Aydoğan E, Ülke S, Yumuşak P, Uygun İlikhan S, Karaahmetoğlu S. Hypertrophic cardiomyopathy in the context of primary hyperaldosteronism, Sjögren’s syndrome, and obstructive uropathy: A case report. World J Clin Cases 2026; 14(11): 119699 [DOI: 10.12998/wjcc.v14.i11.119699]
Corresponding Author of This Article
Sinem Ülke, MD, Consultant, FRCPA, FRCPC, Department of Internal Medicine, Ankara Bilkent City Hospital, University District, Bilkent Boulevard No. 1 Çankaya, Ankara 06800, Türkiye. sinem.karaoglu384@gmail.com
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Endocrinology & Metabolism
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Case Report
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Apr 16, 2026 (publication date) through Apr 15, 2026
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World Journal of Clinical Cases
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Aydoğan E, Ülke S, Yumuşak P, Uygun İlikhan S, Karaahmetoğlu S. Hypertrophic cardiomyopathy in the context of primary hyperaldosteronism, Sjögren’s syndrome, and obstructive uropathy: A case report. World J Clin Cases 2026; 14(11): 119699 [DOI: 10.12998/wjcc.v14.i11.119699]
World J Clin Cases. Apr 16, 2026; 14(11): 119699 Published online Apr 16, 2026. doi: 10.12998/wjcc.v14.i11.119699
Hypertrophic cardiomyopathy in the context of primary hyperaldosteronism, Sjögren’s syndrome, and obstructive uropathy: A case report
Esranur Aydoğan, Sinem Ülke, Pelin Yumuşak, Sevil Uygun İlikhan, Selma Karaahmetoğlu
Esranur Aydoğan, Sinem Ülke, Pelin Yumuşak, Sevil Uygun İlikhan, Selma Karaahmetoğlu, Department of Internal Medicine, Ankara Bilkent City Hospital, Ankara 06690, Türkiye
Author contributions: Uygun İlikhan S and Ülke S contributed to patient evaluation and data collection; Karaahmetoğlu S and Yumuşak P contributed to diagnostic interpretation and clinical assessment; Aydoğan EN contributed to the literature review; Ülke S drafted the manuscript; and all authors critically revised the manuscript and approved the final version.
Informed consent statement: Written informed consent was obtained from the patient for publication of this case report and the accompanying images.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Corresponding author: Sinem Ülke, MD, Consultant, FRCPA, FRCPC, Department of Internal Medicine, Ankara Bilkent City Hospital, University District, Bilkent Boulevard No. 1 Çankaya, Ankara 06800, Türkiye. sinem.karaoglu384@gmail.com
Received: February 3, 2026 Revised: February 20, 2026 Accepted: March 12, 2026 Published online: April 16, 2026 Processing time: 65 Days and 7.9 Hours
Abstract
BACKGROUND
A considerable proportion of patients diagnosed with hypertrophic cardiomyopathy (HCM) or HCM-like phenotypes lack an identifiable genetic mutation and are classified as non-familial cases. This observation suggests that hormonal, autoimmune, and structural mechanisms may contribute to myocardial hypertrophy in selected patients.
CASE SUMMARY
A 45-year-old woman with a history of hypertension and hypothyroidism was evaluated and found to have hypokalemia, metabolic alkalosis, and asymmetric left ventricular hypertrophy. Transthoracic echocardiography revealed dynamic left ventricular outflow tract obstruction, while cardiac magnetic resonance imaging demonstrated diffuse asymmetric hypertrophy with mid-wall late gadolinium enhancement consistent with non-ischemic myocardial fibrosis. Hormonal evaluation showed markedly elevated aldosterone levels with suppressed renin activity, confirming primary hyperaldosteronism. Autoimmune testing and minor salivary gland biopsy established Sjögren’s syndrome. Abdominal imaging revealed a right adrenal adenoma and left-sided obstructive uropathy with severe unilateral renal dysfunction.
CONCLUSION
Endocrine and autoimmune disorders should be considered in patients presenting with HCM-like phenotypes.
Core Tip: Hypertrophic cardiomyopathy-like phenotypes without identifiable genetic mutations may arise from secondary systemic conditions rather than primary sarcomeric disease alone. This case highlights the rare coexistence of primary hyperaldosteronism, Sjögren’s syndrome, and obstructive uropathy contributing synergistically to myocardial hypertrophy and fibrosis. Recognition of endocrine and autoimmune contributors is essential, as targeted treatment may help limit disease progression and improve outcomes.
