The author reported an anesthetic experience of left adrenalectomy for a 37year old man with primary aldosteronism. The patient tolerated fluothane-oxygen via semiclosed circle anesthesia very well. During anesthesia, violent change in blood pressure was not observed.
Adrenalectomy ; Anesthesia ; Blood Pressure ; Humans ; Hyperaldosteronism*

Primary Aldosteronism is characterized by hypertension, hypokalemic alkalosis and increased aldosterone secretion. It is important to distinguish between adenoma and hyperplasia for the treatment of primary aldosteronism because the hypertension associated with the adenomatous form is more likely to respond to operative removal. We report a case of aldosterone producing adrenal adenoma which was diagnosed by postural stimulation test of aldosterone and abdominal computed tomography, and was treated by adrenalectomy. A week after surgery, the blood pressure and laboratory data returned to normal.
Adenoma ; Adrenalectomy ; Aldosterone ; Alkalosis ; Blood Pressure ; Hyperaldosteronism ; Hyperplasia ; Hypertension

Hypertension and atherosclerosis are the most important factors contributing to the development of aortic dissection. Primary aldosteronism is a rare cause of hypertension. The concurrence of aortic dissection is very rare in primary aldosteronism. However, when aortic dissection is found as a life-threatening complication of primary aldosteronism, then the diagnosis of primary aldosteronism is important because the therapeutic intervention can be curative. Only 3 cases of primary aldosteronism with aortic dissection have been reported in the literature. We report here on a case of primary aldosteronism with aortic dissection, which was treated by laparoscopic adrenalectomy. We lowered the blood pressure with antihypertensive drugs and potassium replacement was done to treat the aortic dissection. After stabilization of aortic dissection, we removed his left adrenal mass by laparoscopic adrenalectomy. Postoperatively, the patient's blood pressure has been within normal limits and the serum potassium increased to a normal level without supplementation. The aortic dissection has remained in a stable state
Adrenalectomy ; Antihypertensive Agents ; Atherosclerosis ; Blood Pressure ; Diagnosis ; Hyperaldosteronism* ; Hypertension ; Potassium

Hypertension and atherosclerosis are the most important factors contributing to the development of aortic dissection. Primary aldosteronism is a rare cause of hypertension. The concurrence of aortic dissection is very rare in primary aldosteronism. However, when aortic dissection is found as a life-threatening complication of primary aldosteronism, then the diagnosis of primary aldosteronism is important because the therapeutic intervention can be curative. Only 3 cases of primary aldosteronism with aortic dissection have been reported in the literature. We report here on a case of primary aldosteronism with aortic dissection, which was treated by laparoscopic adrenalectomy. We lowered the blood pressure with antihypertensive drugs and potassium replacement was done to treat the aortic dissection. After stabilization of aortic dissection, we removed his left adrenal mass by laparoscopic adrenalectomy. Postoperatively, the patient's blood pressure has been within normal limits and the serum potassium increased to a normal level without supplementation. The aortic dissection has remained in a stable state
Adrenalectomy ; Antihypertensive Agents ; Atherosclerosis ; Blood Pressure ; Diagnosis ; Hyperaldosteronism* ; Hypertension ; Potassium

Aldosterone ; blood ; Humans ; Hyperaldosteronism ; classification ; diagnosis ; Hypertension ; complications ; Mass Screening ; Renin ; blood ; Renin-Angiotensin System

BACKGOUND: Gitelman's syndrome is manifested by hypokalemia, metabolic alkalosis, normal blood pressure, hyperreninemic hyperaldosteronism, hypomagnesemia and hypocalciuria. This study was carried out to investigate the effects of magnesium supplementation for correcting hypokalemia in Gitelman syndrome. METHODS: A Gitelman patient without hyperaldosteronism in our hospital was studied, oral supplementation periods of regimens for 60 days were divided into eight stages (each stage is at least over 5 days) such as 1 stage:no regimen supplementation period 2 stage:spironolactone 100 mg, alone period 3 stage:spironolactone 100 mg, MgO 1 g mixed period, 4 stage:spironolactone 100 mg, alone period, 5 stage:spironolactone 100 mg, MgO 1 g mixed period, 6 stage:spironolactone 150 mg, MgO 1 g mixed period, 7 stage: spironolactone 150 mg, MgO 1.5 g mixed period, 8 stage:spironolactone 150 mg, MgO 1.5 g, KCl 3.6 g mixed period. RESULTS: The highest value of plasm [K] was 3.3 mEq/L, the lowest value of TTKG was 2.6 during 3 stage, plasm [K] had tendency to increased and TTKG decreased, however next during 4 stage, the tendency of correcting hypokalemia diminished. The highest value of plasm [K] was only 3.3 mEq/L during 7 stage, the highest value of plasm [K] was 4.6 mEq/L during 8 stage. And the highest value of plasm ionized [Mg++] was 0.44 mmol/L during MgO 1.5 g supplementation. CONCLUSION: Magnesium alone fails to completely correct potassium and magnesium depletion despite tendency of correcting. Therefore, the optimal therapeutic regimens for correcting hypokalemia in Gitelman syndrome without hyperaldosteronism would be the magnesium and additional K supplementation.
Alkalosis ; Blood Pressure ; Gitelman Syndrome* ; Humans ; Hyperaldosteronism ; Hypokalemia* ; Magnesium* ; Potassium ; Spironolactone ; Gitelman Syndrome

Primary aldosteronism, characterized by hypertension, hypokalemia and hyperaldosteronemia caused by chronic overproduction of aldosterone independent of normal renin-angiotensin system, due to aldosteronoma, or to bilateral cortical nodular hyperplasia, or to adrenal carcinoma rarely. We report a case of left adrenal adenoma which was diagnosed by classic clinical symptoms, laboratory data, adrenal venography and abdominal computerized tomography. We performed left adrenalectomy with subcostal transperitoneal approach, and then blood pressure and laboratory data were normalized postoperatively.
Adenoma ; Adrenalectomy ; Aldosterone ; Blood Pressure ; Hyperaldosteronism ; Hyperplasia ; Hypertension ; Hypokalemia ; Phlebography ; Renin-Angiotensin System

Pseudo-Bartter syndrome is a rare medical disease of the kidney characterized by normal blood pressure, hypokalemic metabolic alkalosis, hyperreninemia and hyperaldosteronism with drug history of diuretics. We report US, CT and MRI findings of a patient with clinically proved pseudo-Bartter syndrome. The patient was a 37-year-old woman with a history of long term ingestion of the diuretics(furosemide) for 20 years. Renal US revealed hyperechoic renal medulla at both kidneys. The resistive index(RI), calculated from the duplex doppler waveform is 0.61. Unenhanced CT revealed faint high attenuation along the medulla. Tl-weighted MRI revealed indistinct corticomedullary differentiation.
Adult ; Alkalosis ; Blood Pressure ; Diuretics ; Eating ; Female ; Humans ; Hyperaldosteronism ; Kidney ; Magnetic Resonance Imaging

Primary aldosteronism is present in approximately 1% of unselectd hypertensive patients. Adrenal adenoma is a known as one of the surgically curable form of the hypertension. Hypertension is one of the contributing factors for the development of aortic dissection. Cincurrence of aortic dissection in patient with primary aldosteronism is extemely rare. Only one case wasconfirmed by autopsy and reported in the world literature. We report a case of DeBakey type 3 anortic aneursm in a 49-year old hypertensive female patient with primary aldosteronism due to left adrenal adenoma. She underwent left adrenalectomy uneventfully after stabilization of her blood pressure with maximal medical management including nitroprusside, aldactone, enalapril and inderal.
Adenoma ; Adrenalectomy ; Autopsy ; Blood Pressure ; Enalapril ; Female ; Humans ; Hyperaldosteronism ; Hypertension ; Middle Aged ; Nitroprusside ; Propranolol ; Spironolactone

OBJECTIVETo report the clinical characteristics, biochemical profiles, diagnosis and treatment of one Chinese pedigree with glucocorticoid-remediable aldosteronism (GRA) and to study its molecular mechanism.

METHODSPlasma and urinary aldosterone, cortisol and plasma renin activities were dynamically tested and diagnostic therapy with dexamethasone was undergone in 3 affected subjects. Long-distance PCR as well as DNA sequencing were applied to detect the fusion gene in this pedigree.

RESULTSIn this GRA pedigree, there were 4 affected subjects who had hypertension, hypokalemia and low basic and provoked renin activity. Three patients were given dexamethasone treatment, and had a significant decrease in plasma aldosterone concentrations (PACs) (from 192 +/- 9 ng/L to 87 +/- 7ng/L, P < 0.05) after 5 days. Among them, one patient (II -3) responded quite satisfactorily to the therapy, with serum K(+) rising from baseline value of 2.5 to 2.9, 3.8 and 4.15 mEq/L on the 10th, 28th and 35th days after treatment respectively. Three weeks later, his blood pressure decreased from its original level of 146.3 +/- 1 0.7/94.6 +/- 5.3 mm Hg to 138.3 +/- 3.1/87.3 +/- 6.1 mm Hg (P < 0.05). The other 2 members (III -2 and III -4) showed modest improvement although their PACs decreased significantly. Using long-distance PCR, we found a 3.9 kb band in all 4 affected individuals, which was absent in 5 unaffected members from this pedigree or 8 patients with aldosterone-producing adenoma (APA) or idiopathic hyperaldosteronism (IHA). By DNA sequence analysis, we found that the breakpoint of "unequal crossing-over" is both within intron 2 of the 11beta-hydroxylase gene (CYP11B1) and the aldosterone synthase gene (CYP11B2).

CONCLUSIONSThe excess of mineralocorticoid in patients with GRA can be inhibited by exogenous glucocorticoids. The fusion gene resulting from unequal crossing-over between the 11beta-hydroxylase gene and the aldosterone synthase gene is the pathogenesis of this Chinese GRA pedigree.

Adrenocorticotropic Hormone ; physiology ; Adult ; Aldosterone ; blood ; Female ; Glucocorticoids ; therapeutic use ; Humans ; Hyperaldosteronism ; blood ; drug therapy ; genetics ; Mutation ; Pedigree