Beyond ‘essential’ – progression from subclinical hyperthyroidism to T3-thyrotoxicosis presenting as refractory hypertension: a case report

Beyond ‘essential’ – progression from subclinical hyperthyroidism to T3-thyrotoxicosis presenting as refractory hypertension: a case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Beyond ‘essential’ – progression from subclinical hyperthyroidism to T3-thyrotoxicosis presenting as refractory hypertension: a case report Jeremiah Onubi, Blessing Kenechi Myke-Mbata, Bruno Basil, Ugochukwu Josiah Okoli This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8279281/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background : Subclinical hyperthyroidism is often considered a mild condition, yet it may progress to overt thyrotoxicosis with systemic consequences. Hypertension is a recognized though underappreciated cardiovascular complication of thyroid dysfunction. We report a case in which resistant hypertension was ultimately attributable to evolving thyroid disease and was controllable only after anti-thyroid therapy was introduced, emphasizing the need to consider secondary causes in refractory hypertension. Case Presentation : A 48-year-old Nigerian woman with a family history of hyperthyroidism presented with a diffuse anterior neck swelling and known hypertension. At baseline, she had subclinical hyperthyroidism and blood pressure of 140/90 mmHg while on amlodipine and losartan. Over 24 weeks, her thyroid status progressed to overt T3-predominant thyrotoxicosis, during which her blood pressure rose sharply to 170/120 mmHg despite intensifying of antihypertensive therapy. She also developed dyslipidaemia and impaired fasting glucose. Initiation of carbimazole 10–20 mg daily led to rapid blood pressure normalization (120/80 mmHg), improvement in glycaemia, and eventual restoration of euthyroidism by week 36, although mild dyslipidaemia persisted. Aetiology could not be definitively classified due to resource limitations, but the temporal association between thyroid correction and blood pressure improvement suggests that hyperthyroidism may have contributed to her hypertension. Conclusion : This case illustrates that hypertension may be secondary to thyroid dysfunction and remain resistant to conventional treatment until euthyroidism is achieved. It also highlights the cardiovascular potency of T3 thyrotoxicosis and its systemic effects on glucose and lipid metabolism. Clinicians should consider thyroid disease in patients with intractable hypertension, particularly when accompanied by metabolic derangements or family history. Early recognition and timely initiation of anti-thyroid therapy can be decisive in achieving clinical stability and preventing complications. Endocrinology & Metabolism Subclinical hyperthyroidism Refractory hypertension T3 thyrotoxicosis Case report Cardiometabolic effects Background Subclinical hyperthyroidism is defined biochemically by a persistently suppressed serum thyroid-stimulating hormone (TSH) with circulating free thyroxine (FT4) and free triiodothyronine (FT3) levels within the reference range. Although frequently regarded as a mild or benign condition, accumulating evidence suggests that subclinical thyroid dysfunction may have clinically important cardiovascular and metabolic consequences [ 1 ]. Reported complications include atrial fibrillation, increased left ventricular mass, impaired diastolic function, decreased bone mineral density, and progression to overt hyperthyroidism [ 2 ]. Hypertension is a common clinical problem worldwide, and while most cases are due to primary (essential) hypertension, secondary causes must be carefully considered in patients with poor blood pressure control despite appropriate pharmacotherapy [ 3 , 4 ]. Hyperthyroidism is a recognized though often underappreciated secondary cause of hypertension. Thyroid hormone excess can increase cardiac output, reduce systemic vascular resistance, alter renal sodium handling, and potentiate adrenergic activity, all of which may contribute to sustained elevation of blood pressure [ 5 ]. Importantly, in such cases, hypertension may not respond adequately to standard antihypertensive drugs until the underlying thyroid dysfunction is corrected. T3 thyrotoxicosis, characterized by elevated triiodothyronine with normal thyroxine levels, represents a relatively uncommon manifestation of overt hyperthyroidism that can evolve from subclinical disease [ 6 ]. Its cardiovascular effects may be disproportionately pronounced compared to classic thyroxine-driven thyrotoxicosis, making early recognition vital [ 7 ]. We report the case of a 48-year-old woman with a family history of hyperthyroidism who presented with hypertension and subclinical hyperthyroidism. Her hypertension initially appeared resistant to multiple antihypertensive agents, but subsequently improved dramatically once anti-thyroid therapy was introduced and optimized. This case emphasizes the importance of considering hyperthyroidism as a potential secondary cause of hypertension, highlights the progression from subclinical hyperthyroidism to overt T3 thyrotoxicosis, and illustrates the clinical value of timely thyroid-directed treatment in restoring blood pressure control. Case Presentation Patient Information The patient was a 48-year-old Nigerian female civil servant with a known history of hypertension who presented to the metabolic clinic via the general outpatient department with complaints of anterior neck swelling of three months’ duration. She had a family history of hyperthyroidism in her mother who had goitre, but no known family history of diabetes and hypertension. At the time of presentation, she was already on antihypertensive medication, though details of prior treatment response were limited. She denied any overt symptoms of hyperthyroidism such as heat intolerance, palpitations, tremor, or weight loss. There was no history of alcohol or tobacco use, and was not leading a sedentary lifestyle. She had no known allergies and was not on any other concurrent medications other than antihypertensives. Clinical Findings On examination, the patient’s blood pressure was 140/90 mmHg. She had a diffuse anterior neck swelling, but systemic examination was otherwise unremarkable. Initial vital signs included a temperature of 37.6°C and a body weight of 73.3 kg. Her pulse rate was 91 beats per minute and respiratory rate 16 breaths per minute at that time. Blood samples were collected for routine thyroid function tests and other baseline laboratory tests. Over the course of follow-up, her clinical findings evolved in relation to her thyroid status. At 24 weeks, her blood pressure was markedly elevated at 170/120 mmHg despite adherence to multiple antihypertensive agents. Timeline and Therapeutic Interventions Table 1 outlines the chronological progression of the patient’s clinical course, biochemical parameters, and therapeutic interventions. The patient initially presented with subclinical hyperthyroidism, characterized by a suppressed TSH of 0.1 mIU/L with normal FT3 (1.9 pg/dL) and FT4 (1.0 ng/dL). Her blood pressure was mildly elevated, and metabolic assessment revealed impaired fasting glucose (7.7 mmol/L) and dyslipidaemia (total cholesterol 6.29 mmol/L, LDL-C 3.68 mmol/L, triglycerides 2.30 mmol/L). She was managed with lifestyle modification, dietary counselling, and antihypertensive therapy comprising amlodipine 10 mg and losartan 25 mg once daily. At week four, dyslipidaemia was confirmed, prompting the introduction of rosuvastatin 20 mg daily and low-dose aspirin (75 mg daily) for cardiovascular risk reduction. Between weeks four and twenty-four, the patient was temporarily lost to follow-up. Upon re-evaluation at week twenty-four, she had progressed to T3-predominant thyrotoxicosis (FT3 5.4 pg/dL, FT4 0.9 pg/dL, TSH 0.1 mIU/L), which coincided with resistant hypertension (170/120 mmHg) and worsening metabolic derangements, including persistently elevated fasting glucose. At this stage, carbimazole 10 mg daily was initiated, later titrated to 20 mg daily due to persistent biochemical hyperthyroidism, while her antihypertensives, statin, and aspirin were continued. Following initiation of carbimazole, gradual improvements in thyroid indices, blood pressure, and metabolic parameters were observed, suggesting a potential therapeutic effect. By week thirty-six, her FT3 and FT4 had normalized (3.2 pg/dL and 1.0 ng/dL, respectively) with a TSH of 0.7 mIU/L. Blood pressure stabilized at 120/80 mmHg, fasting glucose improved to 5.1 mmol/L, and dyslipidaemia showed partial improvement (total cholesterol 5.20 mmol/L, LDL-C 3.0 mmol/L, triglycerides 1.05 mmol/L). Table 1 Blood pressure, thyroid function, lipid profile, fasting blood glucose, and therapies during the 36-week follow-up Parameter (units) Day 1 4 weeks 24 weeks 25 weeks 32 weeks 36 weeks Blood Pressure (mmHg) 140/90 130/90 170/120 120/80 120/80 130/90 Therapy received Diet control; Amlodipine 10 mg o.d; Losartan 25 mg o.d Amlodipine 10 mg o.d; Losartan 25 mg o.d; Rosuvastatin 20 mg o.d; Aspirin 75 mg o.d Amlodipine 10 mg b.d; Losartan 25 mg b.d; Carbimazole 10 mg o.d; Rosuvastatin 20 mg o.d; Aspirin 75 mg o.d Amlodipine 10 mg o.d; Losartan 25 mg o.d; Carbimazole 20 mg o.d; Rosuvastatin 20 mg o.d; Aspirin 75 mg o.d Same as 25 weeks Same as 25 weeks TSH (0.4–7.0 mIU/L) 0.1 0.1 0.1 0.1 0.3 0.7 FT4 (0.8–2.0 ng/dL) 1.0 1.0 0.9 0.7 0.9 1.0 FT3 (1.4–4.2 pg/dL) 1.9 2.9 5.4 4.2 3.8 3.2 Total Cholesterol (< 5.14 mmol/L) – 6.29 5.35 – 6.84 5.2 Triglycerides ( 0.91 mmol/L) – 1.56 1.43 – 1.97 1.6 LDL-C (< 3.36 mmol/L) – 3.68 3.40 – 4.3 3.0 FBG (4.2–6.1 mmol/L) 7.7 7.2 – 5.0 6.1 5.1 CBC Normal – – – – – Electrolytes (Na⁺/K⁺/Cl⁻/HCO₃⁻) Within reference – – – – – Renal function (Urea, Creatinine, eGFR) Normal – – – – – Liver function (AST, ALT, ALP, Bilirubin, Albumin) Normal – – – – – Urinalysis No proteinuria, no glycosuria – – – – – HbA1c (%) 6.2 – – – – – Therapeutic Rationale Carbimazole was chosen as first-line therapy due to its convenient once-daily dosing, established safety profile, and ready local availability, making it preferable to propylthiouracil in a non-pregnant adult. Rosuvastatin was introduced for primary prevention of atherosclerotic cardiovascular disease in the context of persistent dyslipidaemia and hypertension, while low-dose aspirin was added as prophylaxis against cardiovascular events, given her multiple risk factors. Diagnostic Assessment At initial evaluation, thyroid function tests demonstrated a suppressed TSH (0.1 mIU/L) with normal FT3 (1.9 pg/dL) and FT4 (1.0 ng/dL), a biochemical pattern consistent with subclinical hyperthyroidism. By the fourth week, additional findings included dyslipidaemia (elevated total cholesterol and triglycerides) and impaired fasting glucose (7.2 mmol/L). At 24–25 weeks, her thyroid profile transitioned to overt hyperthyroidism characterized by markedly elevated FT3 (5.4 pg/dL), low-normal FT4 (0.9 ng/dL), and persistently suppressed TSH (0.1 mIU/L), confirming T3 thyrotoxicosis. In this context, her previously resistant hypertension was re-evaluated as secondary to thyrotoxicosis rather than essential hypertension. Differential diagnoses considered included multinodular goitre, thyroiditis, and Graves’ disease. Imaging studies such as thyroid ultrasonography or scintigraphy and immunological screens like Anti-TPO, etc, were not conducted due to financial constraints, and biopsy was not considered necessary for this patient. The major diagnostic challenge was the initial attribution of hypertension to essential causes, rather than recognizing thyroid dysfunction as the underlying driver. Follow-up and Outcomes The patient’s blood pressure initially improved modestly under antihypertensive therapy but remained sub-optimally controlled. Significant improvement occurred only after anti-thyroid treatment was introduced, at which point her blood pressure fell to 120/80 mmHg by the following week. Her lipid profile showed partial improvement under rosuvastatin therapy, though mild dyslipidaemia persisted. At 36 weeks, her thyroid function tests normalized, with TSH 0.7 mIU/L, FT4 0.8 ng/dL, and FT3 3.2 pg/dL. At that time, her blood pressure stabilized at 130/90 mmHg, and she remained clinically well on continued therapy. However, patient did not return for subsequent follow up for reassessment and possible withdrawal of anti-hypertensive therapy. Patient Perspective During the patient’s clinic visit on week 36, she shared her personal experience regarding the illness, diagnosis, and treatment process. She described initial concern about the swelling in her neck and persistent high blood pressure, particularly since she had a family history of thyroid disease. She noted that dietary counselling and medication adjustments were difficult to adapt to at first but appreciated the supportive guidance from the healthcare team. The patient expressed relief at regaining stability in her thyroid function and blood pressure while noting her inability to cope with subsequent follow up visits due to the high cost of management. Discussion This case documents a 48-year-old Nigerian woman who progressed from subclinical hyperthyroidism to overt T3-predominant thyrotoxicosis, accompanied by emergence of dyslipidaemia and fluctuating hyperglycaemia. The most clinically significant observation was that the patient’s hypertension proved resistant to multiple antihypertensive agents and improved following initiation and titration of carbimazole as thyroid function moved toward euthyroidism. This temporal sequence suggests that her elevated BP was mostly secondary to thyroid dysfunction rather than essential hypertension. Comparable reports have suggested that poorly controlled blood pressure should raise suspicion for underlying thyroid disease [ 8 – 10 ]. The cardiovascular effects of thyroid hormone excess are multifactorial. T3 increases cardiac contractility and heart rate through positive inotropic and chronotropic effects, sensitizes the myocardium to catecholamines, expands blood volume, and alters renal sodium handling, in addition to activating the renin–angiotensin–aldosterone system [ 10 ]. These mechanisms typically produce a hemodynamic state of increased cardiac output and reduced systemic vascular resistance. Clinically, this translates into systolic hypertension and widened pulse pressure, which can be difficult to control until the thyrotoxic state is corrected [ 11 ]. Importantly, in T3-predominant thyrotoxicosis, cardiovascular manifestations may be disproportionately severe because T3 is the biologically active thyroid hormone at the tissue level [ 12 ]. In this patient, the sharp reduction in blood pressure after carbimazole initiation is pathophysiologically consistent with reduction in active thyroid hormone burden. The metabolic disturbances observed in this case further highlight the systemic impact of thyroid dysfunction. The patient developed impaired fasting glucose, which improved after euthyroidism was achieved and without use of any hypoglycaemic agents. Hyperthyroidism is known to worsen glycaemic control through mechanisms such as increased hepatic glucose output, enhanced intestinal glucose absorption, and peripheral insulin resistance [ 13 ]. The improvement in glycaemia following anti-thyroid therapy is in line with these mechanisms, although concurrent lifestyle modification may have contributed. Conversely, her lipid profile showed variable abnormalities, including persistence of dyslipidaemia despite statin therapy. This finding is atypical, since overt hyperthyroidism usually lowers LDL and total cholesterol. The persistence of dyslipidaemia may reflect mixed influences such as intermittent thyroid instability, dietary factors, adherence to statins, or genetic predisposition. The case therefore illustrates that while glycaemic disturbances may resolve with thyroid correction, lipid derangements may follow a more complex and less predictable trajectory [ 14 ]. Strengths and Limitations of the Report This case report offers valuable insight into the progression from subclinical hyperthyroidism to overt T3 thyrotoxicosis and its apparent impact on resistant hypertension, documented through serial biochemical and clinical observations. The clear temporal relationship between initiation of anti-thyroid therapy and subsequent blood pressure improvement supports the likelihood of a thyroid-mediated mechanism. Nonetheless, the report has limitations. The absence of thyroid ultrasonography, radionuclide uptake studies, and antibody assays prevented definitive identification of the aetiology. Financial and logistical constraints limited access to advanced cardiometabolic investigations, including echocardiography, repeated HbA1c, and ambulatory blood pressure monitoring, which could have provided additional detail on cardiovascular and metabolic responses. The follow-up gap between weeks 4 and 24 reduced precision in assessing the timing of disease progression, and concurrent adjustment of antihypertensive and lipid-lowering therapies introduces possible confounding. Finally, limited follow-up beyond week 36 restricts conclusions regarding the long-term stability of these improvements. Recommendations In patients with poorly controlled or resistant hypertension, thyroid dysfunction should be considered as a possible secondary cause, and thyroid function tests should be obtained early. Patients with subclinical thyroid disease, particularly those with family history or cardiovascular risk factors, warrant close monitoring given the potential for progression to overt thyrotoxicosis with systemic complications. Clinicians should also provide integrated cardiometabolic care, ensuring assessment of glucose and lipid metabolism alongside thyroid evaluation. Addressing barriers to follow-up and access to diagnostic tests remains critical in resource-limited settings. Lessons Learned and Implications for Clinical Practice Hypertension may be secondary to thyroid dysfunction and may not respond adequately to standard antihypertensive therapy until thyroid status is corrected. T3-predominant thyrotoxicosis can produce pronounced cardiovascular effects even when FT4 remains within the reference range. Thyroid hormone excess can worsen glycaemic control, which often improves after restoration of euthyroidism. Lipid abnormalities in thyroid dysfunction may be variable and influenced by multiple factors, necessitating ongoing monitoring. Continuity of follow-up is essential in chronic endocrine and cardiovascular disease management, particularly in settings where diagnostic and therapeutic resources are constrained. Conclusion This case reinforces the need to consider thyroid dysfunction as a secondary cause of hypertension, especially in patients with resistant blood pressure. The patient’s course demonstrates how subclinical hyperthyroidism can progress to overt T3 thyrotoxicosis with significant cardiovascular and metabolic consequences. Importantly, institution of anti-thyroid therapy was the decisive factor in achieving blood pressure control, alongside improvement in glycaemic indices. Although lipid abnormalities persisted, the case illustrates the complex interplay between thyroid status, cardiovascular health, and metabolic regulation. Early recognition, comprehensive monitoring, and timely initiation of anti-thyroid therapy are critical to preventing morbidity in similar patients. Abbreviations TSH – Thyroid-Stimulating Hormone; FT3 – Free Triiodothyronine; FT4 – Free Thyroxine; T3 – Triiodothyronine; BP – Blood Pressure; bpm – Beats per Minute; od – once daily; bd – twice daily; RAAS – Renin–Angiotensin–Aldosterone System; HbA1c – Glycated Haemoglobin. Declarations Human Ethics and Consent to Participate Declarations: Not applicable. Consent for publication Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Availability of Data and Materials The data from this study will be available upon reasonable request to the corresponding author. Competing Interests The authors declare that they have no conflict of interest. FundingTop of Form This research did not receive any dedicated funding from a public, commercial, or not-for-profit agency. Authors’ contributions All authors collaborated on this case report. JO and BKM conceived the study and were involved in the direct clinical management of the patient. B.B. and UJO were involved in conducting the investigations and reporting the results. All authors participated in drafting and critically revising the manuscript. They collectively approved the final version for publication and accepted responsibility for all aspects of the report. Acknowledgements The authors acknowledge the management of the Bingham University Teaching Hospital, Parklane, staff of the Metabolic Medicine clinic and the patient for cooperating with the unit during the management period. References Kaushik A, Agrawal M (2023) Relationship between subclinical hypothyroidism and the risk of cardiovascular complications. Cureus 15(1):e33708. 10.7759/cureus.33708 Deguchi-Horiuchi H, Ito M, Takahashi S, Kousaka K, Hisakado M, Fukata S, Kudo T, Nishihara E, Nishikawa M, Miyauchi A, Akamizu T (2024) Comparison of pathophysiology in subclinical hyperthyroidism with different etiologies. Endocr J 71(4):373–381. 10.1507/endocrj.EJ23-0497 Buso G, Agabiti-Rosei C, Lemoli M, Corvini F, Muiesan ML (2024) The global burden of resistant hypertension and potential treatment options. Eur Cardiol Rev 19:e07. 10.15420/ecr.2023.51 Dos Teixeira PdFdS PB, Pazos-Moura CC (2020) The role of thyroid hormone in metabolism and metabolic syndrome. Ther Adv Endocrinol Metab 11:2042018820917869. 10.1177/2042018820917869 Rivas AM, Pena C, Kopel J, Dennis JA, Nugent K (2021) Hypertension and hyperthyroidism: association and pathogenesis. Am J Med Sci 361(1):3–7. 10.1016/j.amjms.2020.08.012 Singh SK, Singh R, Bedi S, Pandey AK, Tiwari A, Rai PK (2025) Prevalence of T3 thyrotoxicosis and its management in new onset thyrotoxicosis patients: a prospective observational study. Int J Adv Med 12(1):39–43. 10.18203/2349-3933.ijam20243812 Debmalya S, Saumitra R, Singh MH (2022) Interplay between cardiovascular and thyroid dysfunctions: a review of clinical implications and management strategies. Endocr Regul 56(4):311–328. 10.2478/enr-2022-0033 Prasert N, Manosroi W, Hankamolsiri B, Wae-Uma M, Choonklai P (2025) Factors predicting secondary hypertension in young adults with hypertension: a retrospective study. BMC Cardiovasc Disord 25(1):57. 10.1186/s12872-025-04520-2 Giontella A, Lotta LA, Overton JD, Baras A, Sartorio A, Minuz P et al (2021) Association of Thyroid Function with Blood Pressure and Cardiovascular Disease: A Mendelian Randomization. J Pers Med 11(12):1306. 10.3390/jpm11121306 Berta E, Lengyel I, Halmi S, Zrínyi M, Erdei A, Harangi M, Páll D, Nagy EV, Bodor M (2019) Hypertension in thyroid disorders. Front Endocrinol (Lausanne) 10:482. 10.3389/fendo.2019.00482 Su H, Wang J, Wang ZF, Yang Z, Ma Y (2025) Assessing left ventricular function in patients with hyperthyroidism across varied heart rates via press-strain loop analysis: a retrospective cross-sectional study. Quant Imaging Med Surg 15(2):1632–1640. 10.21037/qims-24-951 Bratu G, Radulescu V, Stanescu-Smocot AP, Mihai R, Badiu C (2025) Challenges in managing severe T3 thyrotoxicosis: a complex case of Graves. In: Endocr Abstracts 110:EP1607. 10.1530/endoabs.110.EP1607 Sarker PK, Sultana N, Islam H, Bashir MS, Ali MS (2025) Thyroid dysfunction and metabolic dysregulation: a cross-sectional study of hormonal and glycemic parameters. Mol Mech Res 3(2):10227. 10.59429/mmr.v3i2.10227 Nagamine T, Tanimura-Inagaki K, Nagao M, Kobayashi S, Shuto Y, Tamura H, Okazaki-Hada M, Fukuda I, Sugihara H, Oikawa S, Iwabu M (2025) Impact of Graves’ hyperthyroidism treatment on lipid profiles and cholesterol dynamics: a prospective observational study. Ther Adv Endocrinol Metab 16:20420188251372381. 10.1177/20420188251372381 Additional Declarations The authors declare no competing interests. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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report\u003c/strong\u003e\u003c/p\u003e","fulltext":[{"header":"Background","content":"\u003cp\u003eSubclinical hyperthyroidism is defined biochemically by a persistently suppressed serum thyroid-stimulating hormone (TSH) with circulating free thyroxine (FT4) and free triiodothyronine (FT3) levels within the reference range. Although frequently regarded as a mild or benign condition, accumulating evidence suggests that subclinical thyroid dysfunction may have clinically important cardiovascular and metabolic consequences [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Reported complications include atrial fibrillation, increased left ventricular mass, impaired diastolic function, decreased bone mineral density, and progression to overt hyperthyroidism [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eHypertension is a common clinical problem worldwide, and while most cases are due to primary (essential) hypertension, secondary causes must be carefully considered in patients with poor blood pressure control despite appropriate pharmacotherapy [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Hyperthyroidism is a recognized though often underappreciated secondary cause of hypertension. Thyroid hormone excess can increase cardiac output, reduce systemic vascular resistance, alter renal sodium handling, and potentiate adrenergic activity, all of which may contribute to sustained elevation of blood pressure [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Importantly, in such cases, hypertension may not respond adequately to standard antihypertensive drugs until the underlying thyroid dysfunction is corrected.\u003c/p\u003e\u003cp\u003eT3 thyrotoxicosis, characterized by elevated triiodothyronine with normal thyroxine levels, represents a relatively uncommon manifestation of overt hyperthyroidism that can evolve from subclinical disease [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Its cardiovascular effects may be disproportionately pronounced compared to classic thyroxine-driven thyrotoxicosis, making early recognition vital [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eWe report the case of a 48-year-old woman with a family history of hyperthyroidism who presented with hypertension and subclinical hyperthyroidism. Her hypertension initially appeared resistant to multiple antihypertensive agents, but subsequently improved dramatically once anti-thyroid therapy was introduced and optimized. This case emphasizes the importance of considering hyperthyroidism as a potential secondary cause of hypertension, highlights the progression from subclinical hyperthyroidism to overt T3 thyrotoxicosis, and illustrates the clinical value of timely thyroid-directed treatment in restoring blood pressure control.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003ePatient Information\u003c/h2\u003e\u003cp\u003eThe patient was a 48-year-old Nigerian female civil servant with a known history of hypertension who presented to the metabolic clinic via the general outpatient department with complaints of anterior neck swelling of three months\u0026rsquo; duration. She had a family history of hyperthyroidism in her mother who had goitre, but no known family history of diabetes and hypertension. At the time of presentation, she was already on antihypertensive medication, though details of prior treatment response were limited. She denied any overt symptoms of hyperthyroidism such as heat intolerance, palpitations, tremor, or weight loss. There was no history of alcohol or tobacco use, and was not leading a sedentary lifestyle. She had no known allergies and was not on any other concurrent medications other than antihypertensives.\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003eClinical Findings\u003c/h3\u003e\n\u003cp\u003eOn examination, the patient\u0026rsquo;s blood pressure was 140/90 mmHg. She had a diffuse anterior neck swelling, but systemic examination was otherwise unremarkable. Initial vital signs included a temperature of 37.6\u0026deg;C and a body weight of 73.3 kg. Her pulse rate was 91 beats per minute and respiratory rate 16 breaths per minute at that time. Blood samples were collected for routine thyroid function tests and other baseline laboratory tests. Over the course of follow-up, her clinical findings evolved in relation to her thyroid status. At 24 weeks, her blood pressure was markedly elevated at 170/120 mmHg despite adherence to multiple antihypertensive agents.\u003c/p\u003e\n\u003ch3\u003eTimeline and Therapeutic Interventions\u003c/h3\u003e\n\u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e outlines the chronological progression of the patient\u0026rsquo;s clinical course, biochemical parameters, and therapeutic interventions. The patient initially presented with subclinical hyperthyroidism, characterized by a suppressed TSH of 0.1 mIU/L with normal FT3 (1.9 pg/dL) and FT4 (1.0 ng/dL). Her blood pressure was mildly elevated, and metabolic assessment revealed impaired fasting glucose (7.7 mmol/L) and dyslipidaemia (total cholesterol 6.29 mmol/L, LDL-C 3.68 mmol/L, triglycerides 2.30 mmol/L). She was managed with lifestyle modification, dietary counselling, and antihypertensive therapy comprising amlodipine 10 mg and losartan 25 mg once daily. At week four, dyslipidaemia was confirmed, prompting the introduction of rosuvastatin 20 mg daily and low-dose aspirin (75 mg daily) for cardiovascular risk reduction.\u003c/p\u003e\u003cp\u003eBetween weeks four and twenty-four, the patient was temporarily lost to follow-up. Upon re-evaluation at week twenty-four, she had progressed to T3-predominant thyrotoxicosis (FT3 5.4 pg/dL, FT4 0.9 pg/dL, TSH 0.1 mIU/L), which coincided with resistant hypertension (170/120 mmHg) and worsening metabolic derangements, including persistently elevated fasting glucose. At this stage, carbimazole 10 mg daily was initiated, later titrated to 20 mg daily due to persistent biochemical hyperthyroidism, while her antihypertensives, statin, and aspirin were continued. Following initiation of carbimazole, gradual improvements in thyroid indices, blood pressure, and metabolic parameters were observed, suggesting a potential therapeutic effect. By week thirty-six, her FT3 and FT4 had normalized (3.2 pg/dL and 1.0 ng/dL, respectively) with a TSH of 0.7 mIU/L. Blood pressure stabilized at 120/80 mmHg, fasting glucose improved to 5.1 mmol/L, and dyslipidaemia showed partial improvement (total cholesterol 5.20 mmol/L, LDL-C 3.0 mmol/L, triglycerides 1.05 mmol/L).\u003c/p\u003e\u003cp\u003e\u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eBlood pressure, thyroid function, lipid profile, fasting blood glucose, and therapies during the 36-week follow-up\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"7\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eParameter (units)\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eDay 1\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003e4 weeks\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\"\u003e\u003cp\u003e24 weeks\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c5\"\u003e\u003cp\u003e25 weeks\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c6\"\u003e\u003cp\u003e32 weeks\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c7\"\u003e\u003cp\u003e36 weeks\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eBlood Pressure (mmHg)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e140/90\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e130/90\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e170/120\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e120/80\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e120/80\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e130/90\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eTherapy received\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eDiet control;\u003c/p\u003e\u003cp\u003eAmlodipine 10 mg o.d;\u003c/p\u003e\u003cp\u003eLosartan 25 mg o.d\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eAmlodipine 10 mg o.d;\u003c/p\u003e\u003cp\u003eLosartan 25 mg o.d;\u003c/p\u003e\u003cp\u003eRosuvastatin 20 mg o.d;\u003c/p\u003e\u003cp\u003eAspirin 75 mg o.d\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eAmlodipine 10 mg b.d;\u003c/p\u003e\u003cp\u003eLosartan 25 mg b.d;\u003c/p\u003e\u003cp\u003eCarbimazole 10 mg o.d;\u003c/p\u003e\u003cp\u003eRosuvastatin 20 mg o.d;\u003c/p\u003e\u003cp\u003eAspirin 75 mg o.d\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003eAmlodipine 10 mg o.d;\u003c/p\u003e\u003cp\u003eLosartan 25 mg o.d;\u003c/p\u003e\u003cp\u003eCarbimazole 20 mg o.d;\u003c/p\u003e\u003cp\u003eRosuvastatin 20 mg o.d;\u003c/p\u003e\u003cp\u003eAspirin 75 mg o.d\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003eSame as 25 weeks\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003eSame as 25 weeks\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eTSH (0.4\u0026ndash;7.0 mIU/L)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e0.1\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e0.1\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e0.1\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e0.1\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e0.3\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e0.7\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eFT4 (0.8\u0026ndash;2.0 ng/dL)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.0\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e1.0\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e0.9\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e0.7\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e0.9\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e1.0\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eFT3 (1.4\u0026ndash;4.2 pg/dL)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e1.9\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e2.9\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e5.4\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e4.2\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e3.8\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e3.2\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eTotal Cholesterol (\u0026lt;\u0026thinsp;5.14 mmol/L)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e6.29\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e5.35\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e6.84\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e5.2\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eTriglycerides (\u0026lt;\u0026thinsp;2.26 mmol/L)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e2.30\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e1.15\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e1.23\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e1.05\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eHDL-C (\u0026gt;\u0026thinsp;0.91 mmol/L)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e1.56\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e1.43\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e1.97\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e1.6\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eLDL-C (\u0026lt;\u0026thinsp;3.36 mmol/L)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e3.68\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e3.40\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e4.3\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e3.0\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eFBG (4.2\u0026ndash;6.1 mmol/L)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e7.7\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e7.2\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e5.0\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e6.1\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e5.1\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eCBC\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eElectrolytes (Na⁺/K⁺/Cl⁻/HCO₃⁻)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eWithin reference\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eRenal function (Urea, Creatinine, eGFR)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eLiver function (AST, ALT, ALP, Bilirubin, Albumin)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eUrinalysis\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eNo proteinuria, no glycosuria\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eHbA1c (%)\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e6.2\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c6\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c7\"\u003e\u003cp\u003e\u0026ndash;\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003c/colgroup\u003e\u003c/table\u003e\u003c/div\u003e\u003c/p\u003e\n\u003ch3\u003eTherapeutic Rationale\u003c/h3\u003e\n\u003cp\u003eCarbimazole was chosen as first-line therapy due to its convenient once-daily dosing, established safety profile, and ready local availability, making it preferable to propylthiouracil in a non-pregnant adult. Rosuvastatin was introduced for primary prevention of atherosclerotic cardiovascular disease in the context of persistent dyslipidaemia and hypertension, while low-dose aspirin was added as prophylaxis against cardiovascular events, given her multiple risk factors.\u003c/p\u003e\n\u003ch3\u003eDiagnostic Assessment\u003c/h3\u003e\n\u003cp\u003eAt initial evaluation, thyroid function tests demonstrated a suppressed TSH (0.1 mIU/L) with normal FT3 (1.9 pg/dL) and FT4 (1.0 ng/dL), a biochemical pattern consistent with subclinical hyperthyroidism. By the fourth week, additional findings included dyslipidaemia (elevated total cholesterol and triglycerides) and impaired fasting glucose (7.2 mmol/L). At 24\u0026ndash;25 weeks, her thyroid profile transitioned to overt hyperthyroidism characterized by markedly elevated FT3 (5.4 pg/dL), low-normal FT4 (0.9 ng/dL), and persistently suppressed TSH (0.1 mIU/L), confirming T3 thyrotoxicosis. In this context, her previously resistant hypertension was re-evaluated as secondary to thyrotoxicosis rather than essential hypertension.\u003c/p\u003e\u003cp\u003eDifferential diagnoses considered included multinodular goitre, thyroiditis, and Graves\u0026rsquo; disease. Imaging studies such as thyroid ultrasonography or scintigraphy and immunological screens like Anti-TPO, etc, were not conducted due to financial constraints, and biopsy was not considered necessary for this patient. The major diagnostic challenge was the initial attribution of hypertension to essential causes, rather than recognizing thyroid dysfunction as the underlying driver.\u003c/p\u003e\u003cdiv id=\"Sec8\" class=\"Section2\"\u003e\u003ch2\u003eFollow-up and Outcomes\u003c/h2\u003e\u003cp\u003eThe patient\u0026rsquo;s blood pressure initially improved modestly under antihypertensive therapy but remained sub-optimally controlled. Significant improvement occurred only after anti-thyroid treatment was introduced, at which point her blood pressure fell to 120/80 mmHg by the following week. Her lipid profile showed partial improvement under rosuvastatin therapy, though mild dyslipidaemia persisted. At 36 weeks, her thyroid function tests normalized, with TSH 0.7 mIU/L, FT4 0.8 ng/dL, and FT3 3.2 pg/dL. At that time, her blood pressure stabilized at 130/90 mmHg, and she remained clinically well on continued therapy. However, patient did not return for subsequent follow up for reassessment and possible withdrawal of anti-hypertensive therapy.\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003ePatient Perspective\u003c/h3\u003e\n\u003cp\u003eDuring the patient\u0026rsquo;s clinic visit on week 36, she shared her personal experience regarding the illness, diagnosis, and treatment process. She described initial concern about the swelling in her neck and persistent high blood pressure, particularly since she had a family history of thyroid disease. She noted that dietary counselling and medication adjustments were difficult to adapt to at first but appreciated the supportive guidance from the healthcare team. The patient expressed relief at regaining stability in her thyroid function and blood pressure while noting her inability to cope with subsequent follow up visits due to the high cost of management.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis case documents a 48-year-old Nigerian woman who progressed from subclinical hyperthyroidism to overt T3-predominant thyrotoxicosis, accompanied by emergence of dyslipidaemia and fluctuating hyperglycaemia. The most clinically significant observation was that the patient\u0026rsquo;s hypertension proved resistant to multiple antihypertensive agents and improved following initiation and titration of carbimazole as thyroid function moved toward euthyroidism. This temporal sequence suggests that her elevated BP was mostly secondary to thyroid dysfunction rather than essential hypertension. Comparable reports have suggested that poorly controlled blood pressure should raise suspicion for underlying thyroid disease [\u003cspan additionalcitationids=\"CR9\" citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eThe cardiovascular effects of thyroid hormone excess are multifactorial. T3 increases cardiac contractility and heart rate through positive inotropic and chronotropic effects, sensitizes the myocardium to catecholamines, expands blood volume, and alters renal sodium handling, in addition to activating the renin\u0026ndash;angiotensin\u0026ndash;aldosterone system [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. These mechanisms typically produce a hemodynamic state of increased cardiac output and reduced systemic vascular resistance. Clinically, this translates into systolic hypertension and widened pulse pressure, which can be difficult to control until the thyrotoxic state is corrected [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Importantly, in T3-predominant thyrotoxicosis, cardiovascular manifestations may be disproportionately severe because T3 is the biologically active thyroid hormone at the tissue level [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. In this patient, the sharp reduction in blood pressure after carbimazole initiation is pathophysiologically consistent with reduction in active thyroid hormone burden.\u003c/p\u003e\u003cp\u003eThe metabolic disturbances observed in this case further highlight the systemic impact of thyroid dysfunction. The patient developed impaired fasting glucose, which improved after euthyroidism was achieved and without use of any hypoglycaemic agents. Hyperthyroidism is known to worsen glycaemic control through mechanisms such as increased hepatic glucose output, enhanced intestinal glucose absorption, and peripheral insulin resistance [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. The improvement in glycaemia following anti-thyroid therapy is in line with these mechanisms, although concurrent lifestyle modification may have contributed.\u003c/p\u003e\u003cp\u003eConversely, her lipid profile showed variable abnormalities, including persistence of dyslipidaemia despite statin therapy. This finding is atypical, since overt hyperthyroidism usually lowers LDL and total cholesterol. The persistence of dyslipidaemia may reflect mixed influences such as intermittent thyroid instability, dietary factors, adherence to statins, or genetic predisposition. The case therefore illustrates that while glycaemic disturbances may resolve with thyroid correction, lipid derangements may follow a more complex and less predictable trajectory [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e\u003cdiv id=\"Sec11\" class=\"Section2\"\u003e\u003ch2\u003eStrengths and Limitations of the Report\u003c/h2\u003e\u003cp\u003eThis case report offers valuable insight into the progression from subclinical hyperthyroidism to overt T3 thyrotoxicosis and its apparent impact on resistant hypertension, documented through serial biochemical and clinical observations. The clear temporal relationship between initiation of anti-thyroid therapy and subsequent blood pressure improvement supports the likelihood of a thyroid-mediated mechanism. Nonetheless, the report has limitations. The absence of thyroid ultrasonography, radionuclide uptake studies, and antibody assays prevented definitive identification of the aetiology. Financial and logistical constraints limited access to advanced cardiometabolic investigations, including echocardiography, repeated HbA1c, and ambulatory blood pressure monitoring, which could have provided additional detail on cardiovascular and metabolic responses. The follow-up gap between weeks 4 and 24 reduced precision in assessing the timing of disease progression, and concurrent adjustment of antihypertensive and lipid-lowering therapies introduces possible confounding. Finally, limited follow-up beyond week 36 restricts conclusions regarding the long-term stability of these improvements.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec12\" class=\"Section2\"\u003e\u003ch2\u003eRecommendations\u003c/h2\u003e\u003cp\u003eIn patients with poorly controlled or resistant hypertension, thyroid dysfunction should be considered as a possible secondary cause, and thyroid function tests should be obtained early. Patients with subclinical thyroid disease, particularly those with family history or cardiovascular risk factors, warrant close monitoring given the potential for progression to overt thyrotoxicosis with systemic complications. Clinicians should also provide integrated cardiometabolic care, ensuring assessment of glucose and lipid metabolism alongside thyroid evaluation. Addressing barriers to follow-up and access to diagnostic tests remains critical in resource-limited settings.\u003c/p\u003e\u003c/div\u003e\u003cdiv id=\"Sec13\" class=\"Section2\"\u003e\u003ch2\u003eLessons Learned and Implications for Clinical Practice\u003c/h2\u003e\u003cp\u003e\u003cul\u003e\u003cli\u003e\u003cp\u003eHypertension may be secondary to thyroid dysfunction and may not respond adequately to standard antihypertensive therapy until thyroid status is corrected.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eT3-predominant thyrotoxicosis can produce pronounced cardiovascular effects even when FT4 remains within the reference range.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eThyroid hormone excess can worsen glycaemic control, which often improves after restoration of euthyroidism.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eLipid abnormalities in thyroid dysfunction may be variable and influenced by multiple factors, necessitating ongoing monitoring.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eContinuity of follow-up is essential in chronic endocrine and cardiovascular disease management, particularly in settings where diagnostic and therapeutic resources are constrained.\u003c/p\u003e\u003c/li\u003e\u003c/ul\u003e\u003c/p\u003e\u003c/div\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case reinforces the need to consider thyroid dysfunction as a secondary cause of hypertension, especially in patients with resistant blood pressure. The patient\u0026rsquo;s course demonstrates how subclinical hyperthyroidism can progress to overt T3 thyrotoxicosis with significant cardiovascular and metabolic consequences. Importantly, institution of anti-thyroid therapy was the decisive factor in achieving blood pressure control, alongside improvement in glycaemic indices. Although lipid abnormalities persisted, the case illustrates the complex interplay between thyroid status, cardiovascular health, and metabolic regulation. Early recognition, comprehensive monitoring, and timely initiation of anti-thyroid therapy are critical to preventing morbidity in similar patients.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eTSH \u0026ndash; Thyroid-Stimulating Hormone; FT3 \u0026ndash; Free Triiodothyronine; FT4 \u0026ndash; Free Thyroxine; T3 \u0026ndash; Triiodothyronine; BP \u0026ndash; Blood Pressure; bpm \u0026ndash; Beats per Minute; od \u0026ndash; once daily; bd \u0026ndash; twice daily; RAAS \u0026ndash; Renin\u0026ndash;Angiotensin\u0026ndash;Aldosterone System; HbA1c \u0026ndash; Glycated Haemoglobin.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cem\u003eHuman Ethics and Consent to Participate Declarations:\u0026nbsp;\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eConsent for publication\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAvailability of Data and Materials\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eThe data from this study will be available upon reasonable request to the corresponding author.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eCompeting Interests\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eFundingTop of Form\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eThis research did not receive any dedicated funding from a public, commercial, or not-for-profit agency.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAuthors\u0026rsquo; contributions\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eAll authors collaborated on this case report. JO and BKM conceived the study and were involved in the direct clinical management of the patient. B.B. and UJO were involved in conducting the investigations and reporting the results. All authors participated in drafting and critically revising the manuscript. They collectively approved the final version for publication and accepted responsibility for all aspects of the report.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAcknowledgements\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eThe authors acknowledge the management of the Bingham University Teaching Hospital, Parklane, staff of the Metabolic Medicine clinic and the patient for cooperating with the unit during the management period.\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eKaushik A, Agrawal M (2023) Relationship between subclinical hypothyroidism and the risk of cardiovascular complications. 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Ther Adv Endocrinol Metab 16:20420188251372381. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1177/20420188251372381\u003c/span\u003e\u003cspan address=\"10.1177/20420188251372381\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"Bingham University, Jos, Nigeria.","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Subclinical hyperthyroidism, Refractory hypertension, T3 thyrotoxicosis, Case report, Cardiometabolic effects","lastPublishedDoi":"10.21203/rs.3.rs-8279281/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8279281/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cem\u003eBackground\u003c/em\u003e: Subclinical hyperthyroidism is often considered a mild condition, yet it may progress to overt thyrotoxicosis with systemic consequences. Hypertension is a recognized though underappreciated cardiovascular complication of thyroid dysfunction. We report a case in which resistant hypertension was ultimately attributable to evolving thyroid disease and was controllable only after anti-thyroid therapy was introduced, emphasizing the need to consider secondary causes in refractory hypertension.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eCase Presentation\u003c/em\u003e: A 48-year-old Nigerian woman with a family history of hyperthyroidism presented with a diffuse anterior neck swelling and known hypertension. At baseline, she had subclinical hyperthyroidism and blood pressure of 140/90 mmHg while on amlodipine and losartan. Over 24 weeks, her thyroid status progressed to overt T3-predominant thyrotoxicosis, during which her blood pressure rose sharply to 170/120 mmHg despite intensifying of antihypertensive therapy. She also developed dyslipidaemia and impaired fasting glucose. Initiation of carbimazole 10–20 mg daily led to rapid blood pressure normalization (120/80 mmHg), improvement in glycaemia, and eventual restoration of euthyroidism by week 36, although mild dyslipidaemia persisted. Aetiology could not be definitively classified due to resource limitations, but the temporal association between thyroid correction and blood pressure improvement suggests that hyperthyroidism may have contributed to her hypertension.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eConclusion\u003c/em\u003e: This case illustrates that hypertension may be secondary to thyroid dysfunction and remain resistant to conventional treatment until euthyroidism is achieved. It also highlights the cardiovascular potency of T3 thyrotoxicosis and its systemic effects on glucose and lipid metabolism. Clinicians should consider thyroid disease in patients with intractable hypertension, particularly when accompanied by metabolic derangements or family history. Early recognition and timely initiation of anti-thyroid therapy can be decisive in achieving clinical stability and preventing complications.\u003c/p\u003e","manuscriptTitle":"Beyond ‘essential’ – progression from subclinical hyperthyroidism to T3-thyrotoxicosis presenting as refractory hypertension: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-05 07:29:11","doi":"10.21203/rs.3.rs-8279281/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"9685c7cf-3f7d-4912-8e76-f8727330cad3","owner":[],"postedDate":"December 5th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":59094499,"name":"Endocrinology \u0026 Metabolism"}],"tags":[],"updatedAt":"2025-12-05T07:29:11+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-05 07:29:11","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8279281","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8279281","identity":"rs-8279281","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}