetal/neonatal
risk even if mom is euthyroid.
Postpartum: Graves' relapses in roughly 1 in 3 women within 12 months of delivery, often masked as "new-mom" fatigue or anxiety.
Re-check TSH, FT4, and TRAK at 6 weeks and 6 months postpartum β even if you felt fine through pregnancy.
What to ask your doctor & follow-ups
Questions for each visit, the labs that matter, and the symptoms that mean "call today, don't wait."
TSH lags weeks behind your symptoms, antibodies wax and wane, and antithyroid drugs have their own risks. Going in with a list and tracking your own numbers between visits makes a real difference.
At diagnosis / before choosing treatment
What is my TRAK / TRAb level, and what does the magnitude mean for my prognosis?
Are my TPO and thyroglobulin antibodies also positive? (overlap with Hashimoto's)
What's my TSH, FT4, FT3 β and how far outside reference are they?
Is there a goiter or nodule? Do I need a thyroid ultrasound or RAIU scan?
Any signs of eye involvement? Should I see an ophthalmologist familiar with Graves' orbitopathy?
Given my age & pregnancy plans, which treatment fits β ATD vs RAI vs surgery?
Baseline DEXA (bone density), ECG, and vitamin D?
What's my plan if I get pregnant on treatment?
At each follow-up visit
What are my latest TSH / FT4 / FT3 β and what's the trend vs last visit?
Is my TRAK rising or falling? (especially before stopping ATD)
Any change to drug dose? When's the next blood draw?
If on ATD: when is my next CBC and LFT? Any new bruising, sore throat, or jaundice?
How are my heart rate, weight, sleep, periods, mood?
If post-RAI / surgery: am I on the right levothyroxine dose?
Are we close to the point where I can try to stop ATD? What does my TRAK say?
Any updates I should know on guidelines or new options (e.g., teprotumumab for eye disease)?
Fatigue and hair loss have many causes β rule out non-thyroid contributors.
If symptoms persist after euthyroid
π¦΄Calcium & PTH
Post-thyroidectomy hypoparathyroidism risk; baseline bone health.
Day 1, week 1, month 1 post-surgery; annually if osteoporosis
π¦΄DEXA (bone density)
Long-standing hyperthyroidism accelerates bone loss β major issue post-menopause.
Baseline if post-menopausal or prolonged hyper; repeat every 1β2 yrs
πECG
Screen for atrial fibrillation β increased risk during active disease.
At diagnosis; if palpitations or age > 50
πLipid panel
Hyperthyroidism lowers cholesterol; hypothyroidism (post-RAI) raises it.
Baseline & annually
π€°HCG (pregnancy test)
Before any RAI scan/treatment. Period changes can mask pregnancy.
Before RAI; if cycles irregular
Call your doctor the same day if
π€
Fever + sore throat while on antithyroid drug
Possible agranulocytosis β stop the drug, get a CBC same day.
π‘
Yellowing of skin or eyes, severe nausea
Possible drug-induced liver toxicity β stop the drug, get LFTs.
π
Severe palpitations, chest pain, or new irregular heartbeat
Possible atrial fibrillation or thyrotoxic heart failure.
ποΈ
New double vision, eye pain, or vision loss
Possible active Graves' orbitopathy β needs urgent ophthalmology review.
π¨
Confusion, high fever, severe vomiting
Possible thyroid storm β call emergency services. Up to 25% mortality if untreated.
Self-tracking tip: Keep a simple spreadsheet β date, TSH, FT4, FT3, TRAK, drug dose, resting heart rate, weight, period date.
Bring it to every visit. Trends matter more than any single reading.
Natural remedies & lifestyle
Adjuncts only β these don't replace antithyroid drugs, RAI, or surgery. But three of them have strong enough evidence to matter.
Bottom line β the three highest-evidence moves
π
Stop smoking
Halves the progression of Graves' eye disease. Single biggest modifiable risk.
Already downloaded into ./datasets/. To redo from scratch:
# bash
mkdir -p datasets && cd datasets
BASE=https://archive.ics.uci.edu/ml/machine-learning-databases/thyroid-disease
for f in allhyper allbp sick-euthyroid hypothyroid sick allhypo; do
curl -sSLO $BASE/$f.data
curl -sSLO $BASE/$f.names 2>/dev/null
done# index of all files
curl -s $BASE/ | grep -oE 'href="[^"]+"' | head -40
NHANES (CDC)No login
Official US health survey. Files are SAS XPT format; needs pyreadstat or haven to read.
Submit an Access Management System (AMS) application describing your project (~6β8 weeks review).
Pay access fee (currently Β£3,000β9,000 depending on data scope).
Download via the UKB Research Analysis Platform (cloud) or bulk files for approved fields. Thyroid-relevant fields: 20002 (self-reported diagnosis), ICD codes E05.x (hyperthyroid), serum TSH/FT4.
ClinicalTrials.govOpen API
Bulk-download summary results for all Graves' trials:
# JSON API β no login
curl -sSL "https://clinicaltrials.gov/api/v2/studies?query.cond=Graves+Disease&pageSize=100" \
-o datasets/clinicaltrials_graves.json
python3 -c "
import json
d = json.load(open('datasets/clinicaltrials_graves.json'))
print('Studies:', len(d['studies']))
for s in d['studies'][:5]:
print('-', s['protocolSection']['identificationModule']['briefTitle'])"
ImmPort β immunology studiesFree account
Has several thyroid autoimmunity studies. Register at immport.org, then use their Aspera client or the web download for studies tagged "Graves' disease".
Sources
Patient resources, clinical guidelines, and the research papers behind the numbers on this page.