Atorvastatin induced gynecomastia in a dyslipidemic patient.

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Omar Alomari, Arzu Cennet Işık, Sinem Nur Ertan, Ali Karagöz This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6083956/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 Statins, widely used for lowering low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, have demonstrated significant cardiovascular benefits. However, recent case reports have associated statins with gynecomastia, a condition characterized by benign breast tissue enlargement in males. Gynecomastia can cause significant discomfort and emotional distress. We present the case of a 66-year-old male who developed gynecomastia after two months of atorvastatin therapy at 20 mg/day. The patient, with a history of recent coronary artery bypass graft surgery, experienced pain, sensitivity, and growth in both mammary glands. Clinical examination and imaging revealed an increase in fibroglandular tissue, with no cystic or solid lesions. Laboratory tests ruled out other potential causes, including liver disease, hormonal imbalances, and the use of other medications known to cause gynecomastia. After switching the patient’s medication from atorvastatin to rosuvastatin 10 mg/day, a follow-up showed a reduction in pain, sensitivity, and mammary gland enlargement. This case underscores the importance of considering drug-induced gynecomastia when evaluating male patients on statin therapy. While rare, statin-induced gynecomastia is reversible upon discontinuation or modification of the treatment. Clinicians should be aware of this potential side effect to prevent unnecessary investigations and alleviate patient distress. Statin-induced gynecomastia Atorvastatin Cholesterol-lowering therapy Drug side effects Figures Figure 1 Introduction Statins (HMG-CoA reductase inhibitors) have been used for the treatment of hypercholesterolemia for more than two decades. Statin therapy has demonstrated efficacy in reducing low-density lipoprotein cholesterol (LDL-C) levels by 20–50%, along with a reduction in triglyceride levels by 10–20% (1). Additionally, it may lead to an increase in serum high-density lipoprotein cholesterol (HDL-C) levels by 5–10% (2). Recently, some case reports have associated statins with an elevated risk of gynecomastia (3–6). Gynecomastia, characterized by the benign enlargement of male breast tissue, poses considerable discomfort for affected individuals (7, 8). This condition can exert a notable emotional and social toll on men. Pharmacologically induced gynecomastia accounts for 10–20% of cases, with drugs like statins, a highly effective class of lipid-lowering medications, contributing to 10–25% of these instances (9). Here we present a 66 years old male with pain, sensitivity and growth in both mammary glands secondary to the use of atorvastatin. Case Presentation The patient was referred to our clinic upon the cardiology department request. The patient experienced pain, sensitivity and growth in both mammary glands secondary to the use of atorvastatin 20 mg/day for two months. The medical history of the patient included a recent three-vessel coronary artery bypass graft (CABG) surgery due to experiencing exertional shortness of breath for the past three months. Additionally, aspirin, a beta-blocker, and atorvastatin are currently prescribed. After a thorough physical examination, the only abnormal finding noted was the presence of mammary gland growth. In the conducted blood tests, the biochemical results were as follow: total cholesterol 282 mg/dl, triglycerides 112 mg/dl, HDL 60 mg/dl, LDL 200 mg/dl, and VLDL 22mg/dl. The total blood count, coagulation parameters, and hormone levels were all within normal ranges. In the echocardiography, there was no systolic or diastolic deficiency observed. Both mammary glands show an increase in fibroglandular tissue without any cystic or solid lesions detected in the ultrasonography. Additionally, there were no vascular pathologies found in the doppler ultrasound, and no other pathological findings in the mammography were observed (Fig. 1 ). No evidence of chronic liver disease, congestive heart disease, genetic disorders, adrenal, testicular, or thyroid abnormalities, nor is there a history of psychiatric or herbal drug use, or the use of aldosterone antagonist drugs was detected. Anti-HIV and hepatitis markers were also within normal limits. The patient's statin medication was switched from atorvastatin to rosuvastatin 10 mg/day, and follow-up blood tests were scheduled for fifteen days later. After the follow-up, there was a decrease in pain and sensitivity in the mammary gland. Furthermore, mammary gland enlargement was reduced on the third-month ultrasound examination. Discussion This case highlights that gynecomastia related to statin treatment is a rare occurrence, with very few documented cases in the literature. If diagnosed, it is crucial to assess all medications and underlying chronic conditions. Changing the statin to an alternative medication is advisable, as gynecomastia is reversible, and clinical and radiological regression typically occur within months. Gynecomastia should be distinguished in adulthood from pseudogynecomastia, which refers to fat deposition without glandular proliferation and typically does not necessitate evaluation, as well as from the rare occurrence of breast carcinoma (8). Medications may contribute to 10–20% of gynecomastia cases, either by increasing estrogen production, enhancing estrogenic activity, or reducing testosterone synthesis or effectiveness (8,4). The difference between the statins in terms of adverse reactions may be due to the high 20-mg/day starting dosage of rosuvastatin in contrast to recommendations of several regulatory agencies and to the package insert for rosuvastatin, which suggests a starting dosage of 10 mg/day for the first 4 weeks (10). Atorvastatin and rosuvastatin are thought to inhibit steroidogenesis more strongly than other statins because of their relatively potent lipid lowering effects. In the literature, 14 cases have been documented as statin-induced gynecomastia up to date. Seven of these cases were related to atorvastatin (4,11–13), six of them were related to rosuvastatin (5,6,12), and 1 was related to pravastatin (3). It is believed that statins suppress adrenal or gonadal steroid production by impacting cholesterol synthesis, which leads to a higher estradiol to testosterone ratio (5). Another potential cause is increased secretion of prolactin from the pituitary gland, with a blockade of dopaminergic activity on lactotrope cell groups, as dopamine is the prolactin-inhibiting factor in the anterior pituitary (14). However, in many instances, the underlying mechanism remains unknown. In our patient, the onset of gynecomastia after initiating atorvastatin and its resolution upon discontinuation of this medication suggest a potential causal relationship. Clinicians should, however, bear in mind the possibility of drug-induced exacerbating gynecomastia when assessing patients treated with statins who present with such symptoms. Discontinuation of the medication or transitioning to a less potent agent within the class may result in symptom relief and prevent unnecessary investigation and patient distress. Nonetheless, laboratory evaluation should include assessment of the free androgen index to rule out potential pre-existing hypogonadism unmasked by statin use. Declarations CONSENT: We confirm that written informed consent for participation and publication was obtained from the patient. No ethical approval was required for this case report due to the policies of our Hospital ( Kartal Dr. Lutfi Kırdar Research and Training Hospital). Conflict of Interest Statement: The authors declare no conflicts of interest in preparing this paper. Funding information: This research received no specific grants from any funding agency in the public, commercial, or not-profit-sectors. Data availability Statement: The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request. Acknowledgements: None References Taylor F, Huffman MD, Macedo AF, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2013;1(1) Huang WC, Lin TW, Chiou KR, et al. The effect of intensified low density lipoprotein cholesterol reduction on recurrent myocardial infarction and cardiovascular mortality. Acta Cardiol Sin. 2013;29(5):404–412. Aerts J, Karmochkine M, Raguin G. Gynécomastie attribuable à la pravastatine [Gynecomastia due to pravastatin]. Presse Med. 1999 Apr 17;28(15):787. French. PMID: 10325934. Hammons KB, Edwards RF, Rice WY. Golf-inhibiting gynecomastia associated with atorvastatin therapy. Pharmacotherapy. 2006 Aug;26(8):1165-8. doi: 10.1592/phco.26.8.1165. PMID: 16863492. Oteri A, Catania MA, Travaglini R, Russo A, Giustini SE, Caputi AP, Polimeni G. Gynecomastia possibly induced by rosuvastatin. Pharmacotherapy. 2008 Apr;28(4):549 − 51. doi: 10.1592/phco.28.4.549. PMID: 18363539. Picolos MK, Zeniou V, Michalis A. Rosuvastatin-induced gynaecomastia. Clin Endocrinol (Oxf). 2010 Sep;73(3):421-2. doi: 10.1111/j.1365-2265.2010.03802.x. Epub 2010 Mar 13. PMID: 20346003. Dickson G. Gynecomastia. Am Fam Physician. 2012 Apr 1;85(7):716 − 22. PMID: 22534349. Braunstein GD. Clinical practice. Gynecomastia. N Engl J Med. 2007 Sep 20;357(12):1229-37. doi: 10.1056/NEJMcp070677. PMID: 17881754. Rallidis LS, Lekakis J. PCSK9 inhibition as an emerging lipid lowering therapy: Unanswered questions. Hellenic J Cardiol. 2016 Mar-Apr;57(2):86–91. doi: 10.1016/j.hjc.2016.03.002. Epub 2016 Apr 11. PMID: 27445021. Astrazeneca SpA. Crestor (rosuvastatin) package insert. Basiglio, Italy; 2004. Bostanitis I, Tsalidou M. Atorvastatin-induced gynecomastia in a dyslipidemic patient: A case report. Hellenic J Cardiol. 2019 May-Jun;60(3):194–195. doi: 10.1016/j.hjc.2018.08.003. Epub 2018 Aug 24. PMID: 30145234. Roberto G, Biagi C, Montanaro N, Koci A, Moretti U, Motola D. Statin-associated gynecomastia: evidence coming from the Italian spontaneous ADR reporting database and literature. Eur J Clin Pharmacol. 2012 Jun;68(6):1007-11. doi: 10.1007/s00228-012-1218-5. PMID: 22286160. Famularo G, Sarrecchia C. Atorvastatin-Associated Gynecomastia. Ann Pharmacother. 2021 Oct;55(10):1300–1301. doi: 10.1177/1060028021988994. Epub 2021 Jan 20. PMID: 33472378. Thompson DF, Carter JR. Drug-induced gynecomastia. Pharmacotherapy 1993;13:37–45. 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. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6083956","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":419371886,"identity":"e3273255-bb44-4ec4-9858-f15e49de9271","order_by":0,"name":"Omar Alomari","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA5UlEQVRIiWNgGAWjYDCCA2BSQo6NmbHxAZDFw0esFmN+9uZmA5AWNiK1MCTO7DneJgFiEdTCd/vw0Q0/91gwbriR2Fb5NcdOho2B+eGjG3i0SJ5LS7vZ80yC2QCo5bbstmSgw9iMjXPwaDE4w2N2g+eABBtYi+Q2ZqAWHjZpQlpu/jkgwQPSUiy5rZ44LbeBtkhI9hxsY/y47TBhLZJn2NJuyxyQMOBnb2yWZtx2nIeNmYBf+M4wH7v55kBdfRsz+8OPP7dV2wMj6OFjfFpQADMPmCRWOQgw/iBF9SgYBaNgFIwYAABWfEpTngTQ1QAAAABJRU5ErkJggg==","orcid":"","institution":"Hamidiye International School of Medicine, University of Health Sciences, 3400, Istanbul, Türkiye","correspondingAuthor":true,"prefix":"","firstName":"Omar","middleName":"","lastName":"Alomari","suffix":""},{"id":419371887,"identity":"b89a3408-562b-435c-968b-fc1f24d093e1","order_by":1,"name":"Arzu Cennet Işık","email":"","orcid":"","institution":"Department of Internal Medicine, Kartal Dr. Lutfi Kirdar City Hospital, University of Health Sciences, Istanbul, Turkey","correspondingAuthor":false,"prefix":"","firstName":"Arzu","middleName":"Cennet","lastName":"Işık","suffix":""},{"id":419371888,"identity":"0f87d1c1-135a-434a-b47e-37eb284b2df3","order_by":2,"name":"Sinem Nur Ertan","email":"","orcid":"","institution":"Hamidiye International School of Medicine, University of Health Sciences, 3400, Istanbul, Türkiye","correspondingAuthor":false,"prefix":"","firstName":"Sinem","middleName":"Nur","lastName":"Ertan","suffix":""},{"id":419371889,"identity":"40981258-5ad9-4b58-ab68-c9f57a71df5e","order_by":3,"name":"Ali Karagöz","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Ali","middleName":"","lastName":"Karagöz","suffix":""}],"badges":[],"createdAt":"2025-02-22 07:41:54","currentVersionCode":1,"declarations":{"humanSubjects":true,"vertebrateSubjects":false,"conflictsOfInterestStatement":false,"humanSubjectEthicalGuidelines":true,"humanSubjectConsent":true,"humanSubjectClinicalTrial":false,"humanSubjectCaseReport":true,"vertebrateSubjectEthicalGuidelines":false},"doi":"10.21203/rs.3.rs-6083956/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6083956/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":77355564,"identity":"2cd1ac6c-9173-4e63-854d-fd688a3a2b76","added_by":"auto","created_at":"2025-02-27 17:56:25","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":373254,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eMammography of the presented case\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-6083956/v1/ca2b82b16b3d1f562d3e9eca.png"},{"id":77356989,"identity":"336acbdb-f402-4e38-ab89-dcf00dfee2e2","added_by":"auto","created_at":"2025-02-27 18:12:32","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":4695108,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6083956/v1/5166cae9-df45-4e76-95a5-ebf12defb606.pdf"}],"financialInterests":"The authors declare no competing interests.","formattedTitle":"\u003cp\u003e\u003cstrong\u003eAtorvastatin induced gynecomastia in a dyslipidemic patient.","fulltext":[{"header":"Introduction","content":"\u003cp\u003eStatins (HMG-CoA reductase inhibitors) have been used for the treatment of hypercholesterolemia for more than two decades. Statin therapy has demonstrated efficacy in reducing low-density lipoprotein cholesterol (LDL-C) levels by 20\u0026ndash;50%, along with a reduction in triglyceride levels by 10\u0026ndash;20% (1). Additionally, it may lead to an increase in serum high-density lipoprotein cholesterol (HDL-C) levels by 5\u0026ndash;10% (2). Recently, some case reports have associated statins with an elevated risk of gynecomastia (3\u0026ndash;6). Gynecomastia, characterized by the benign enlargement of male breast tissue, poses considerable discomfort for affected individuals (7, 8). This condition can exert a notable emotional and social toll on men. Pharmacologically induced gynecomastia accounts for 10\u0026ndash;20% of cases, with drugs like statins, a highly effective class of lipid-lowering medications, contributing to 10\u0026ndash;25% of these instances (9). Here we present a 66 years old male with pain, sensitivity and growth in both mammary glands secondary to the use of atorvastatin.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eThe patient was referred to our clinic upon the cardiology department request. The patient experienced pain, sensitivity and growth in both mammary glands secondary to the use of atorvastatin 20 mg/day for two months. The medical history of the patient included a recent three-vessel coronary artery bypass graft (CABG) surgery due to experiencing exertional shortness of breath for the past three months. Additionally, aspirin, a beta-blocker, and atorvastatin are currently prescribed. After a thorough physical examination, the only abnormal finding noted was the presence of mammary gland growth.\u003c/p\u003e \u003cp\u003eIn the conducted blood tests, the biochemical results were as follow: total cholesterol 282 mg/dl, triglycerides 112 mg/dl, HDL 60 mg/dl, LDL 200 mg/dl, and VLDL 22mg/dl. The total blood count, coagulation parameters, and hormone levels were all within normal ranges. In the echocardiography, there was no systolic or diastolic deficiency observed. Both mammary glands show an increase in fibroglandular tissue without any cystic or solid lesions detected in the ultrasonography. Additionally, there were no vascular pathologies found in the doppler ultrasound, and no other pathological findings in the mammography were observed (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eNo evidence of chronic liver disease, congestive heart disease, genetic disorders, adrenal, testicular, or thyroid abnormalities, nor is there a history of psychiatric or herbal drug use, or the use of aldosterone antagonist drugs was detected. Anti-HIV and hepatitis markers were also within normal limits. The patient's statin medication was switched from atorvastatin to rosuvastatin 10 mg/day, and follow-up blood tests were scheduled for fifteen days later. After the follow-up, there was a decrease in pain and sensitivity in the mammary gland. Furthermore, mammary gland enlargement was reduced on the third-month ultrasound examination.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis case highlights that gynecomastia related to statin treatment is a rare occurrence, with very few documented cases in the literature. If diagnosed, it is crucial to assess all medications and underlying chronic conditions. Changing the statin to an alternative medication is advisable, as gynecomastia is reversible, and clinical and radiological regression typically occur within months.\u003c/p\u003e \u003cp\u003eGynecomastia should be distinguished in adulthood from pseudogynecomastia, which refers to fat deposition without glandular proliferation and typically does not necessitate evaluation, as well as from the rare occurrence of breast carcinoma (8). Medications may contribute to 10\u0026ndash;20% of gynecomastia cases, either by increasing estrogen production, enhancing estrogenic activity, or reducing testosterone synthesis or effectiveness (8,4).\u003c/p\u003e \u003cp\u003eThe difference between the statins in terms of adverse reactions may be due to the high 20-mg/day starting dosage of rosuvastatin in contrast to recommendations of several regulatory agencies and to the package insert for rosuvastatin, which suggests a starting dosage of 10 mg/day for the first 4 weeks (10). Atorvastatin and rosuvastatin are thought to inhibit steroidogenesis more strongly than other statins because of their relatively potent lipid lowering effects. In the literature, 14 cases have been documented as statin-induced gynecomastia up to date. Seven of these cases were related to atorvastatin (4,11\u0026ndash;13), six of them were related to rosuvastatin (5,6,12), and 1 was related to pravastatin (3). It is believed that statins suppress adrenal or gonadal steroid production by impacting cholesterol synthesis, which leads to a higher estradiol to testosterone ratio (5). Another potential cause is increased secretion of prolactin from the pituitary gland, with a blockade of dopaminergic activity on lactotrope cell groups, as dopamine is the prolactin-inhibiting factor in the anterior pituitary (14). However, in many instances, the underlying mechanism remains unknown.\u003c/p\u003e \u003cp\u003eIn our patient, the onset of gynecomastia after initiating atorvastatin and its resolution upon discontinuation of this medication suggest a potential causal relationship. Clinicians should, however, bear in mind the possibility of drug-induced exacerbating gynecomastia when assessing patients treated with statins who present with such symptoms. Discontinuation of the medication or transitioning to a less potent agent within the class may result in symptom relief and prevent unnecessary investigation and patient distress. Nonetheless, laboratory evaluation should include assessment of the free androgen index to rule out potential pre-existing hypogonadism unmasked by statin use.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eCONSENT: We confirm that written informed consent for participation and publication was obtained from the patient. No ethical approval was required for this case report due to the policies of our Hospital ( Kartal Dr. Lutfi Kırdar Research and Training Hospital).\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eConflict of Interest Statement:\u003c/strong\u003e The authors declare no conflicts of interest in preparing this paper.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding information:\u003c/strong\u003e This research received no specific grants from any funding agency in the public, commercial, or not-profit-sectors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData availability Statement:\u003c/strong\u003e The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements:\u003c/strong\u003e None\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003e Taylor F, Huffman MD, Macedo AF, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2013;1(1)\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Huang WC, Lin TW, Chiou KR, et al. The effect of intensified low density lipoprotein cholesterol reduction on recurrent myocardial infarction and cardiovascular mortality. Acta Cardiol Sin. 2013;29(5):404\u0026ndash;412.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Aerts J, Karmochkine M, Raguin G. Gyn\u0026eacute;comastie attribuable \u0026agrave; la pravastatine [Gynecomastia due to pravastatin]. Presse Med. 1999 Apr 17;28(15):787. French. PMID: 10325934.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Hammons KB, Edwards RF, Rice WY. Golf-inhibiting gynecomastia associated with atorvastatin therapy. Pharmacotherapy. 2006 Aug;26(8):1165-8. doi: 10.1592/phco.26.8.1165. PMID: 16863492.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Oteri A, Catania MA, Travaglini R, Russo A, Giustini SE, Caputi AP, Polimeni G. Gynecomastia possibly induced by rosuvastatin. Pharmacotherapy. 2008 Apr;28(4):549\u0026thinsp;\u0026minus;\u0026thinsp;51. doi: 10.1592/phco.28.4.549. PMID: 18363539.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Picolos MK, Zeniou V, Michalis A. Rosuvastatin-induced gynaecomastia. Clin Endocrinol (Oxf). 2010 Sep;73(3):421-2. doi: 10.1111/j.1365-2265.2010.03802.x. Epub 2010 Mar 13. PMID: 20346003.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Dickson G. Gynecomastia. Am Fam Physician. 2012 Apr 1;85(7):716\u0026thinsp;\u0026minus;\u0026thinsp;22. PMID: 22534349.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Braunstein GD. Clinical practice. Gynecomastia. N Engl J Med. 2007 Sep 20;357(12):1229-37. doi: 10.1056/NEJMcp070677. PMID: 17881754.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Rallidis LS, Lekakis J. PCSK9 inhibition as an emerging lipid lowering therapy: Unanswered questions. Hellenic J Cardiol. 2016 Mar-Apr;57(2):86\u0026ndash;91. doi: 10.1016/j.hjc.2016.03.002. Epub 2016 Apr 11. PMID: 27445021.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Astrazeneca SpA. Crestor (rosuvastatin) package insert. Basiglio, Italy; 2004.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Bostanitis I, Tsalidou M. Atorvastatin-induced gynecomastia in a dyslipidemic patient: A case report. Hellenic J Cardiol. 2019 May-Jun;60(3):194\u0026ndash;195. doi: 10.1016/j.hjc.2018.08.003. Epub 2018 Aug 24. PMID: 30145234.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Roberto G, Biagi C, Montanaro N, Koci A, Moretti U, Motola D. Statin-associated gynecomastia: evidence coming from the Italian spontaneous ADR reporting database and literature. Eur J Clin Pharmacol. 2012 Jun;68(6):1007-11. doi: 10.1007/s00228-012-1218-5. PMID: 22286160.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Famularo G, Sarrecchia C. Atorvastatin-Associated Gynecomastia. Ann Pharmacother. 2021 Oct;55(10):1300\u0026ndash;1301. doi: 10.1177/1060028021988994. Epub 2021 Jan 20. PMID: 33472378.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003e Thompson DF, Carter JR. Drug-induced gynecomastia. Pharmacotherapy 1993;13:37\u0026ndash;45.\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":"Sağlık Bilimleri Üniversitesi","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":"Statin-induced gynecomastia, Atorvastatin, Cholesterol-lowering therapy, Drug side effects","lastPublishedDoi":"10.21203/rs.3.rs-6083956/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6083956/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eStatins, widely used for lowering low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, have demonstrated significant cardiovascular benefits. However, recent case reports have associated statins with gynecomastia, a condition characterized by benign breast tissue enlargement in males. Gynecomastia can cause significant discomfort and emotional distress. We present the case of a 66-year-old male who developed gynecomastia after two months of atorvastatin therapy at 20 mg/day.\u003c/p\u003e \u003cp\u003eThe patient, with a history of recent coronary artery bypass graft surgery, experienced pain, sensitivity, and growth in both mammary glands. Clinical examination and imaging revealed an increase in fibroglandular tissue, with no cystic or solid lesions. Laboratory tests ruled out other potential causes, including liver disease, hormonal imbalances, and the use of other medications known to cause gynecomastia. After switching the patient\u0026rsquo;s medication from atorvastatin to rosuvastatin 10 mg/day, a follow-up showed a reduction in pain, sensitivity, and mammary gland enlargement.\u003c/p\u003e \u003cp\u003eThis case underscores the importance of considering drug-induced gynecomastia when evaluating male patients on statin therapy. While rare, statin-induced gynecomastia is reversible upon discontinuation or modification of the treatment. Clinicians should be aware of this potential side effect to prevent unnecessary investigations and alleviate patient distress.\u003c/p\u003e","manuscriptTitle":"Atorvastatin induced gynecomastia in a dyslipidemic patient.","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-02-27 17:56:20","doi":"10.21203/rs.3.rs-6083956/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":"78121893-8b9c-4bbb-a290-d43aaee23298","owner":[],"postedDate":"February 27th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-02-27T17:56:20+00:00","versionOfRecord":[],"versionCreatedAt":"2025-02-27 17:56:20","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6083956","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6083956","identity":"rs-6083956","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}