A Rare Presentation of multiple endocrine neoplasia with Concurrent Aldosterone-Producing Adrenal Adenoma: a case report

A Rare Presentation of multiple endocrine neoplasia with Concurrent Aldosterone-Producing Adrenal Adenoma: 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 A Rare Presentation of multiple endocrine neoplasia with Concurrent Aldosterone-Producing Adrenal Adenoma: a case report Xiaoli Liu, Kuanhong Zeng, Lijuan Wang, Tingbin Cao, Zhigang Zhao, and 4 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-3993682/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 Multiple endocrine neoplasia type 1 (MEN1) is a disorder characterized by the occurrence of tumours in two or more endocrine glands of a patient. Coexistence of different endocrine tumors warrants additional screening for multiple endocrine neoplasia syndromes, especially in patients with adrenal apparent adenoma. Case presentation We present the case of a 52-year-old male was admitted to Army Specialty Medical Center because of neck pain that had persisted for 4 months and aggravated muscle pain for 3 days. After admission, the patient showed hypertension and hypokalemia. The plasma aldosterone levels increased, and the renin levels decreased. Adrenal contrast-enhanced CT showed a nodule shadow on the left external branch of the adrenal gland, suggesting the possibility of adrenal adenoma. Other imaging examination suggested that the patient had thyroid nodules, parathyroid nodules, pituitary microadenomasm. The adrenal vein sampling (AVS) results indicated dominant secretion from the left adrenal gland. The patient was diagnosed as: 1. Primary aldosteronism-induced hypertension; 2. multiple endocrine neoplasia; 3. rhabdomyolysis; 4. hyperlipidemia; 5. fatty liver disease; 6. lumbar disc herniation; 7. fascia inflammation of the lower back. The Whole-exome sequencing of the peripheral blood from the patient showed the heterozygous variant of the genes CACNA1D and MYH8. The patient was performed left adrenal resection surgery in the Urology Department. Postoperative pathological specimen examination suggested a (left adrenal tumor) cortical adenoma. He achieved complete biochemical success and partial clinical success. Conclusions Our findings confirm the need for careful genetic analysis of patients with MEN1 and establish a likely pathogenic role for the new heterozygous variant of the genes CACNA1D and MYH8, at least in the rare subset of MEN1 associated with primary aldosteronism. primary aldosteronism multiple endocrine neoplasia Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Background Multiple endocrine neoplasia (MEN) is a group of syndromes with a genetic predisposition to the appearance of endocrine tumors, and shows autosomal dominant transmission, mainly involving the parathyroid gland, pancreatic islets and pituitary gland. It is a rare disease, with an estimated prevalence of one in 30 000 individuals and a high penetrance and an equal sex distribution ( 1 ). The types of MEN mainly include MEN-1, MEN-2, and MEN-4, depending on the specific endocrine glands affected and the involved gene mutations. While most patients diagnosed with MEN inherit the condition as an autosomal dominant trait, sporadic cases can occur even without family history. Adrenal lesions have been reported in about 36–73% of MEN1 patients, while the majority of adrenal tumours have been reported as non-hyperfunctioning ( 1 ). The objective of the present study was to report on a MEN1 case characterized by primary aldosteronism, with particular concern on the possible predisposing genetic defects. Case Presentation A 52-year-old male was admitted to Army Specialty Medical Center because of neck pain that had persisted for 4 months and aggravated muscle pain for 3 days. The patient began experiencing neck pain, muscle stiffness, limited mobility, and lower limb fatigue 4 months prior. Cervical spine MRI in our outpatient department indicated the following: 1. Degenerative changes in the cervical spine: Cervical disc herniation from 3/4 to 6/7; and 2. a Schemer's nodule that had formed at the lower edge of the cervical vertebral body. An outpatient doctor diagnosed neck muscle strain, which improved significantly, and the patient was treated symptomatically with drugs such as etoposide. Three days prior, the patient experienced muscle pain and fatigue in the proximal left upper arm, which worsened after activity. Two days prior, the patient experienced worsening pain in the left upper arm and muscle pain in the proximal right upper arm. One day prior, the patient experienced lower back pain and aggravated traction pain while walking. Past history The patient had a history of gout without regular uric acid lowering treatment. Family history None. Routine laboratory tests During hospitalization, the serum K+ concentration fluctuated between 1.84 and 3.14 mmol/L. When the serum K+ concentration was 3.14 mmol/L, the 24-hour urine potassium concentration was 19.27 mmol/24 hours, and the red blood cell sedimentation rate was 20.0 mm/h. The myocardial enzyme spectrum was as follows: creatine kinase 3631 U/L and creatine kinase isoenzyme-MB 30.7 U/L. Blood lipids were as follows: triglyceride was 3.97 mmol/L; low-density lipoprotein cholesterol was 2.4 mmol/L; and high-density lipoprotein cholesterol was 0.91 mmol/L His liver function was as follows: total bilirubin 24.2 µmol/L, indirect bilirubin 20.1 µmol/L, and aspartate aminotransferase 55.8 U/L. His inorganic ion levels were as follows: total calcium, 1.98 mmol/L and inorganic phosphorus, 0.65 mmol/L. The urine microalbuminuria concentration was 85 mg/L, and the urine microalbuminuria/creatinine ratio was 93.69 mg/g. (Table 1). There were no significant abnormalities in thyroid function; prolactin, parathyroid hormone, or male hormone levels; the growth hormone levels; renal function; coagulation; and blood test results were normal. Adrenal endocrine hormone and function testing The cortisol and ACTH hormone rhythms were both normal. According to both the upright and supine RAAS hormone measurements, the aldosterone levels increased (33 ng/dl (upright) and 37.2 ng/dl (supine)), and the renin levels decreased (< 0.5 mU/L) (Table 2). A low-dose dexamethasone suppression test showed complete inhibition (Table 3). Based on the comparison of the results after saline load test and before test, the blood pressure was 149/95 vs. 152/98 mmHg; aldosterone was 75.9 vs. 53.5 ng/dl; and renin was <0.5 vs. <0.5 mU/L. The serum potassium levels were 3.12 vs. 2.98 mmol/L (Table 4). These findings indicated that saline loading did not reduce the patient’s aldosterone levels. Imaging examination Adrenal contrast-enhanced CT showed a nodule shadow on the left external branch of the adrenal gland, suggesting the possibility of adrenal adenoma (Figure 1). Pituitary magnetic resonance imaging (MRI) revealed an abnormal signal in the pituitary gland, suggesting a pituitary microadenoma (Figure 2). Parathyroid ultrasound revealed that the morphology of the right parathyroid gland was enlarged, and the echo was decreased, suggesting an adenoma or a cyst (Figure 3). Thyroid ultrasound revealed a cystic solid echogenic nodule in the right lobe of the thyroid (inclined toward the TI-RADS 3 type) and a cystic echogenic nodule in the left lobe of the thyroid (inclined toward the TI-RADS 2 type) (Figure 4). Cervical spine MRI indicated the following: 1. degenerative changes in the cervical spine and cervical disc herniation from 3/4 to 6/7. 2. A Shermer's nodule had formed at the lower edge of the cervical vertebral body. Electrocardiogram examination revealed sinus rhythm and ST-T changes. A chest X-ray showed no obvious abnormalities. Genetic testing Whole-exome sequencing was performed on the peripheral blood of the patient (Figure 5), and the results indicated the presence of the pathogenic genes CACNA1D and MYH8. The heterozygous variant of CACNA1D; NM_000720.2:c.4750+18G>A. CACNA1D mutations were associated with developmental delay, elevated aldosterone levels and transient hypoglycemia (2). This gene has not yet been reported to be associated with multiple endocrine neoplasia. However, this gene has been confirmed to be pathogenic for primary aldosteronism, epileptic seizures, and neurological abnormalities (OMIM: 615474). Another heterozygous variant of MYH8, NM_ 002472.2: c.5351G>A (p.Arg1784Gln), was detected, but there are no relevant reports about multiple endocrine neoplasia harboring this variant. Based on the improved inspection results, the doctors in the Endocrinology Department diagnosed the patient as follows: 1. Primary aldosteronism-induced hypertension; 2. multiple endocrine neoplasia; 3. rhabdomyolysis; 4. hyperlipidemia; 5. fatty liver disease; 6. lumbar disc herniation; 7. fascia inflammation of the lower back. Further treatment Based on the above diagnostic and treatment steps, the patient was subjected to adrenal vein sampling (AVS) and localization examination. The AVS results indicated dominant secretion from the left adrenal gland, which was consistent with the morphological manifestations of adrenal CT (Table 5). The main treatment method for functional MEN is surgery. The adrenal tumors of this MEN1 patient were unilateral lesions, so unilateral resection was feasible. Therefore, the patient had indications for surgical intervention. The next step was to perform left adrenal resection surgery in the Urology Department. Postoperative pathological specimen examination suggested a (left adrenal tumor) cortical adenoma (Figure 6). Follow-up The patient underwent a follow-up examination of serum potassium (3.91 mmol/L) on the second day after surgery. Additionally, spironolactone and potassium chloride supplementation therapy were discontinued. Regular postoperative follow-up was performed. At 1 month after surgery, his blood pressure was 130/80 mmHg, his serum potassium concentration was 4.88 mmol/L, his aldosterone concentration was 5.6 ng/dl, and his renin concentration was 15.9 mU/L (Table 6). This patient achieved complete biochemical success and partial clinical success. Final Diagnosis 1. Primary aldosteronism-induced hypertension; 2. multiple endocrine neoplasia; 3. rhabdomyolysis; 4. hyperlipidemia; 5. fatty liver disease; 6. lumbar disc herniation; 7. fascia inflammation of the lower back. Discussion This study reported a 52-year-old male sought medical because of neck and muscle pain. The main manifestations of this patient were hypokalemia and hypertension with elevated plasma aldosterone and decreased renin. Main diagnosises were primary aldosteronism-induced hypertension and multiple endocrine neoplasia. Whole-exome sequencing indicated the heterozygous variant of CACNA1D; NM_000720.2:c.4750 + 18G > A and heterozygous variant of MYH8, NM_ 002472.2: c.5351G > A (p.Arg1784Gln). The patient underwent left adrenal resection surgery. Postoperative pathological specimen examination suggested a (left adrenal tumor) cortical adenoma. Postoperative follow-up suggested the patient achieved complete biochemical success and partial clinical success. MEN1 is an autosomal dominant disorder characterized by the presence of endocrine tumors in several organs. Although previous studies report that 20 to 73% of the MEN1 patients could develop adrenocortical tumors depending on laboratory and imaging examination methods, only few of them are functional or become functional during followup ( 3 ). Our case is an extremely unusual presentation because the patient developed these two infrequent features: multiple endocrine neoplasia and functional adrenal adnoma, and they presented synchronously in a middle aged patient. When MEN diagnosis is a possibility, clinical suspicion allows for other tumors to be detected early, in mild or subclinical stages, and they usually turn out to be treatable. However, the more the comorbidities are found, the more difficult the treatment is and the worse the prognosis is. Diagnostic criteria for MEN1 were proposed in the recommendations for clinical practice published in 2012. Thus, a diagnosis of MEN1 can be made based on ( 4 ). The pathological/clinical significance of mild adrenal enlargement, sporadic and asymptomatic incidentalomas in MEN1 patients is unknown ( 5 ). Besides adrenal tumors are mostly benign in MEN1 patients, consensus about the management of adrenal lesions as not yet been reached ( 1 ). Surgery is still the first-line treatment whenever it is possible. Conclusion This study, performed on patients with genetically confirmed MEN1, demonstrates that adrenal lesions are a common feature of this syndrome regardless of their genotype. Although a predominance of stable adrenal disease was observed in terms of size and hormonal secretion, some of them may cause hormonal hypersecretion and, as such, may be associated with higher morbidity and mortality and may contribute to patients’ impaired quality of life. Considering the variable prevalence of adrenal lesions reported by different authors and their potential to be hormonally active, adrenal evaluation should be considered in MEN1 patients; their prompt diagnosis would avoid delays and will enable an adequate treatment and follow-up of the affected patients. Abbreviations MEN multiple endocrine neoplasia; MRI magnetic resonance imaging; AVS adrenal vein sampling; MEN1 multiple endocrine neoplasia type 1 Declarations Author contributions Conception and design:X.L.L., L.L.. Analysis and interpretation of the data: K.H.Z.,L.J.W., and T.B.C.. Drafting of the article: X.L.L., L.L. and Z.C.Y.. Critical revision of the article for important intellectual content: Z.G.Z. and H.B.H. Obtaining of funding: L.L.. Administrative, technical, or logistic support: H.B.H. and Y.L.X. Funding This research was supported by grants from the National Natural Science Foundation of China (81873657) Declarations of competing interests Ethics approval and consent to participate 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 of this journal. Competing interests None. Acknowledgements Not Applicable. References Ventura M, Melo M, Carrilho F. Outcome and long-term follow-up of adrenal lesions in multiple endocrine neoplasia type 1. Arch Endocrinol Metab. 2019;63(5):516–23. Scholl UI. Genetics of Primary Aldosteronism. Hypertension. 2022;79(5):887–97. Zhao YX, Wang O, Song A, Wang LJ, Gong FY, Duan L, Yang HB, Pan H, Zhu HJ. The risk of concurrent malignancies in patients with multiple endocrine neoplasia type 1: insights into clinical characteristics of those with multiple endocrine neoplasia type 1. J Endocrinol Invest. 2023. Sahakian N, Castinetti F, Romanet P, Reznik Y, Brue T. Updates on the genetics of multiple endocrine neoplasia. Ann Endocrinol (Paris). 2024. Gatta-Cherifi B, Chabre O, Murat A, Niccoli P, Cardot-Bauters C, Rohmer V, Young J, Delemer B, Du Boullay H, Verger MF, Kuhn JM, Sadoul JL, Ruszniewski P, Beckers A, Monsaingeon M, Baudin E, Goudet P, Tabarin A. Adrenal involvement in MEN1. Analysis of 715 cases from the Groupe d'etude des Tumeurs Endocrines database. Eur J Endocrinol. 2012;166(2):269–79. Tables Table 1. Laboratory Data Variable Reference Range† On Admission Serum K+ (mmol/L) 3.5-5.3 3.14 24-hour urine potassium (mmol/24 hours) 35-100 19.27 Red blood cell sedimentation rate (mm/h) 27-34 20.0 Myocardial enzyme spectrum Creatine kinase (U/L) 50-310 3631 Creatine kinase isoenzyme-MB (U/L) 1-25 30.7 Blood lipids Triglyceride (mmol/L) 0.3-1.7 3.97 Low-density lipoprotein cholesterol (mmol/L) 1.55-3.12 2.4 High-density lipoprotein cholesterol (mmol/L) 1.16-1.42 0.91 Liver function Total bilirubin (umol/L) 1.7-23 24.2 Indirect bilirubin (umol/L) 0.00-16.2 20.1 Aspartate aminotransferase (U/L) 15-40 55.8 Inorganic ions Total calcium (mmol/L) 3.11-2.52 1.98 Inorganic phosphorus (mmol/L) 0.85-1.51 0.65 Urine Microalbuminuria (mg/L) 0.00-23.00 85 Urine Microalbuminuria/creatinine (mg/g) 0.00-30.00 93.69 Autoantibody Anti ScI-70 antibody Negative Positive (++) Antinuclear antibody Negative Weakly positive Urine osmolality (mOsm/L) 600-1000 290 †Reference values are affected by many variables, including patient population and laboratory methods used. The ranges used at Army Specialty Medical Center are for adults who were not pregnant and did not have medical conditions that could affect the results. Therefore, these methods may not be appropriate for all patients. Table 2. Additional Laboratory Data. Variable Reference Range On Admission Cortisol rhythm 8:00 (nmol/L) 185-624 279.73 16:00 (nmol/L) 185-624 199.78 0:00 (nmol/L) <276 198.09 ACTH rhythm 8:00 (pg/mL) 4.7-48.8 2.91 16:00 (pg/mL) 4.7-48.8 24.81 0:00 (pg/mL) 4.7-48.8 23.99 growth hormone 8:00 (ng/mL) 0.003-0.971 0.02 16:00 (ng/mL) 0.003-0.971 0.01 0:00 (ng/mL) 0.003-0.971 0.1 Insulin growth factor (ng/mL) 46-230 124.1 RAAS hormone in supine position Aldosterone (ng/dl) 3.0-23.6 37.2 Renin (mU/L) 2.8-39.9 < 0.5 RAAS hormone in the upright position Aldosterone (ng/dl) 3-40 33 Renin (mU/L) 4.4-46.1 < 0.5 Table 3. Low-dose dexamethasone suppression test Reference Range Before test After test Plasma cortisol (nmol/L) 185-624 279.73 21.38 ACTH (pg/mL) 4.7-48.8 3.91 2.91 Table 4. Saline load inhibition test Before test After test Blood pressure（mmHg） 149/95 152/98 Aldosterone（ng/dl） 75.9 53.5 Renin（mU/L） <0..5 <0.5 Serum potassium（mmol/L） 3.12 2.98 Table 5. Localization examination of adrenal vein samples. ALD（ng/dL） DRC（mU/L） Cor（nmol/L） Standardization ALD % Periphery 106 <0.5 314.91 33.66 Left 1 366 <0.5 10703.6 3.42 Left 2 498 <0.5 11015.69 4.52 Right 127 2 Left dominant secretion Notes: ALD: plasma aldosterone; DRC: direct renin; Cor: plasma cortisol; SI: selectivity index; To: right or left adrenal cortisol right adrenal cortisol/peripheral cortisol; LI: lateralization index; L1: normalized aldosterone in the left and right adrenal glands; CI: nondominant aldosterone cortisol ratio/inferior vena cava aldosterone cortisol. Table 6. Postoperative follow-up examination results Before surgery 2 days after surgery 1 month after surgery Serum potassium (mmol/L) 1.84 3.91 4.88 SBP/DBP (mmHg) 153/83 140/90 130/80 Aldosterone (ng/dl) 33 — 5.6 DRC (mU/L) <0.5 — 15.9 ARR — — 0.35 medical treatment nifedipine GITs 30 mg, Irbesartan 300 mg, Spironolactone 100 mg Irbesartan 150 mg Irbesartan 150 mg Notes: ARR: plasma aldosterone/direct renin; SBP, systolic blood pressure; DBP, diastolic blood pressure. Additional Declarations No competing interests reported. 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. 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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-3993682","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":275812109,"identity":"575febf1-3788-4d78-8d93-9e2240a5a77c","order_by":0,"name":"Xiaoli Liu","email":"","orcid":"","institution":"Army Medical University","correspondingAuthor":false,"prefix":"","firstName":"Xiaoli","middleName":"","lastName":"Liu","suffix":""},{"id":275812110,"identity":"4feadc57-d73f-4cda-94fb-91e21b29c21a","order_by":1,"name":"Kuanhong Zeng","email":"","orcid":"","institution":"Army Medical University","correspondingAuthor":false,"prefix":"","firstName":"Kuanhong","middleName":"","lastName":"Zeng","suffix":""},{"id":275812111,"identity":"5892994c-d432-4d48-ac88-1e1e9424e194","order_by":2,"name":"Lijuan Wang","email":"","orcid":"","institution":"Army Medical University","correspondingAuthor":false,"prefix":"","firstName":"Lijuan","middleName":"","lastName":"Wang","suffix":""},{"id":275812112,"identity":"bb9b68b7-19c8-4897-a101-099e63af8234","order_by":3,"name":"Tingbin Cao","email":"","orcid":"","institution":"Army Medical University","correspondingAuthor":false,"prefix":"","firstName":"Tingbin","middleName":"","lastName":"Cao","suffix":""},{"id":275812113,"identity":"d43e8cf4-b20b-4c61-827e-d5627c0a9248","order_by":4,"name":"Zhigang Zhao","email":"","orcid":"","institution":"Army Medical 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11:02:39","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-3993682/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-3993682/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":52034493,"identity":"198e9e19-56fa-43b3-a4d4-bef194075f57","added_by":"auto","created_at":"2024-03-05 16:50:03","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":27354,"visible":true,"origin":"","legend":"\u003cp\u003eAdrenal contrast-enhanced CT.\u003c/p\u003e\n\u003cp\u003eNote: adrenal contrast-enhanced CT showed a nodule shadow on the left external branch of the adrenal gland, suggesting the possibility of adrenal adenoma.\u003c/p\u003e","description":"","filename":"groupimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/20424ec22dd732777122b9b0.jpeg"},{"id":52033623,"identity":"49749479-b653-43e2-bfb9-b03b6ae3825b","added_by":"auto","created_at":"2024-03-05 16:42:03","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":35438,"visible":true,"origin":"","legend":"\u003cp\u003ePituitary MR image.\u003c/p\u003e\n\u003cp\u003eNote: An abnormal signal in the pituitary gland was considered a pituitary microadenoma.\u003c/p\u003e","description":"","filename":"groupimage2.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/321d9d8d09a8ab78abf78c60.jpeg"},{"id":52033619,"identity":"dbc96b85-4809-43c7-9203-ad247fb3781d","added_by":"auto","created_at":"2024-03-05 16:42:03","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":14043,"visible":true,"origin":"","legend":"\u003cp\u003eParathyroid ultrasound\u003c/p\u003e\n\u003cp\u003eNote: The morphology of the right parathyroid gland was enlarged, and the echo was decreased, suggesting an adenoma or a cyst.\u003c/p\u003e","description":"","filename":"groupimage3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/0af33d1596038cba42cd2dc5.jpeg"},{"id":52033620,"identity":"1cf1fb8c-e0a0-45ab-b36b-a38c93218630","added_by":"auto","created_at":"2024-03-05 16:42:03","extension":"jpeg","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":13019,"visible":true,"origin":"","legend":"\u003cp\u003eThyroid ultrasound\u003c/p\u003e\n\u003cp\u003eNotes: A cystic solid echogenic nodule in the right lobe of the thyroid (inclined toward the TI-RADS 3 type) and a cystic echogenic nodule in the left lobe of the thyroid (inclined toward the TI-RADS 2 type) are shown.\u003c/p\u003e","description":"","filename":"groupimage4.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/d3cca3236038b3df73073611.jpeg"},{"id":52033617,"identity":"f7c653a8-3ee2-426d-ab2a-4188cb617502","added_by":"auto","created_at":"2024-03-05 16:42:03","extension":"jpg","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":46992,"visible":true,"origin":"","legend":"\u003cp\u003eClinical whole-exome detection\u003c/p\u003e\n\u003cp\u003eNote: The variations related to clinical phenotype. The MYH8;NM_ 002472.2:c.5351G\u0026gt;A (p.Arg1784Gln) mutation was detected. There were no reports of this mutation. According to the ACMG guidelines (appendix), this variant was identified as a variant of unknown significance, PM2+PP3, with the following evidence items: PM2: Mutations (or extremely low frequency loci in recessive genetic diseases) not found in the normal control population in the ESP databases, thousand person databases, and EXAC databases. PP3: Multiple statistical methods predict that this mutation will have harmful effects on genes or gene products, including conservative prediction, evolutionary prediction, and splicing site influence. For example, in the case of CACNA1D, the mutation NM_ 000720.2:c.4750+18G\u0026gt;A was detected, but there are no reports of this mutation. According to the ACMG guidelines (appendix), this variant has been identified as a significant unknown variant, PM2, with the following evidence items: PM2: Variations (or extremely low frequency loci in recessive genetic diseases) not found in the normal control population in the ESP databases, thousand person databases, and EXAC databases.\u003c/p\u003e","description":"","filename":"5.jpg","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/e6be6d009e4ca76fe1c4098a.jpg"},{"id":52033621,"identity":"031af93f-f815-485b-af61-f4ff6eac4b26","added_by":"auto","created_at":"2024-03-05 16:42:03","extension":"jpeg","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":30748,"visible":true,"origin":"","legend":"\u003cp\u003eGross and pathological specimen.\u003c/p\u003e\n\u003cp\u003eNote: The gross specimen was removed during surgery (left); the tumor was stained with HE.\u003c/p\u003e","description":"","filename":"groupimage5.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/99146465c620b882e7a1420e.jpeg"},{"id":52036141,"identity":"2c5fb6e6-d79d-4fdd-98de-ef4cfe04748a","added_by":"auto","created_at":"2024-03-05 17:06:06","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":344699,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-3993682/v1/1c8aeeae-5925-4779-afba-3550d46688be.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"A Rare Presentation of multiple endocrine neoplasia with Concurrent Aldosterone-Producing Adrenal Adenoma: a case report","fulltext":[{"header":"Background","content":"\u003cp\u003eMultiple endocrine neoplasia (MEN) is a group of syndromes with a genetic predisposition to the appearance of endocrine tumors, and shows autosomal dominant transmission, mainly involving the parathyroid gland, pancreatic islets and pituitary gland. It is a rare disease, with an estimated prevalence of one in 30 000 individuals and a high penetrance and an equal sex distribution (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). The types of MEN mainly include MEN-1, MEN-2, and MEN-4, depending on the specific endocrine glands affected and the involved gene mutations. While most patients diagnosed with MEN inherit the condition as an autosomal dominant trait, sporadic cases can occur even without family history. Adrenal lesions have been reported in about 36\u0026ndash;73% of MEN1 patients, while the majority of adrenal tumours have been reported as non-hyperfunctioning (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). The objective of the present study was to report on a MEN1 case characterized by primary aldosteronism, with particular concern on the possible predisposing genetic defects.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 52-year-old male was admitted to Army Specialty Medical Center because of neck pain that had persisted for 4 months and aggravated muscle pain for 3 days. The patient began experiencing neck pain, muscle stiffness, limited mobility, and lower limb fatigue 4 months prior. Cervical spine MRI in our outpatient department indicated the following: 1. Degenerative changes in the cervical spine: Cervical disc herniation from 3/4 to 6/7; and 2. a Schemer\u0026apos;s nodule that had formed at the lower edge of the cervical vertebral body. An outpatient doctor diagnosed neck muscle strain, which improved significantly, and the patient was treated symptomatically with drugs such as etoposide. Three days prior, the patient experienced muscle pain and fatigue in the proximal left upper arm, which worsened after activity. Two days prior, the patient experienced worsening pain in the left upper arm and muscle pain in the proximal right upper arm. One day prior, the patient experienced lower back pain and aggravated traction pain while walking.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003ePast history \u0026nbsp; \u0026nbsp;\u003c/em\u003eThe patient had a history of gout without regular uric acid lowering treatment.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eFamily history \u0026nbsp; \u0026nbsp;\u003c/em\u003eNone.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eRoutine laboratory tests \u0026nbsp;\u0026nbsp;\u003c/em\u003eDuring hospitalization, the serum K+ concentration fluctuated between 1.84 and 3.14 mmol/L. When the serum K+ concentration was 3.14 mmol/L, the 24-hour urine potassium concentration was 19.27 mmol/24 hours, and the red blood cell sedimentation rate was 20.0 mm/h. The myocardial enzyme spectrum was as follows: creatine kinase 3631 U/L and creatine kinase isoenzyme-MB 30.7 U/L. Blood lipids were as follows: triglyceride was 3.97 mmol/L; low-density lipoprotein cholesterol was 2.4 mmol/L; and high-density lipoprotein cholesterol was 0.91 mmol/L His liver function was as follows: total bilirubin 24.2 \u0026micro;mol/L, indirect bilirubin 20.1 \u0026micro;mol/L, and aspartate aminotransferase 55.8 U/L. His inorganic ion levels were as follows: total calcium, 1.98 mmol/L and inorganic phosphorus, 0.65 mmol/L. The urine microalbuminuria concentration was 85 mg/L, and the urine microalbuminuria/creatinine ratio was 93.69 mg/g. \u0026nbsp;(Table 1). There were no significant abnormalities in thyroid function; prolactin, parathyroid hormone, or male hormone levels; the growth hormone levels; renal function; coagulation; and blood test results were normal.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAdrenal endocrine hormone and function testing \u0026nbsp;\u003c/em\u003eThe cortisol and ACTH hormone rhythms were both normal. According to both the upright and supine RAAS hormone measurements, the aldosterone levels increased (33 ng/dl (upright) and 37.2 ng/dl (supine)), and the renin levels decreased (\u0026lt; 0.5 mU/L) (Table 2). A low-dose dexamethasone suppression test showed complete inhibition (Table 3). Based on the comparison of the results after saline load test and before test, the blood pressure was 149/95 vs. 152/98 mmHg; aldosterone was 75.9 vs. 53.5 ng/dl; and renin was \u0026lt;0.5 vs. \u0026lt;0.5 mU/L. The serum potassium levels were 3.12 vs. 2.98 mmol/L (Table 4). These findings indicated that saline loading did not reduce the patient\u0026rsquo;s aldosterone levels.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eImaging examination \u0026nbsp;\u003c/em\u003eAdrenal contrast-enhanced CT showed a nodule shadow on the left external branch of the adrenal gland, suggesting the possibility of adrenal adenoma (Figure 1). Pituitary magnetic resonance imaging (MRI) revealed an abnormal signal in the pituitary gland, suggesting a pituitary microadenoma (Figure 2). Parathyroid ultrasound revealed that the morphology of the right parathyroid gland was enlarged, and the echo was decreased, suggesting an adenoma or a cyst (Figure 3). Thyroid ultrasound revealed a cystic solid echogenic nodule in the right lobe of the thyroid (inclined toward the TI-RADS 3 type) and a cystic echogenic nodule in the left lobe of the thyroid (inclined toward the TI-RADS 2 type) (Figure 4). Cervical spine MRI indicated the following: 1. degenerative changes in the cervical spine and cervical disc herniation from 3/4 to 6/7. 2. A Shermer\u0026apos;s nodule had formed at the lower edge of the cervical vertebral body. Electrocardiogram examination revealed sinus rhythm and ST-T changes. A chest X-ray showed no obvious abnormalities.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eGenetic testing\u003c/em\u003e\u0026nbsp; Whole-exome sequencing was performed on the peripheral blood of the patient (Figure 5), and the results indicated the presence of the pathogenic genes CACNA1D and MYH8. The heterozygous variant of CACNA1D; NM_000720.2:c.4750+18G\u0026gt;A. CACNA1D mutations were associated with developmental delay, elevated aldosterone levels and transient hypoglycemia\u0026nbsp;(2). This gene has not yet been reported to be associated with multiple endocrine neoplasia. However, this gene has been confirmed to be pathogenic for primary aldosteronism, epileptic seizures, and neurological abnormalities (OMIM: 615474). Another heterozygous variant of MYH8, NM_ 002472.2: c.5351G\u0026gt;A (p.Arg1784Gln), was detected, but there are no relevant reports about multiple endocrine neoplasia harboring this variant.\u003c/p\u003e\n\u003cp\u003eBased on the improved inspection results, the doctors in the Endocrinology Department diagnosed the patient as follows: 1. Primary aldosteronism-induced hypertension; 2. multiple endocrine neoplasia; 3. rhabdomyolysis; 4. hyperlipidemia; 5. fatty liver disease; 6. lumbar disc herniation; 7. fascia inflammation of the lower back.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eFurther treatment\u003c/em\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e Based on the above diagnostic and treatment steps, the patient was subjected to adrenal vein sampling (AVS) and localization examination. The AVS results indicated dominant secretion from the left adrenal gland, which was consistent with the morphological manifestations of adrenal CT (Table 5). The main treatment method for functional MEN is surgery. The adrenal tumors of this MEN1 patient were unilateral lesions, so unilateral resection was feasible. Therefore, the patient had indications for surgical intervention. The next step was to perform left adrenal resection surgery in the Urology Department. Postoperative pathological specimen examination suggested a (left adrenal tumor) cortical adenoma (Figure 6).\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eFollow-up\u003cstrong\u003e\u0026nbsp;\u0026nbsp;\u003c/strong\u003e\u003c/em\u003eThe patient underwent a follow-up examination of serum potassium (3.91 mmol/L) on the second day after surgery. Additionally, spironolactone and potassium chloride supplementation therapy were discontinued. Regular postoperative follow-up was performed. At 1 month after surgery, his blood pressure was 130/80 mmHg, his serum potassium concentration was 4.88 mmol/L, his aldosterone concentration was 5.6 ng/dl, and his renin concentration was 15.9 mU/L (Table 6). This patient achieved complete biochemical success and partial clinical success.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eFinal Diagnosis \u0026nbsp;\u003c/em\u003e1. Primary aldosteronism-induced hypertension; 2. multiple endocrine neoplasia; 3. rhabdomyolysis; 4. hyperlipidemia; 5. fatty liver disease; 6. lumbar disc herniation; 7. fascia inflammation of the lower back.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis study reported a 52-year-old male sought medical because of neck and muscle pain. The main manifestations of this patient were hypokalemia and hypertension with elevated plasma aldosterone and decreased renin. Main diagnosises were primary aldosteronism-induced hypertension and multiple endocrine neoplasia. Whole-exome sequencing indicated the heterozygous variant of CACNA1D; NM_000720.2:c.4750\u0026thinsp;+\u0026thinsp;18G\u0026thinsp;\u0026gt;\u0026thinsp;A and heterozygous variant of MYH8, NM_ 002472.2: c.5351G\u0026thinsp;\u0026gt;\u0026thinsp;A (p.Arg1784Gln). The patient underwent left adrenal resection surgery. Postoperative pathological specimen examination suggested a (left adrenal tumor) cortical adenoma. Postoperative follow-up suggested the patient achieved complete biochemical success and partial clinical success.\u003c/p\u003e \u003cp\u003eMEN1 is an autosomal dominant disorder characterized by the presence of endocrine tumors in several organs. Although previous studies report that 20 to 73% of the MEN1 patients could develop adrenocortical tumors depending on laboratory and imaging examination methods, only few of them are functional or become functional during followup (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Our case is an extremely unusual presentation because the patient developed these two infrequent features: multiple endocrine neoplasia and functional adrenal adnoma, and they presented synchronously in a middle aged patient. When MEN diagnosis is a possibility, clinical suspicion allows for other tumors to be detected early, in mild or subclinical stages, and they usually turn out to be treatable. However, the more the comorbidities are found, the more difficult the treatment is and the worse the prognosis is.\u003c/p\u003e \u003cp\u003eDiagnostic criteria for MEN1 were proposed in the recommendations for clinical practice published in 2012. Thus, a diagnosis of MEN1 can be made based on (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). The pathological/clinical significance of mild adrenal enlargement, sporadic and asymptomatic incidentalomas in MEN1 patients is unknown (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). Besides adrenal tumors are mostly benign in MEN1 patients, consensus about the management of adrenal lesions as not yet been reached (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Surgery is still the first-line treatment whenever it is possible.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis study, performed on patients with genetically confirmed MEN1, demonstrates that adrenal lesions are a common feature of this syndrome regardless of their genotype. Although a predominance of stable adrenal disease was observed in terms of size and hormonal secretion, some of them may cause hormonal hypersecretion and, as such, may be associated with higher morbidity and mortality and may contribute to patients\u0026rsquo; impaired quality of life. Considering the variable prevalence of adrenal lesions reported by different authors and their potential to be hormonally active, adrenal evaluation should be considered in MEN1 patients; their prompt diagnosis would avoid delays and will enable an adequate treatment and follow-up of the affected patients.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eMEN \u0026nbsp;multiple endocrine neoplasia; MRI \u0026nbsp;magnetic resonance imaging; AVS \u0026nbsp;adrenal vein sampling; MEN1 \u0026nbsp;multiple endocrine neoplasia type 1\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAuthor contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eConception and design:X.L.L., L.L.. Analysis and interpretation of the data: K.H.Z.,L.J.W., and T.B.C.. Drafting of the article: X.L.L., L.L. and Z.C.Y.. Critical revision of the article for important intellectual content: Z.G.Z. and H.B.H. Obtaining of funding: L.L.. Administrative, technical, or logistic support: H.B.H. and Y.L.X.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research was supported by grants from the National Natural Science Foundation of China (81873657)\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDeclarations of competing interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\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 of this journal.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot Applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eVentura M, Melo M, Carrilho F. Outcome and long-term follow-up of adrenal lesions in multiple endocrine neoplasia type 1. Arch Endocrinol Metab. 2019;63(5):516\u0026ndash;23.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eScholl UI. Genetics of Primary Aldosteronism. Hypertension. 2022;79(5):887\u0026ndash;97.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhao YX, Wang O, Song A, Wang LJ, Gong FY, Duan L, Yang HB, Pan H, Zhu HJ. The risk of concurrent malignancies in patients with multiple endocrine neoplasia type 1: insights into clinical characteristics of those with multiple endocrine neoplasia type 1. J Endocrinol Invest. 2023.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSahakian N, Castinetti F, Romanet P, Reznik Y, Brue T. Updates on the genetics of multiple endocrine neoplasia. Ann Endocrinol (Paris). 2024.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGatta-Cherifi B, Chabre O, Murat A, Niccoli P, Cardot-Bauters C, Rohmer V, Young J, Delemer B, Du Boullay H, Verger MF, Kuhn JM, Sadoul JL, Ruszniewski P, Beckers A, Monsaingeon M, Baudin E, Goudet P, Tabarin A. Adrenal involvement in MEN1. Analysis of 715 cases from the Groupe d'etude des Tumeurs Endocrines database. Eur J Endocrinol. 2012;166(2):269\u0026ndash;79.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"},{"header":"Tables","content":"\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"100%\" colspan=\"3\" valign=\"top\"\u003e\n \u003cp\u003eTable 1. \u0026nbsp;Laboratory Data\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eVariable\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003eReference Range\u0026dagger;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003eOn Admission\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eSerum K+ (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e3.5-5.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e3.14\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003e24-hour urine potassium (mmol/24 hours)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e35-100\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e19.27\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eRed blood cell sedimentation rate (mm/h)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e27-34\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e20.0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eMyocardial enzyme spectrum\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eCreatine kinase \u0026nbsp;(U/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e50-310\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e3631\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eCreatine kinase isoenzyme-MB \u0026nbsp; (U/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e1-25\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e30.7\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eBlood lipids\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eTriglyceride (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e0.3-1.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e3.97\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eLow-density lipoprotein cholesterol (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e1.55-3.12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e2.4\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eHigh-density lipoprotein cholesterol (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e1.16-1.42\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e0.91\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eLiver function\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eTotal bilirubin (umol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e1.7-23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e24.2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eIndirect bilirubin (umol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e0.00-16.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e20.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eAspartate aminotransferase (U/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e15-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e55.8\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eInorganic ions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eTotal calcium (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e3.11-2.52\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e1.98\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eInorganic phosphorus (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e0.85-1.51\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e0.65\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eUrine Microalbuminuria (mg/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e0.00-23.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e85\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eUrine Microalbuminuria/creatinine (mg/g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e0.00-30.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e93.69\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eAutoantibody\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eAnti ScI-70 antibody\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003eNegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003ePositive (++)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eAntinuclear antibody\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003eNegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003eWeakly positive\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"49.8046875%\" valign=\"top\"\u003e\n \u003cp\u003eUrine osmolality (mOsm/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.5390625%\" valign=\"top\"\u003e\n \u003cp\u003e600-1000\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.65625%\" valign=\"top\"\u003e\n \u003cp\u003e290\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026dagger;Reference values are affected by many variables, including patient population and laboratory methods used. The ranges used at Army Specialty Medical Center are for adults who were not pregnant and did not have medical conditions that could affect the results. Therefore, these methods may not be appropriate for all patients.\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eTable 2. Additional Laboratory Data.\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eVariable\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003eReference Range\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003eOn Admission\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eCortisol rhythm\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e8:00 (nmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e185-624\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e279.73\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e16:00 (nmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e185-624\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e199.78\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e0:00 (nmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026lt;276\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e198.09\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eACTH rhythm\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e8:00 (pg/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e4.7-48.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e2.91\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e16:00 (pg/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e4.7-48.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e24.81\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e0:00 (pg/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e4.7-48.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e23.99\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003egrowth hormone\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e8:00 (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e0.003-0.971\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e16:00 (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e0.003-0.971\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e0.01\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003e0:00 (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e0.003-0.971\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e0.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eInsulin growth factor (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e46-230\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e124.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eRAAS hormone in supine position\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eAldosterone (ng/dl)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e3.0-23.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e37.2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eRenin (mU/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e2.8-39.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026lt; 0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eRAAS hormone in the upright position\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eAldosterone (ng/dl)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e3-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e33\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"44.973544973544975%\" valign=\"top\" style=\"width: 48.6434%;\"\u003e\n \u003cp\u003eRenin (mU/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"29.45326278659612%\" valign=\"top\" style=\"width: 31.7829%;\"\u003e\n \u003cp\u003e4.4-46.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"18.1657848324515%\" valign=\"top\" style=\"width: 19.5736%;\"\u003e\n \u003cp\u003e\u0026lt; 0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTable 3. Low-dose dexamethasone suppression test\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"554\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"30.32490974729242%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.256317689530686%\" valign=\"top\"\u003e\n \u003cp\u003eReference Range\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"20.3971119133574%\" valign=\"top\"\u003e\n \u003cp\u003eBefore test\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.021660649819495%\" valign=\"top\"\u003e\n \u003cp\u003eAfter test\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"30.32490974729242%\" valign=\"top\"\u003e\n \u003cp\u003ePlasma cortisol (nmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.256317689530686%\" valign=\"top\"\u003e\n \u003cp\u003e185-624\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"20.3971119133574%\" valign=\"top\"\u003e\n \u003cp\u003e279.73\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.021660649819495%\" valign=\"top\"\u003e\n \u003cp\u003e21.38\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"30.32490974729242%\" valign=\"top\"\u003e\n \u003cp\u003eACTH (pg/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.256317689530686%\" valign=\"top\"\u003e\n \u003cp\u003e4.7-48.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"20.3971119133574%\" valign=\"top\"\u003e\n \u003cp\u003e3.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"22.021660649819495%\" valign=\"top\"\u003e\n \u003cp\u003e2.91\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTable 4. Saline load inhibition test\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"515\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"38.95348837209303%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.906976744186046%\" valign=\"top\"\u003e\n \u003cp\u003eBefore test\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"33.13953488372093%\" valign=\"top\"\u003e\n \u003cp\u003eAfter test\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"38.95348837209303%\" valign=\"top\"\u003e\n \u003cp\u003eBlood pressure（mmHg）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.906976744186046%\" valign=\"top\"\u003e\n \u003cp\u003e149/95\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"33.13953488372093%\" valign=\"top\"\u003e\n \u003cp\u003e152/98\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"38.95348837209303%\" valign=\"top\"\u003e\n \u003cp\u003eAldosterone（ng/dl）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.906976744186046%\" valign=\"top\"\u003e\n \u003cp\u003e75.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"33.13953488372093%\" valign=\"top\"\u003e\n \u003cp\u003e53.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"38.95348837209303%\" valign=\"top\"\u003e\n \u003cp\u003eRenin（mU/L）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.906976744186046%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0..5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"33.13953488372093%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"38.95348837209303%\" valign=\"top\"\u003e\n \u003cp\u003eSerum potassium（mmol/L）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"27.906976744186046%\" valign=\"top\"\u003e\n \u003cp\u003e3.12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"33.13953488372093%\" valign=\"top\"\u003e\n \u003cp\u003e2.98\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTable 5. Localization examination of adrenal vein samples.\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003eALD（ng/dL）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003eDRC（mU/L）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003eCor（nmol/L）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003eStandardization ALD %\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003ePeriphery\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003e106\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003e314.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e33.66\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003eLeft 1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003e366\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003e10703.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e3.42\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003eLeft 2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003e498\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003e11015.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e4.52\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003eRight\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003e127\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003e11641.85\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e1.09\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003eSI\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003eCI\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003eL1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003eRight/inferior vena cava\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003e36.97\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e0.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003eRight/left 1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e0.32\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003eLeft 1/inferior vena cava\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003e33.99\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e0.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003eLeft 1/Right\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e3.13\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"20.361247947454842%\" valign=\"top\"\u003e\n \u003cp\u003eLI\u0026gt;2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.912972085385878%\" valign=\"top\"\u003e\n \u003cp\u003eLeft dominant secretion\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"16.25615763546798%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"19.86863711001642%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.600985221674875%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eNotes: ALD: plasma aldosterone; DRC: direct renin; Cor: plasma cortisol; SI: selectivity index; To: right or left adrenal cortisol right adrenal cortisol/peripheral cortisol; LI: lateralization index; L1: normalized aldosterone in the left and right adrenal glands; CI: nondominant aldosterone cortisol ratio/inferior vena cava aldosterone cortisol.\u003c/p\u003e\n\u003cp\u003eTable 6. Postoperative follow-up examination results\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"589\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003eBefore surgery\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003e2 days after surgery\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e1 month after surgery\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003eSerum potassium (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003e1.84\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003e3.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e4.88\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003eSBP/DBP (mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003e153/83\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003e140/90\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e130/80\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003eAldosterone (ng/dl)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003e33\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e5.6\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003eDRC (mU/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026lt;0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e15.9\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003eARR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003e0.35\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003emedical treatment\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"30.560271646859082%\" valign=\"top\"\u003e\n \u003cp\u003enifedipine GITs 30 mg, Irbesartan 300 mg, Spironolactone 100 mg\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"17.147707979626485%\" valign=\"top\"\u003e\n \u003cp\u003eIrbesartan 150 mg\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd width=\"26.146010186757216%\" valign=\"top\"\u003e\n \u003cp\u003eIrbesartan 150 mg\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eNotes: ARR: plasma aldosterone/direct renin; SBP, systolic blood pressure; DBP, diastolic blood pressure.\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","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":"primary aldosteronism, multiple endocrine neoplasia","lastPublishedDoi":"10.21203/rs.3.rs-3993682/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-3993682/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eMultiple endocrine neoplasia type 1 (MEN1) is a disorder characterized by the occurrence of tumours in two or more endocrine glands of a patient. Coexistence of different endocrine tumors warrants additional screening for multiple endocrine neoplasia syndromes, especially in patients with adrenal apparent adenoma.\u003c/p\u003e\u003ch2\u003eCase presentation\u003c/h2\u003e \u003cp\u003eWe present the case of a 52-year-old male was admitted to Army Specialty Medical Center because of neck pain that had persisted for 4 months and aggravated muscle pain for 3 days. After admission, the patient showed hypertension and hypokalemia. The plasma aldosterone levels increased, and the renin levels decreased. Adrenal contrast-enhanced CT showed a nodule shadow on the left external branch of the adrenal gland, suggesting the possibility of adrenal adenoma. Other imaging examination suggested that the patient had thyroid nodules, parathyroid nodules, pituitary microadenomasm. The adrenal vein sampling (AVS) results indicated dominant secretion from the left adrenal gland. The patient was diagnosed as: 1. Primary aldosteronism-induced hypertension; 2. multiple endocrine neoplasia; 3. rhabdomyolysis; 4. hyperlipidemia; 5. fatty liver disease; 6. lumbar disc herniation; 7. fascia inflammation of the lower back. The Whole-exome sequencing of the peripheral blood from the patient showed the heterozygous variant of the genes CACNA1D and MYH8. The patient was performed left adrenal resection surgery in the Urology Department. Postoperative pathological specimen examination suggested a (left adrenal tumor) cortical adenoma. He achieved complete biochemical success and partial clinical success.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003eOur findings confirm the need for careful genetic analysis of patients with MEN1 and establish a likely pathogenic role for the new heterozygous variant of the genes CACNA1D and MYH8, at least in the rare subset of MEN1 associated with primary aldosteronism.\u003c/p\u003e","manuscriptTitle":"A Rare Presentation of multiple endocrine neoplasia with Concurrent Aldosterone-Producing Adrenal Adenoma: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-03-05 16:41:58","doi":"10.21203/rs.3.rs-3993682/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":"b59d0836-6637-4242-9028-a7072d3b476c","owner":[],"postedDate":"March 5th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2024-03-05T16:42:01+00:00","versionOfRecord":[],"versionCreatedAt":"2024-03-05 16:41:58","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-3993682","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-3993682","identity":"rs-3993682","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}