title: Clinical characteristics of primary hyperaldosteronism due to adrenal microadenoma.
abstract: An increasing number of patients are being diagnosed with primary aldosteronism (PA) due to aldosterone-producing macroadenoma (APA). However, there are only limited data available on the clinical characteristics of PA that are associated with adrenal microadenoma. Of the 55 patients that were diagnosed with PA in our study, 22 patients showed a unilateral adrenal over-production of aldosterone. The histopathology of the surgically removed adrenal tissues led to six patients being diagnosed with microadenoma, and the clinical features of microadenoma, macroadenoma and idiopathic hyperaldosteronism (IHA) were studied. The expression levels of CYP11B2, CYP17, CYP21 and 3β-hydroxysteroid dehydrogenase 2 (HSD3B2) mRNA in the adrenal cortices (n=5 and 6, respectively) that remained attached to the adrenal microadenomas or macroadenomas were examined by real time-PCR and then compared to the expression levels in the adrenal cortices (n=5) of non-functioning adrenal adenomas (NF). The patients with microadenoma (n=6) had significantly higher diastolic blood pressure than the patients with macroadenoma (n=16) or IHA (n=33) (p<0.05). The systolic blood pressure, plasma aldosterone concentration, serum potassium level and renal function did not differ between the PA sub-groups. The levels of CYP11B2 and CYP17 mRNA were significantly increased in the adjacent tissues of microadenomas, as compared with macroadenomas or NF (p<0.05), whereas no significant differences in the CYP21 and HSD3B2 mRNA levels were found between the PA sub-groups. The tumor size did not influence the clinical characteristics of APA. The non-tumor portions of the microadenomas showed marked and sustained CYP11B2 mRNA expression under the suppressed renin-angiotensin system. We suggest that an increased number of microadenomas should be sampled, and the immunohistochemistry for steoridogenic enzymes should be investigated to clarify the etiology of microadenoma.
authors.affiliation: Department of Internal Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa 920-8641, Japan.
authors.forename: Shigehiro
authors.initials: S
authors.lastname: Karashima
authors.forename: Yoshiyu
authors.initials: Y
authors.lastname: Takeda
authors.forename: Yuan
authors.initials: Y
authors.lastname: Cheng
authors.forename: Takashi
authors.initials: T
authors.lastname: Yoneda
authors.forename: Masashi
authors.initials: M
authors.lastname: Demura
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Kometani
authors.forename: Masashi
authors.initials: M
authors.lastname: Ohe
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Mori
authors.forename: Kunimasa
authors.initials: K
authors.lastname: Yagi
authors.forename: Masakazu
authors.initials: M
authors.lastname: Yamagishi
mesh_terms: D000306:Adrenal Cortex Neoplasms / Q000150:complications*; D018246:Adrenocortical Adenoma / Q000150:complications*; D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D001794:Blood Pressure; D019405:Cytochrome P-450 CYP11B2 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015870:Gene Expression; D006801:Humans; D006929:Hyperaldosteronism / Q000201:enzymology* / Q000209:etiology / Q000473:pathology*; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D011375:Progesterone Reductase / Q000235:genetics / Q000378:metabolism; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics / Q000378:metabolism; D013255:Steroid 21-Hydroxylase / Q000235:genetics / Q000378:metabolism
chemical_list: D000450:Aldosterone; C533068:3 beta-hydroxysteroid dehydrogenase type II; D011375:Progesterone Reductase; D013255:Steroid 21-Hydroxylase; D013254:Steroid 17-alpha-Hydroxylase; D019405:Cytochrome P-450 CYP11B2; D011188:Potassium