Medication- and immunotherapy-induced thyroiditis comprises a heterogeneous group of conditions in which pharmacological exposure causes thyroid inflammation, resulting in a transient or persistent alteration of gland function. In clinical practice, the most frequent mechanism is destructive thyroiditis, characterized by follicular damage and the release of preformed thyroid hormones into the circulation. This produces an initial phase of thyrotoxicosis, which may progress to hypothyroidism because of depletion of hormone stores and reduced secretory capacity. In other settings, the medication may act as a trigger or amplifier of thyroid autoimmunity, producing clinical pictures that overlap with chronic autoimmune thyroiditis or, less frequently, immune-mediated hyperthyroidism.
This field has acquired increasing relevance with the widespread use of modern oncological therapies. In particular, immune checkpoint inhibitors represent one of the most common causes of iatrogenic thyroid dysfunction in oncology, with presentations including destructive thyrotoxicosis, primary hypothyroidism, and biphasic patterns. Correct identification of the underlying mechanism is essential because it guides differential diagnosis and treatment, preventing the inappropriate use of antithyroid medications when thyrotoxicosis results from hormone release.
The epidemiology of medication-induced thyroiditis is closely related to prescribing patterns and the increasing use of biological and oncological therapies. Unlike “classic” forms of thyroiditis, it is not a single nosological entity, but a group of adverse events whose frequency varies according to the medication, duration of exposure, treated population, and sensitivity of monitoring strategies. In many patients, particularly those with cancer, thyroid dysfunction is detected at a subclinical stage through serial measurements of thyroid-stimulating hormone (TSH) and free thyroxine (FT4), resulting in an apparently higher incidence than in settings where testing is performed only when symptoms develop.
Immune checkpoint inhibitors are among the principal contemporary epidemiological determinants. Thyroid dysfunction associated with anti-programmed cell death protein 1 (anti-PD-1) and anti-programmed death-ligand 1 (anti-PD-L1) therapy is reported with significant frequency and often includes an episode of destructive thyroiditis followed by hypothyroidism, whereas combinations with anti-cytotoxic T-lymphocyte-associated protein 4 (anti-CTLA-4) therapy may increase the overall probability of endocrine adverse events. The clinical impact is amplified by the fact that symptoms may overlap with cancer-related fatigue, systemic adverse effects, or disease progression, making proactive monitoring essential.
Another major category includes non-immune oncological therapies that affect thyroid function, particularly tyrosine kinase inhibitors and certain targeted agents. Hypothyroidism is frequently observed in these patients, sometimes preceded by a thyrotoxic phase or associated with changes in the thyroid parenchyma. The underlying mechanisms include vascular alterations, follicular damage, interference with hormone transport and metabolism, and modulation of autoimmunity. Frequency varies widely among medications and clinical settings, and the condition becomes particularly relevant when tumour control requires prolonged therapeutic continuity.
Outside oncology, several medications are historically and clinically important causes of thyroid dysfunction. Lithium is associated predominantly with hypothyroidism and goitre, through possible facilitation of autoimmunity or interference with hormone secretion. Amiodarone, because of its high iodine content and its direct effects on thyroid parenchyma and peripheral hormone metabolism, may cause destructive thyrotoxicosis, increased hormone synthesis in a predisposed thyroid gland, or iodine-induced hypothyroidism. Interferons and other immunomodulatory therapies may also trigger autoimmune thyroid processes with variable phenotypes.
Among individual risk factors, the presence of thyroid autoantibodies at baseline increases the probability of developing thyroid dysfunction with several classes of medication, particularly immune checkpoint inhibitors. Age, female sex, and a personal or family history of autoimmune thyroid disease may also contribute, but the most clinically useful stratification remains based on autoantibody status and pre-treatment assessment of thyroid function.
An important epidemiological feature is the possible persistence of hypothyroidism after a phase of destructive thyroiditis. The proportion of patients requiring long-term levothyroxine varies according to the type of medication, severity of the damage, and pre-existing thyroid reserve. Management must therefore extend beyond the acute event and include structured follow-up, particularly in patients with cancer who continue treatment or experience prolonged survival.
Medication- and immunotherapy-induced thyroiditis can be interpreted through two major pathogenetic pathways, which frequently coexist in different proportions: direct or mediated destructive damage and the initiation or reactivation of thyroid autoimmunity. In the first setting, the primary event is follicular injury, with disruption of colloid and release of stored thyroxine (T4) and triiodothyronine (T3). In the second, pharmacological exposure alters immune tolerance or regulatory pathways, promoting the development of autoantibodies and lymphocytic infiltration with features overlapping those of chronic autoimmune thyroiditis.
Immune checkpoint inhibitors provide the clearest model of immune-mediated pathogenesis. Blockade of programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) reduces the physiological restraints on lymphocyte activation, facilitating a stronger immune response against tumour antigens, but also against self-antigens. The thyroid may become the target of an inflammatory process characterized by lymphocytic infiltration and cytotoxicity, resulting in destructive thyroiditis. In many patients, the event follows a typical pathophysiological sequence: transient release-related thyrotoxicosis with suppressed TSH, followed by hypothyroidism because of depletion of hormone stores and reduced secretory capacity.
From a biochemical perspective, destructive thyrotoxicosis has distinctive characteristics. The increase in thyroid hormones results from passive release rather than increased synthesis, and thyroid iodine uptake is therefore generally reduced, while antithyroid medications are ineffective. The thyrotoxic phase is usually limited because intrathyroidal stores are progressively depleted. Progression to hypothyroidism depends on the extent of tissue damage and the regenerative capacity of the remaining thyroid tissue. When the autoimmune component is pronounced or thyroid reserve was already reduced, hypothyroidism is more likely to become persistent.
Tyrosine kinase inhibitors and certain targeted agents may induce thyroid dysfunction through multiple mechanisms. Some interfere with thyroid vascularization and endothelial biology, promoting subclinical ischaemia and follicular damage. Others modify the expression of transporters and deiodinases or alter peripheral hormone turnover. In other cases, the thyroid becomes more vulnerable to inflammatory and autoimmune processes. The most common clinical outcome is hypothyroidism, which may develop gradually and require hormone replacement to maintain metabolic stability during prolonged oncological treatment.
Lithium acts through a different pathophysiological mechanism, interfering with thyroid hormone synthesis and, particularly, with hormone release, thereby promoting intrathyroidal accumulation. It may also increase susceptibility to autoimmune thyroiditis in predisposed individuals. The clinical picture is dominated by hypothyroidism and goitre, with relevant practical implications because hypothyroid symptoms may overlap with mood disturbances and psychiatric adverse effects, complicating recognition.
Amiodarone is an example in which destructive pathogenesis and iodine-mediated alterations may coexist. Its iodine load and structural similarity to thyroid hormones, together with cytotoxic effects on thyroid parenchyma and interference with peripheral conversion, may cause destructive thyrotoxicosis, increased hormone synthesis in a predisposed thyroid gland, or hypothyroidism. Pathophysiological distinction is therefore essential because treatment depends on the underlying mechanism and directly affects the patient’s cardiovascular risk.
Overall, the pathophysiology of these disorders supports a general clinical principle: iatrogenic thyroid dysfunction must not be treated according to diagnostic labels alone, but according to its mechanism. The same biochemical picture of thyrotoxicosis may require beta-blockade and observation when it is destructive, or antithyroid therapy when it results from hormone overproduction. This approach reduces unnecessary interventions, prevents iatrogenic deterioration, and allows endocrine management to be integrated with continuation of the causative therapy, particularly in oncology.
The clinical manifestations of medication- and immunotherapy-induced thyroiditis depend on the type of thyroid dysfunction, the speed of onset, and the patient’s clinical context. In many cases, particularly in oncology, thyroid dysfunction is identified before overt symptoms develop because of scheduled monitoring. When symptoms are present, however, they may significantly affect quality of life, treatment tolerance, and cardiovascular stability.
During the thyrotoxic phase of destructive thyroiditis, the clinical history may include palpitations, tachycardia, tremor, irritability, insomnia, heat intolerance, and weight loss. In patients with cancer, these symptoms may be confused with anxiety, physical deconditioning, anaemia, infections, or systemic effects of treatment. Clinicians should recognize that even moderate thyrotoxicosis may amplify cardiovascular vulnerability and impair exercise tolerance, producing a clinical impact disproportionate to the degree of biochemical abnormality.
On physical examination, the thyroid is generally painless and not markedly enlarged in thyroiditis associated with immune checkpoint inhibitors, while signs of adrenergic overactivity may be present. Ophthalmopathy, when present, favours Graves disease rather than destructive thyroiditis, although the absence of ocular signs alone does not establish the mechanism. In some patients, particularly those with predominant hypothyroidism, physical findings may be limited and diagnosis depends on laboratory testing and the therapeutic context.
The hypothyroid phase, which is often more prolonged and clinically relevant, may present with fatigue, somnolence, psychomotor slowing, cold intolerance, dry skin, constipation, weight gain, or difficulty losing weight. In patients with cancer, these symptoms frequently overlap with disease-related and treatment-related fatigue, but correction of hypothyroidism may significantly improve performance status and well-being. Similarly, in patients receiving lithium, hypothyroid symptoms may be interpreted as worsening mood or reduced energy related to the underlying psychiatric condition, requiring a high index of suspicion.
In some settings, the dominant clinical presentation is not isolated thyroid dysfunction but its coexistence with other iatrogenic endocrinopathies. In patients receiving immune checkpoint inhibitors, hypophysitis, adrenal insufficiency, or immune-mediated diabetes may coexist. The presence of hypotension, nausea, hyponatraemia, or hypoglycaemia requires consideration of glucocorticoid deficiency because its clinical severity and urgency are greater. This distinction is crucial to avoid attributing all symptoms to thyroid dysfunction and overlooking a potentially dangerous endocrine adverse event.
In more severe cases, particularly in patients with cardiovascular disease, thyrotoxicosis may precipitate arrhythmias or haemodynamic instability, while hypothyroidism may contribute to bradycardia, reduced functional capacity, and deterioration of the lipid profile. Clinical presentation must therefore be interpreted systemically, taking comorbidities, concomitant medications, and individual vulnerability into account.
A final distinctive clinical feature is the temporal pattern. Many iatrogenic forms of thyroiditis, particularly those associated with immune checkpoint inhibitors, follow a biphasic course, with progression from thyrotoxicosis to hypothyroidism over weeks or months. Recognizing this pattern allows serial testing and treatment adjustments to be planned appropriately, avoiding decisions based on a single blood test that may represent only a transient phase of the process.
Medication- or immunotherapy-induced thyroiditis should be suspected whenever thyroid dysfunction develops in a patient exposed to agents known to interfere with thyroid function, particularly when the temporal relationship is compatible and no convincing alternative explanation is present. In oncology, suspicion should be systematic in patients treated with immune checkpoint inhibitors and in those receiving targeted therapies associated with thyroid dysfunction, because the event may be frequent, underdiagnosed, and clinically relevant even when symptoms are subtle.
The threshold for suspicion should be particularly low in the presence of cardiovascular signs such as persistent tachycardia, palpitations, worsening angina, or new-onset arrhythmias, because even transient thyrotoxicosis may have disproportionate consequences in vulnerable patients. In patients with cancer, the development of tremor, insomnia, and somatic anxiety should prompt rapid assessment of TSH and FT4 rather than automatic attribution of symptoms to stress or nonspecific treatment-related adverse effects.
Iatrogenic thyroiditis should also be suspected when symptoms of hypothyroidism predominate, particularly marked fatigue, psychomotor slowing, and cold intolerance. In patients receiving oncological treatment, fatigue is multifactorial and is often regarded as unavoidable. However, correctable hypothyroidism represents a treatable cause that may significantly improve well-being and treatment tolerance. Similarly, in patients receiving lithium, reduced energy, weight gain, and somnolence require thyroid assessment because dysfunction may be insidious and progressive.
A specific setting requiring suspicion is the development of thyroid dysfunction together with signs of other immunotherapy-related endocrinopathies. Systemic symptoms such as persistent nausea, vomiting, hypotension, hyponatraemia, or mental confusion should not automatically be attributed to thyroid dysfunction because they may indicate adrenal insufficiency or hypophysitis, conditions in which timely diagnosis and treatment are essential. In these circumstances, morning cortisol assessment and investigation for hypophysitis take clinical priority.
Suspicion is further increased by markers of autoimmune predisposition, such as positive thyroid autoantibodies at baseline or a personal history of autoimmune thyroiditis. In many clinical strategies, positive autoantibody status does not necessarily contraindicate the causative therapy, but it identifies a patient who requires closer monitoring and in whom thyroid dysfunction should be considered early when nonspecific symptoms develop.
In summary, medication-induced thyroiditis should be suspected when thyroid dysfunction is temporally related to relevant pharmacological exposure, with particular attention to patients with cancer receiving immunotherapy, patients treated with lithium, and individuals receiving agents with a recognized effect on thyroid function. The key is to recognize the temporal pattern and integrate symptoms with the therapeutic context, preventing diagnostic delays that may impair treatment tolerance and increase clinical risk.
The diagnosis of medication- and immunotherapy-induced thyroiditis is based on a sequential approach integrating medication history, thyroid biochemistry, and investigations that distinguish release-related thyrotoxicosis from hormone overproduction. First-line testing includes TSH and FT4, together with free triiodothyronine (FT3) when thyrotoxicosis is present or clinically suspected. Testing must be repeated over time because many presentations are dynamic and the transition from thyrotoxicosis to hypothyroidism may occur within a few weeks.
A central diagnostic step, particularly in patients receiving immunotherapy, is the distinction between destructive thyroiditis and Graves disease because their therapeutic implications differ. Measurement of TSH receptor antibodies is highly informative: positivity supports Graves disease, while negativity, in an appropriate clinical context and with a biphasic course, supports destructive thyroiditis. Thyroid peroxidase antibodies and thyroglobulin antibodies may identify an autoimmune background, but they do not independently distinguish hormone overproduction from passive hormone release.
When greater certainty regarding the mechanism is required, assessment of thyroid iodine uptake or appropriate thyroid scintigraphy, when feasible, may be decisive. Uptake is typically low in destructive thyroiditis, consistent with the absence of hormone overproduction and reduced iodine organification. Alternatively, Doppler ultrasonography may provide indirect evidence. A pattern compatible with thyroiditis and the absence of marked hypervascularity makes destructive thyrotoxicosis more likely, whereas a substantial increase in blood flow may suggest Graves disease. Ultrasonography is also useful for assessing the structural substrate, identifying goitre and nodules, and estimating the likelihood of persistent hypothyroidism when features of chronic thyroiditis are present.
Accurate reconstruction of pharmacological exposure is essential. Diagnosis requires identification of potentially causative agents, duration of exposure, timing of symptom onset or laboratory abnormalities, and the possible presence of concomitant medications that modify hormone metabolism or protein binding. In oncology, diagnosis must be integrated with the therapeutic protocol and recommended monitoring plans, because continuation of antitumour therapy often depends more on appropriate management of endocrine adverse events than on their mere identification.
In patients receiving immunotherapy, diagnosis should include a targeted assessment for other associated endocrinopathies. When the clinical picture includes hypotension, persistent nausea, hyponatraemia, or hypoglycaemia, assessment of morning cortisol and pituitary function becomes a priority to exclude adrenal insufficiency or hypophysitis. This step is crucial because treatment of hypothyroidism with levothyroxine in a patient with unrecognized glucocorticoid deficiency may worsen clinical stability by increasing cortisol requirements and vulnerability to physiological stress.
The differential diagnosis includes painful subacute thyroiditis, factitious thyrotoxicosis, iodine excess, and previously unrecognized thyroid dysfunction. A well-structured diagnostic process permits treatment to be aligned with the underlying mechanism and allows appropriate follow-up to be planned for functional transition, particularly when progression to persistent hypothyroidism is likely.
Classification of medication- and immunotherapy-induced thyroiditis is useful for guiding diagnosis, management, and follow-up. A first fundamental distinction is between dysfunction caused predominantly by a destructive mechanism and dysfunction caused predominantly by an autoimmune mechanism with hormone overproduction. In the first setting, thyrotoxicosis results from hormone release, tends to be transient, and often progresses to hypothyroidism. In the second, hyperfunction is sustained by immune-mediated stimulation and requires specific therapeutic strategies, including antithyroid treatment and assessment of treatment duration and recurrence risk.
A second classification axis concerns the temporal pattern, distinguishing monophasic thyrotoxic forms, monophasic hypothyroid forms, and biphasic forms. Biphasic presentations are typical of many destructive forms of thyroiditis associated with immune checkpoint inhibitors, with an initial thyrotoxic peak followed by transition to hypothyroidism. Isolated hypothyroid forms are common with agents that progressively alter thyroid physiology, including some targeted therapies and lithium. Isolated thyrotoxic forms require particular attention to the differential diagnosis with Graves disease and iodine excess.
Severity may be classified according to clinical and biochemical parameters. During the thyrotoxic phase, severity is determined primarily by cardiovascular and neurological effects rather than by the degree of hormone elevation, because vulnerable patients may develop complications despite moderate biochemical abnormalities. During the hypothyroid phase, severity depends on the reduction in FT4 and the functional impact, with particular attention to patients with cancer in whom hypothyroidism may impair performance status and treatment tolerance.
A further practical classification concerns the probability of reversibility. Some destructive forms of thyroiditis resolve with recovery of euthyroidism, whereas others progress to permanent hypothyroidism, particularly when pre-existing autoimmunity is present or tissue damage is extensive. In patients receiving immunotherapy, post-thyroiditis hypothyroidism is often persistent and requires long-term replacement. In patients treated with lithium, reversibility varies and depends on duration of exposure, autoimmune status, and decisions regarding continuation of the causative medication.
Finally, classification should account for the coexistence of other iatrogenic endocrinopathies, particularly in oncology. A patient with thyroid dysfunction caused by immune checkpoint inhibitors may also develop hypophysitis or adrenal insufficiency, which modify the clinical presentation and establish a hierarchy of diagnostic and therapeutic priorities. Iatrogenic thyroiditis is therefore not merely a thyroid diagnosis, but may indicate a broader state of immune activation involving multiple endocrine glands.
Treatment of medication- and immunotherapy-induced thyroiditis must be mechanism-dependent, distinguishing release-related thyrotoxicosis, immune-mediated hormone overproduction, and hypothyroidism. In destructive thyrotoxicosis, antithyroid medications are not indicated because they do not reduce hormone release and do not modify the pathophysiology of follicular damage. The therapeutic objective is to control symptoms and prevent complications, particularly cardiovascular complications, during the transient phase.
During the thyrotoxic phase, the main therapeutic measure is the use of beta-blockers to reduce tachycardia, tremor, and adrenergic symptoms. Selection and dosage depend on cardiovascular comorbidities and symptom severity. When thyrotoxicosis is mild and the patient is clinically stable, close monitoring without pharmacological treatment may be sufficient, particularly when rapid transition to euthyroidism or hypothyroidism is expected. In selected cases with more pronounced inflammation and significant symptoms, glucocorticoids may be considered, but the decision must be carefully contextualized, particularly in patients with cancer, taking into account interactions with the causative therapy and the possible presence of other endocrinopathies.
When thyrotoxicosis is caused by Graves disease or immune-mediated hormone overproduction, treatment follows standard hyperthyroidism strategies, including antithyroid medications and, when appropriate, other therapeutic options. This scenario requires diagnostic confirmation through TSH receptor antibody testing and functional assessment because incorrect treatment may be ineffective and increase the risk of complications during the subsequent phase. In iatrogenic settings, the most frequent error is treating destructive thyrotoxicosis with antithyroid medications, thereby delaying effective symptomatic control and complicating management of the hypothyroidism that frequently follows.
During the hypothyroid phase, the principal therapeutic decision concerns initiation of levothyroxine. Treatment is indicated when hypothyroidism is clinically significant, FT4 is reduced, or symptoms have a substantial impact. In patients with cancer, correction of hypothyroidism may improve performance status and adherence to the therapeutic pathway. Dosage must be individualized according to age, cardiovascular comorbidities, and severity of hormone deficiency, with gradual dose escalation in vulnerable patients.
Management of the causative medication must be integrated with an assessment of the risk-benefit balance. In oncological immunotherapy, thyroid dysfunction can often be managed without discontinuing antitumour treatment, provided that the patient is clinically stable and the endocrine adverse event is controlled. Similarly, during targeted therapy, the objective is to preserve therapeutic continuity by correcting thyroid dysfunction with adequate hormone replacement. With lithium, the decision to continue treatment depends on the psychiatric indication, severity of thyroid dysfunction, and response to replacement therapy, within a multidisciplinary approach.
An essential practical principle concerns therapeutic hierarchy when multiple endocrinopathies coexist. In patients with suspected adrenal insufficiency or hypophysitis, glucocorticoid coverage must be ensured before initiating or increasing levothyroxine, in order to prevent clinical destabilization. This step is particularly relevant in patients receiving immune checkpoint inhibitors, in whom the association of several endocrine adverse events is clinically plausible and potentially dangerous.
Follow-up of medication- and immunotherapy-induced thyroiditis is essential because thyroid function may change rapidly and a significant proportion of patients progress to persistent hypothyroidism. Monitoring should be based on TSH and FT4, with testing frequency adapted to the clinical phase. During the thyrotoxic phase, close monitoring allows identification of the transition to hypothyroidism and timely adjustment of symptomatic management. During the hypothyroid phase, testing guides initiation and adjustment of levothyroxine and facilitates stabilization of metabolic status.
In patients receiving immunotherapy, follow-up must be incorporated into oncological care pathways and coordinated with the team managing immune-related adverse events. Thyroid dysfunction may develop early or later during treatment and may persist after immunotherapy has been discontinued. Serial monitoring prevents nonspecific symptoms from being attributed to disease progression or non-endocrine toxicity and allows oncological treatment to continue more safely.
In patients receiving levothyroxine, follow-up must assess signs of both undertreatment and overtreatment. In patients with cancer and in those with cardiovascular disease, excessive replacement may be poorly tolerated, and dose adjustment should therefore be cautious and guided by TSH and FT4. Variability in thyroid function during active treatment requires more frequent reassessment than in stable, non-iatrogenic hypothyroidism.
A specific issue is the assessment of hypothyroidism reversibility after destructive thyroiditis. Some patients recover thyroid function, whereas others develop permanent hypothyroidism. When clinically appropriate, any attempt to reduce or discontinue levothyroxine should be planned according to clear criteria and accompanied by close monitoring. In settings where persistence is highly likely, as in many cases of thyroiditis associated with immune checkpoint inhibitors, follow-up focuses primarily on stabilizing replacement therapy rather than discontinuing it.
Follow-up should also include targeted assessment for associated endocrinopathies, particularly during immunotherapy. The development of systemic symptoms or electrolyte abnormalities should prompt consideration of adrenal insufficiency or hypophysitis, with focused testing. This approach reduces the risk of major clinical events and improves the quality of multidisciplinary care.
Finally, in patients receiving chronic therapies such as lithium, follow-up must be continuous and integrated into the overall care pathway because thyroid dysfunction may develop gradually and remain subclinical for prolonged periods. Periodic TSH and FT4 measurements, combined with clinical assessment, allow early diagnosis and prevention of functional impairment that might otherwise be incorrectly attributed to the underlying psychiatric disorder.
The prognosis of medication- and immunotherapy-induced thyroiditis is generally favourable when thyroid dysfunction is recognized promptly and managed according to the underlying pathophysiological mechanism. Prognosis nevertheless depends significantly on the clinical context, particularly in oncology, where the objective is to maintain continuity of antitumour therapy while managing the endocrine adverse event as a treatable condition. In many patients, particularly those receiving immune checkpoint inhibitors, post-thyroiditis hypothyroidism tends to persist and requires long-term replacement and prolonged monitoring.
The most frequent and clinically relevant complication is the development of permanent hypothyroidism. This outcome is more likely when follicular damage is extensive, pre-existing autoimmunity is present, or the hypothyroid phase is severe. Untreated hypothyroidism may worsen fatigue, functional capacity, lipid profile, and exercise tolerance, with a potentially significant impact in already vulnerable patients. Prevention of these consequences relies on structured follow-up and appropriate replacement therapy.
During the thyrotoxic phase, the principal complications are cardiovascular. Tachyarrhythmias and haemodynamic instability may occur particularly in patients with cardiovascular disease, older adults, and patients with cancer and multiple comorbidities. Although destructive thyrotoxicosis is frequently transient, it may be clinically intense for a limited period and requires prompt beta-blockade and monitoring. Another potential complication is reduced tolerance of oncological treatment and an increase in urgent healthcare use when thyroid dysfunction is not recognized and corrected.
A conceptually important complication is inappropriate management resulting from diagnostic error. Treating destructive thyrotoxicosis with antithyroid medications is ineffective and may delay adequate symptomatic control. Conversely, failure to recognize Graves disease in a patient receiving immunotherapy may prolong hyperthyroidism and increase the risk of complications. The best prognosis is therefore closely linked to accurate aetiological diagnosis based on TSH receptor antibodies and, when indicated, functional testing.
In the context of immune checkpoint inhibitors, a clinically critical complication is the possible coexistence of other endocrinopathies, particularly adrenal insufficiency or hypophysitis. Failure to recognize these conditions may result in significant clinical instability. Outcomes depend on the ability of the clinical team to identify systemic warning signs promptly and initiate comprehensive endocrine management with the correct hierarchy of hormone replacement.
Overall, medication- and immunotherapy-induced thyroiditis represents a group of frequent and usually manageable, but not trivial, endocrine adverse events. Prognosis is optimal when care is structured around proactive monitoring in high-risk settings, mechanism-based diagnosis, targeted treatment with beta-blockers and levothyroxine when indicated, and multidisciplinary integration in patients with cancer to preserve therapeutic continuity without compromising clinical safety.