Introduction
I was diagnosed about 2 years ago with Hashimoto’s disease. About a year later I developped symptoms that suggested to much thyroid hormone, specifically Atrial Fibrilation with blood tests showing elevated T3 and T4 with TSH <0.01. Testing for Graves disease came back positive and at the same time testing again for Hashimoto’s also returned positive.
I am a male in early 60’s which I understand is also fairly rate (about 10% of patients with Thyroid problems).
With the new deep research feature in chatGPT decided to ask it about the prevelance of both diseases. This is the result.
Please note, this is my journey as a patient. You should consult your doctor for information about you. You can show your doctor this article if you like.
How common is it for a person to have both Hashimoto’s disease and graves disease?
ChatGPT said:
Are you looking for general statistics on the prevalence of having both Hashimoto’s disease and Graves’ disease, or are you interested in specific risk factors, case studies, or medical explanations of how both conditions can coexist?
You said:
statistics and case studies please
ChatGPT said:
Research completed in 10m · 23 sources
I will find statistics on the prevalence of individuals having both Hashimoto’s disease and Graves’ disease, along with case studies that explore this rare coexistence. This will include medical research findings, documented patient cases, and potential risk factors. I will update you once I have the information.Research completed in 10m · 23 sources
Coexistence of Hashimoto’s Disease and Graves’ Disease
Prevalence and Frequency of Dual Diagnosis
Having both Hashimoto’s thyroiditis and Graves’ disease in the same individual is uncommon, documented mostly in case reports. Medical literature describes the simultaneous occurrence of Hashimoto’s (an autoimmune hypothyroid condition) and Graves’ (autoimmune hyperthyroid) as rare.

There is no exact population prevalence for concurrent presentation, but it is considered an exceptional finding. More often, the two conditions occur sequentially over a patient’s lifetime rather than truly at the same time. For example, approximately 15–20% of Graves’ disease patients eventually develop Hashimoto’s thyroiditis and resultant hypothyroidism spontaneously over the course of their illnesspubmed.ncbi.nlm.nih.gov.
In contrast, progression from Hashimoto’s thyroiditis to Graves’ hyperthyroidism is much rarer – only on the order of dozens of cases reported in the literature pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov. An endocrine review notes that “a small percentage” of Hashimoto’s patients might later switch to Graves’ disease after years of hypothyroidism ncbi.nlm.nih.gov, underscoring how infrequent this transition is. Even transient hyperthyroid phases can sometimes occur in Hashimoto’s patients (a phenomenon called “Hashitoxicosis”), but this too is uncommon (on the order of ~5% of Hashimoto’s cases) and usually short-lived ncbi.nlm.nih.gov.
Overall, individuals diagnosed with both autoimmune thyroid conditions are a minority among thyroid patients, highlighting the rarity of this coexistence.
Documented Case Studies of Coexistence
Because concurrent or sequential Hashimoto’s and Graves’ disease is unusual, the medical literature contains numerous case reports and small series detailing such occurrences. These reports help illustrate how the dual pathology manifests. For instance, Majumder et al. described a 60-year-old woman who initially presented with symptoms of hyperthyroidism (tremors, weight loss, goiter) and was found to have lab evidence of both diseases: elevated thyroid hormones with low TSH (consistent with Graves’), plus strongly positive anti-thyroid peroxidase (TPO) antibodies and TSH-receptor antibodies. pmc.ncbi.nlm.nih.gov

Thyroid imaging in that case showed a diffusely increased radioiodine uptake (a hallmark of Graves’ overactivity) with patchy “cold” areas, and a biopsy revealed lymphocytic thyroiditis consistent with Hashimoto’s pmc.ncbi.nlm.nih.gov. In other words, the patient simultaneously had the gland-destructive autoimmune process of Hashimoto’s alongside the stimulatory process of Graves’ disease.
Another published case report referred to this scenario as a “hot and cold” thyroid, where a hyperfunctioning gland on scan harbored focal autoimmune destruction pmc.ncbi.nlm.nih.gov.
There are also documented sequential cases: for example, pediatric cases of Hashimoto’s thyroiditis that later converted to Graves’ hyperthyroidism after several years pubmed.ncbi.nlm.nih.gov, or adults with long-standing Graves’ disease who eventually became hypothyroid due to developing Hashimoto’s pubmed.ncbi.nlm.nih.gov.
In one series of four patients with Graves’ disease in remission, all developed Hashimoto’s chronic thyroiditis 7 to 25 years later pubmed.ncbi.nlm.nih.gov. Such case studies collectively confirm that while rare, one person can indeed experience both autoimmune thyroid conditions.
Clinicians are advised to be aware of this possibility so that, for example, a new onset of hyperthyroid symptoms in a known Hashimoto’s patient (or vice versa) is properly recognized rather than dismissed as an anomaly pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov.
Pathophysiology: How Both Conditions Can Manifest Together
Hashimoto’s thyroiditis and Graves’ disease represent two ends of the autoimmune thyroid disease (AITD) spectrum, and they share a common underlying immune origin despite causing opposite thyroid dysfunctions pmc.ncbi.nlm.nih.gov juniperpublishers.com. In both disorders, the body’s immune system attacks the thyroid gland, but the autoantibody profiles differ in their effects:
- In Graves’ disease, the immune system produces stimulating antibodies (often called thyroid-stimulating immunoglobulins, TSI) against the TSH receptor on thyroid cells. These antibodies activate the receptor, causing the gland to grow and secrete excess thyroid hormones (leading to hyperthyroidism)pubmed.ncbi.nlm.nih.gov. This is why Graves’ patients have high hormone levels and symptoms of thyrotoxicosis.
- In Hashimoto’s thyroiditis, the immune response is characterized by antibodies (e.g. anti-TPO and anti-thyroglobulin) and T-cells that destroy thyroid tissue. There are also sometimes blocking antibodies to the TSH receptor (TSH-blocking Ab) that interfere with TSH signalingpubmed.ncbi.nlm.nih.gov. The result is progressive thyroid damage, glandular atrophy, and an eventual inability to produce enough hormone (hypothyroidism)pubmed.ncbi.nlm.nih.gov.
Given this common autoimmune basis, it is medically plausible for an individual to produce both types of antibodies – stimulating and blocking – either simultaneously or at different times. In fact, research has shown overlapping antibody presence: for example, many Graves’ patients also have high titers of anti-thyroid peroxidase (TPO) antibodies seen in Hashimoto’s, and a subset of Hashimoto’s patients have measurable TSH-receptor antibodies pmc.ncbi.nlm.nih.gov.
In one large study of autoimmune thyroid cases, about 10 patients (roughly 1% of those studied) had both TSH-receptor–stimulating and –blocking antibodies detectable at the same time pmc.ncbi.nlm.nih.gov. The balance between these opposing immune factors can determine the clinical picture.
If thyroid-stimulating antibodies dominate, the person will be hyperthyroid (Graves’-like); if destructive and blocking antibodies prevail, hypothyroidism (Hashimoto’s) ensues. This dynamic can cause a person’s thyroid function to oscillate or shift over time.
Indeed, in rare instances patients have alternated between hyperthyroid and hypothyroid states for years, reflecting fluctuations in their immune response (“oscillating” between Graves’ and Hashimoto’s) juniperpublishers.com juniperpublishers.com. Most commonly, a patient might initially have one condition and later transition to the other as the immune attack changes. For example, a Graves’ disease patient in remission may later develop high TPO antibodies and lymphocytic thyroiditis, moving into Hashimoto’s hypothyroidism pubmed.ncbi.nlm.nih.gov. Conversely, a long-standing Hashimoto’s patient with thyroid atrophy might, on rare occasion, begin producing TSH-receptor stimulatory antibodies, causing a swing into hyperthyroidism ncbi.nlm.nih.gov.
The medical community considers these phenomena a continuum of autoimmune thyroid disease, with both disorders sharing genetic predispositions (such as certain HLA genes and other immune-regulating genes).
In summary, one individual can manifest both conditions because the underlying autoimmunity is capable of targeting the thyroid in multiple ways – either stimulating it or destroying it – sometimes even concurrently. This also explains why laboratory findings can show a mix of antibodies, and why clinical signs may sometimes be atypical (for instance, a Graves’ patient who doesn’t become as hyperthyroid as expected might have coexisting Hashimoto’s dampening the thyroid’s output) pmc.ncbi.nlm.nih.gov.
Risk Factors and Contributing Factors for Dual Autoimmunity
Who is at risk for developing both Hashimoto’s and Graves’ disease? In general, the risk factors overlap with those for autoimmune thyroid disease in general, since both conditions share etiological factors:
- Genetic predisposition: Family and twin studies indicate a strong genetic component to autoimmune thyroid disorders. Having a family history of thyroid autoimmunity (either Graves’ or Hashimoto’s) increases one’s susceptibility to autoimmune thyroid disease, and by extension could allow the emergence of both conditions in the same person pubmed.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov. Certain HLA genes and other immune-regulatory gene polymorphisms are linked to AITDs and may influence whether a person develops one, the other, or even transitions between them. Notably, cases of Hashimoto-to-Graves conversion show a female predominance (~90% female)pubmed.ncbi.nlm.nih.gov, similar to the usual female bias in both diseases (women are much more affected than men), suggesting sex-linked genetic or hormonal factors play a role.
- Presence of one autoimmune thyroid disease: Simply having one of the two disorders is a risk factor for later developing the other. As discussed, about 15–20% of Graves’ patients eventually become hypothyroid due to Hashimoto’spubmed.ncbi.nlm.nih.gov, indicating that the immune response can broaden over time. Likewise, while far less common, a small fraction of Hashimoto’s patients may later show signs of Graves’ hyperthyroidismncbi.nlm.nih.gov. Patients who are positive for TSH-receptor antibodies even when hypothyroid (as was seen in some Hashimoto’s cases) are considered at risk of transitioning to hyperthyroid Graves’ disease laterpubmed.ncbi.nlm.nih.gov. In essence, the more types of thyroid autoantibodies one has, the higher the chance of dual manifestations.
- Other autoimmune diseases (polyglandular autoimmunity): Individuals with multiple autoimmune conditions (e.g. type 1 diabetes, adrenal insufficiency/Addison’s disease, etc.) have a generalized immune dysregulation that can affect the thyroid in complex ways. For instance, in the context of Schmidt’s syndrome (autoimmune polyendocrine syndrome type II, which classically includes adrenal and thyroid autoimmunity), patients might present with features of both Graves’ and Hashimoto’s disease concurrentlypmc.ncbi.nlm.nih.gov. One case report of coexistent Graves’ and Hashimoto’s occurred alongside primary adrenal failure (Addison’s), illustrating how a broad autoimmune milieu can facilitate unusual combinations of thyroid dysfunctionpmc.ncbi.nlm.nih.govpmc.ncbi.nlm.nih.gov. Thus, having any autoimmune condition makes it more likely to develop another – in one large study, 10–15% of autoimmune thyroid patients had a second autoimmune disorderpubmed.ncbi.nlm.nih.gov – and this “clustering” can include the two thyroid-specific diseases in the same patient.
- Environmental and life factors: Various external factors known to trigger or modulate autoimmune thyroid disease could contribute to shifting the immune balance. Iodine exposure is one example – high iodine intake has been linked to increased Hashimoto’s incidence, and in predisposed individuals could potentially precipitate autoimmune thyroiditis on top of preexisting Graves’ (or vice versa)ncbi.nlm.nih.govncbi.nlm.nih.gov. Stress and infection are sometimes implicated in triggering Graves’ disease; in a patient with underlying Hashimoto’s antibodies, such triggers might spark the development of Graves’ symptoms. The postpartum period is another well-known trigger: women with underlying Hashimoto’s often experience postpartum thyroiditis (a transient hyperthyroid phase followed by hypothyroidism) due to immune rebound after pregnancyncbi.nlm.nih.gov. In rare instances, this could manifest as true Graves’ hyperthyroidism postpartum in someone with prior Hashimoto’s. Immune-modulating medications have also been reported to cause shifts – for example, the drug alemtuzumab (used in multiple sclerosis) can induce Graves’ disease in some patients and hypothyroidism in others, and even cause oscillation between the twopmc.ncbi.nlm.nih.gov. Changes in the immune system with aging or other immunomodulatory therapies might tip the balance from one condition to anotherpmc.ncbi.nlm.nih.govpmc.ncbi.nlm.nih.gov. In summary, any factor that perturbs the immune system or thyroid antigen exposure (including iodine, infections, stress, and pregnancy) in a susceptible individual could contribute to the coexistence or sequential development of both Graves’ and Hashimoto’s.
Management and Treatment Considerations
Managing a patient who has features of both Graves’ disease and Hashimoto’s thyroiditis can be challenging, and treatment must be tailored to the current dominant thyroid state while anticipating shifts. Key considerations include:
- Treating the active phase: If the patient is presently hyperthyroid (due to Graves’ activity), initial therapy focuses on controlling hyperthyroidism. Standard Graves’ treatments apply – typically anti-thyroid medications (like methimazole) to reduce thyroid hormone production, beta-blockers to alleviate symptoms (tremor, palpitations), and in some cases definitive therapy with radioactive iodine (I-131) or surgerypmc.ncbi.nlm.nih.gov. For example, one reported patient with concurrent Graves’/Hashimoto’s was started on low-dose carbimazole to manage hyperthyroidism and later underwent radioiodine ablation pmc.ncbi.nlm.nih.gov. Radioiodine is an effective definitive treatment for Graves’ hyperthyroidismpmc.ncbi.nlm.nih.gov, though clinicians must be mindful that inducing hypothyroidism is highly likely (these patients may already have Hashimoto’s-related damage that will make them permanently hypothyroid after ablation). If the hyperthyroidism is mild or expected to be transient (such as a case of hashitoxicosis or early coexistent Hashimoto’s limiting the severity of Graves’), some physicians may choose a conservative approach – using only beta-blockers for symptom relief and closely observing thyroid levelspmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov. This was the strategy in the case by Majumder et al., where despite clear evidence of Graves’ hyperthyroidism, the coexistence of Hashimoto’s led doctors to monitor on beta-blockers, anticipating an eventual spontaneous resolution of the overactive phasepmc.ncbi.nlm.nih.gov. On the other hand, if the patient is hypothyroid (Hashimoto’s dominant) with only subtle signs of past Graves’ activity, the appropriate treatment is thyroid hormone replacement. All documented cases of Graves’ turning into Hashimoto’s are managed long-term with levothyroxine to restore normal thyroid levelspubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov. Thyroid hormone replacement is straightforward once the patient is definitively hypothyroid. The challenge is during the transition or if some hyperfunction remains.
- Monitoring and adjustment: Close monitoring of thyroid function is crucial in patients with dual pathology, since their status can fluctuate. These individuals may require periodic re-testing of TSH, Free T4/T3, and antibody levels to gauge which autoimmune process is active. As one case series noted, a clue to impending transition from Hashimoto’s to Graves’ was the need to taper down the levothyroxine dose (because the patient’s thyroid started producing hormone again)scielo.br. Similarly, a Graves’ patient who unexpectedly develops high TSH (indicating hypothyroidism) after a period of stability should be evaluated for new-onset Hashimoto’s. Tracking TSH-receptor antibody levels (TSI or TBII assays) in a Hashimoto’s patient can help predict a swing toward Graves’ if those antibodies start rising pubmed.ncbi.nlm.nih.govpubmed.ncbi.nlm.nih.gov. In short, dynamic management is often needed, with therapy adjusted as the patient shifts from hyperthyroid to euthyroid to hypothyroid states or vice versa.
- Comprehensive approach: Because these patients have an underlying autoimmune tendency, physicians might also address general autoimmune support (e.g. ensuring sufficient selenium and vitamin D, which have roles in thyroid autoimmunity ncbi.nlm.nih.gov ncbi.nlm.nih.gov, though evidence is evolving). Any co-occurring autoimmune disorders (like adrenal insufficiency or type 1 diabetes) must be managed in parallel to avoid compounding metabolic problems (for instance, untreated adrenal insufficiency in a Graves’ patient can be dangerous if hyperthyroidism isn’t controlled). Patient education is key as well – individuals with both Graves’ and Hashimoto’s may experience confusing swings in symptoms (from hyperthyroid symptoms like anxiety and weight loss to hypothyroid symptoms like fatigue and weight gain). Educating them on the importance of follow-ups and symptom reporting can improve outcomes.
- Diagnostic vigilance: From a diagnostic standpoint, clinicians use multiple modalities to confirm the coexistence. Thyroid ultrasound and scintigraphy (uptake scans) can help differentiate active Graves’ vs. thyroiditis. A diffusely high uptake on radioiodine scan indicates Graves’ disease activity, whereas low uptake would suggest a thyroiditis-driven thyrotoxicosis (non-Graves)pmc.ncbi.nlm.nih.gov. In a patient with known Hashimoto’s who becomes hyperthyroid, a high uptake scan or the presence of TSH-receptor stimulating antibodies would confirm that Graves’ has developed on top of the chronic thyroiditis pmc.ncbi.nlm.nih.gov. This is important for guiding treatment (since true Graves’ hyperthyroidism might warrant anti-thyroid drugs or radioiodine, while hashitoxicosis would not). Fine-needle aspiration biopsy is sometimes done if imaging shows unusual thyroid nodules, to rule out other pathologies and to look for lymphocytic infiltration consistent with Hashimoto’s pmc.ncbi.nlm.nih.govpmc.ncbi.nlm.nih.gov.
In summary, treatment of coexisting Hashimoto’s and Graves’ is individualized. The primary goal is to maintain the patient in a euthyroid state (normal thyroid function) and address whichever autoimmune process is currently causing dysfunction. This may mean antithyroid therapy initially, followed by lifelong hormone replacement, or vice versa. Many patients who go through a hyper-to-hypo transition ultimately end up simply on stable levothyroxine therapy once the thyroid is burnt out pubmed.ncbi.nlm.nih.gov. What makes these cases complex is the need for flexibility and careful observation – physicians must be alert to changes, as one disorder can “mask” or complicate the other pmc.ncbi.nlm.nih.gov. Fortunately, with appropriate monitoring and therapy, even this rare dual condition can be effectively managed, as evidenced by case reports of patients achieving long-term stability (either via remission of one component or definitive treatment of Graves’ followed by replacement for Hashimoto’s) pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov.
Sources: Medical journal articles and reviews were used to compile these statistics and insights, including endocrinology case reports and research on autoimmune thyroid disease (e.g. Indian J Endocrinol Metab., Medicina (Kaunas), Acta Med Indones, and others)
pubmed.ncbi.nlm.nih.gov. Authoritative endocrinology sources and thyroid disease guidelines were also consulted to explain mechanisms and management
ncbi.nlm.nih.gov. These references document the rare coexistence of Graves’ and Hashimoto’s, the immunological interplay, and recommended clinical approaches to care for affected individuals. Each cited source comes from reputable medical literature or established health organizations in the field of endocrinology.
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