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Objective There are a few reports on surgical treatment of idiopathic hyperaldosteronism (IHA),pathological profile and prognosis. The clinical and pathological characteristics and prognosis of 23 patients with IHA were retrospectively analyzed in order to support potential improvement of diagnosis and treatment outcome. Methods Clinical characteristics of 23 patients with IHA were analyzed retrospectively. HE staining and CYP11B2 immunostaining were performed for pathological microsocopic observation. Pathological features and surgical prognosis were analyzed. Results All samples were categorized as nonclassic pathology, including 12 cases with multiple aldosterone-producing nodules,10 cases with multiple or single aldosterone-producing micronodules. Only one case had aldosterone-producing diffuse hyperplasia. Unilateral adrenal resection was performed in all patients. Postoperatively, blood pressure and serum potassium recovered to normal range in 6 patients with a cure rate 26%. Blood pressure decreased but did not return to normal in 17 patients (improve rate 74%). Compared with the improved group, patients in the cured group had a lower pre-operative blood pressure (P＜0.05). Conclusions Multiple functional nodules and micronodules are the main types in adrenal pathology of IHA. Unilateral adrenal resections probably bring clinical benefits in these patients.

Objective To identify the genetic mutations of aldosterone- and cortisol-coproducing adrenal adenoma in a young boy by whole-exome sequencing. Methods The clinical data of a boy with aldosterone- and cortisol-coproducing adrenal adenoma were collected. Whole-exome sequencing was performed with DNA extracted from the blood and tumor tissue to identify germline and somatic mutations. Results A 13-year-old boy with hypertension and hypokalemia was diagnosed as primary aldosteronism complicated with sub-clinical Cushing's syndrome diagnosed by clinical manifestations and adrenal hormone testing. CT scan found a 4.5 cm×3.6 cm mass in right adrenal gland. The mass was surgically removed and adenoma was proved by pathologic microscopy. A somatic CTNNB1 c.133T＞C (p.S45P) mutation was detected in the adenoma tissue. Somatic mutations, such as KCNJ5, ATP1A1, ATP2B3 and CACNA1D were not detected. Conclusions Somatic CTNNB1 mutation is probably the main cause of this rare disease characterized by aldosterone- and cortisol-coproducing adrenal adenoma. But the profound mechanism needs further study.

Objective Aldosterone-producing adrenocortical carcinoma(ACC) is an uncommon disease.In this paper, the genetic mutations of aldosterone-producing ACC are studied by whole-exome sequencing. Methods Clinical data of the patient with aldosterone-producing ACC were collected. DNA was extracted from paraffin-embedded tissues and peripheral blood, then the whole-exome sequencing was carried out to identify germline and somatic mutations. Results There was no mutation associated with hereditary adrenocortical tumors and familial hyperaldosteronism in peripheral blood DNA. A total of 349 somatic mutations were found in tumor tissues, which were mainly enriched in tumorigenesis and calcium signaling pathways. Mutations related to the growth of adrenocortical tumor, CTNNB1, CDKN2A and MSH6, were detected, while no mutation related to aldosterone synthesis as KCNJ5, ATP1A1, ATP2B3 and CACNA1D was found in the tumor tissue. Conclusions The tumor- igenesis of aldosterone-producing ACC is related to CTNNB1, CDKN2A and MSH6, but the mechanism of promoting aldosterone production is still uncertain.

Objective To explore the clinical characteristics of patients with paroxysmal hypertension caused by panic attacks. Methods The clinical data of 24 patients with panic attack treated in Peking Union Medical College Hospital were retrospectively analyzed. Results Nineteen patients presented paroxysmal aggravation of hypertension. Blood pressure of the patients was usually controlled at (136±12/84±9)mmHg with antihypertensive therapy, and rose to (181±13)/(105±15)mmHg during panic attack. The other 5 patients were usually normotensive with average blood pressure (125±10)/(76±6)mmHg, and their blood pressure rose to (175±26)/(92±14)mmHg at panic attack. The surge of blood pressure last from more than ten seconds to six hours. And the attacks were irregular with the frequency ranging from once a few years to several times a day. The attack was triggered by psycho-emotional changes in 54% patients. The proportions of palpitation/panic, dizziness and chest tightness were 92%, 75% and 33% respectively. 24 hours urine catecholamines were normal in all patients. Conclusions Blood pressure of the patients may significantly enhance during panic attacks, mostly accompanying with palpitation/panic, dizziness, chest tightness. The attack may be triggered by psycho-emotional changes. Necessary biochemical tests are needed to exclude other diseases such as pheochromocytoma.

To evaluate the effects of abdominal massage on gastrointestinal function in the intensive care unit (ICU) patients.