Clinical and pathological analysis of 116 cases of adult adrenal cortical adenoma and literature review.

BACKGROUND: The aim of this study is to investigate origin, gross features, microscopic features, immunohistochemical properties, and differential diagnosis of adrenal cortical adenoma (ACA) in patients ≥20 years old. METHODS: The clinicopathological features of 116 cases of ACA and the immunohistochemical features of 50 cases of ACA were evaluated, and the relevant literature was reviewed. RESULTS: In our cohort, 76.72% (89/116) of the cases were functional, and 27 cases had non-functional, benign adrenal adenomas. ACA presented as an island tumor with an envelope, and the mean tumor size was 3.6 cm (range 1-5 cm), with a mean tumor weight of 9.28 g (range 5-113 g). The shape of the tumor cells was consistent, and mitosis was rarely observed. Forty of the 46 patients with cortisol-secreting ACA had tumors containing granule cells. Primary aldosteronism was observed in 43 cases. Thirty-eight cases had endoscopically visible tumors, with clear cells and lipid-rich cytoplasm arranged in irregular patches or strips. Cortisol-producing ACAs were associated with atrophy of the non-tumorous cortex. Adrenocortical adenomas displayed positive immunohistochemical staining for MELAN-A, Syn (46 of 50 cases of ACA), NSE (44 of 50 cases of ACA), Vim (42 of 50 cases of ACA) and Ki-67 <5% (24 of 50 cases of ACA; the remaining 26 cases were negative for Ki-67). CONCLUSION: Prediction of endocrine syndrome in functional ACA was possible based on its structure and morphologic features, which could prevent an unanticipated postoperative crisis. However, a clinical study is needed to validate these findings.

Relationship between adiponectin and testosterone in patients with type 2 diabetes.

INTRODUCTION: This study was designed to investigate the relationship between serum adiponectin and testosterone in patients with type 2 diabetes. MATERIALS AND METHODS: Serum level of adiponectin and testosterone were prospectively measured in 65 patients with type 2 diabetes and in 20 healthy subjects. Testosterone was determined by the radio-immunoassay whereas adiponectin levels were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: The average serum testosterone did not differ between the diabetes and the control group, but the average adiponectin in the diabetes group was lower (14.6 (14.2-15.0) vs. 24.3 (24.05-24.55) ng/mL, P = 0.001). In the diabetes group, the serum adiponectin level in patients with renal dysfunction (22.3 (21.5-23.1) ng/mL) was higher than in patients with no complications (12.1 (11.45-12.75) ng/mL) and than in patients with coronary artery disease (11.2 (10.25-12.15) ng/mL) (P = 0.009). Univariate correlation analysis showed an inverse weak correlation between adiponectin and testosterone concentrations in male diabetic patients (r = -0.27, P = 0.009). There was no significant correlation between adiponectin and testosterone in female patients (r = -0.05, P = 0.167). CONCLUSIONS: We conclude that patients with type 2 diabetes have lower serum adiponectin concentration than healthy individuals, and that there is a weak inverse correlation between adiponectin and testosterone serum concentrations in male diabetics.

[Study on the change of myocardial cell and matrix in the rats with insulin resistance and type 2 diabetes mellitus].

OBJECTIVE: To explore the injury of insulin resistance on cardiac muscle cell and matrix, and the relationship between insulin resistance and diabetic cardiomyopathy. METHODS: Twenty four Wistar rats of 6 months were randomly divided into normal control (N), insulin resistance group (I), diabetic group (D). Euglycemic insulin clamp technique (EICT) was used to determine insulin resistance (IR). Cadiocyte apoptosis was evaluated by TUNEL. Heart weight (HW) and body weight (BW) were measured to calculate HW/BW. Ultra-microstructure of cardiac muscle cell and structure of heart was observed. Masson dyeing, hydroxyproline detection and immunohistochemistry were used to measure the levels of collagen protein. RESULTS: Compared with controls, GIR decreased remarkably in D group and I group (P < 0.01). The number of apoptosis cell in I group was lower than that of D group (P < 0.01), and higher than that of N group (P < 0.01). Injury change of ultramicrostructure of myocardial cell was observed in the rats with type 2 diabetes mellitus or insulin resistance. Interstitial fibrosis of heart occurred in D group and I group. Content of Hydroxyproline, the level of I , III type of collagen, and the total level of collagen in I group were lower than those in D group, and higher than those in N group (P < 0.05). CONCLUSION: Insulin resistance in the rats with type 2 diabetes mellitus or insulin resistance can injury myocardial cell and matrix.