BackgroundAldosterone has been shown to substantially contribute to the accumulation of different types of collagen fibers and growth factors in the arterial wall, which increase wall stiffness. We previously showed that arterial wall stiffness is increased in primary aldosteronism (PA) independently of concomitant hypertension. This study was aimed at assessing the effects of specific treatment of PA on the arterial stiffness.MethodsTwenty-nine patients with confirmed PA (15 with aldosterone-producing adenoma treated by unilateral laparoscopic adrenalectomy, 14 treated with spironolactone (mainly idiopathic aldosteronism) were investigated by Sphygmocor applanation tonometer (using measurement of carotid-femoral pulse wave velocity (PWV) and augmentation index (AI)) at the time of the diagnosis and then approximately 1 year after the specific treatment.ResultsThe office blood pressure (BP) decreased from 167 +/- 18/96 +/- 9 to 136 +/- 12/80 +/- 7 mm Hg after adrenalectomy (P = 0.001), and from 165 +/- 21/91 +/- 13 to 151 +/- 22/88 +/- 8 mm Hg (not significant (n.s.)) on spironolactone. The mean 24-h BP decreased from 150 +/- 18/93 +/- 11 mm Hg to 126 +/- 17/80 +/- 10 mm Hg after adrenalectomy (P < 0.01), and from 155 +/- 16/94 +/- 12 to 139 +/- 18/88 +/- 8 mm Hg (n.s.) on spironolactone. The PWV significantly decreased after surgery from 9.5 +/- 2.7 m/s to 7.6 +/- 2 m/s (P = 0.001), and the AI (recalculated for heart rate 75/min) decreased significantly from 27 +/- 10 to 19 +/- 9% (P < 0.01). On the other hand, we did not find significant change of arterial stiffness indices in patients treated with spironolactone (PWV: 9.3 +/- 1.6 m/s vs. 8.8 +/- 1.3 m/s (n.s.); AI: 25 +/- 9% vs. 25 +/- 8% (n.s.)).ConclusionsSurgical but not conservative treatment of PA led to a significant decrease of BP and arterial stiffness parameters.American Journal of Hypertension (2008). doi:10.1038/ajh.2008.243American Journal of Hypertension (2008); 21, 10, 1086-1092. doi 10.1038/ajh.2008.243.

This work discusses the clinical performance of chromogranin A (CGA), a commonly measured marker in neuroendocrine neoplasms, for the diagnosis of pheochromocytoma/ paraganglioma (PPGL). Plasma CGA (cut-off value 150 µg/L) was determined by an immunoradiometric assay. Free metanephrine (cut-off value 100 ng/L) and normetanephrine (cut-off value 170 ng/L) were determined by radioimmunoassay. Blood samples were collected from PPGL patients preoperatively, one week, six months, one year and two years after adrenal gland surgery. The control patients not diagnosed with PPGL suffered from adrenal problems or from MEN2 and thyroid carcinoma. The clinical sensitivity in the PPGL group of patients (n = 71) based on CGA is 90% and is below the clinical sensitivity determined by metanephrines (97%). The clinical specificity based on all plasma CGA values after surgery (n = 98) is 99% and is the same for metanephrines assays. The clinical specificity of CGA in the control group (n = 85) was 92% or 99% using metanephrines tests. We can conclude that plasma CGA can serve as an appropriate complement to metanephrines assays in laboratory diagnosis of PPGL patients. CGA is elevated in PPGLs, as well as in other neuroendocrine or non-neuroendocrine neoplasia and under clinical conditions increasing adrenergic activity.

TRH-like peptides are characterized by substitution of basic amino acid histidine (related to authentic TRH) with neutral or acidic amino acid, like glutamic acid, phenylalanine, glutamine, tyrosine, leucin, valin, aspartic acid and asparagine. The presence of extrahypothalamic TRH-like peptides was reported in peripheral tissues including gastrointestinal tract, placenta, neural tissues, male reproductive system and certain endocrine tissues. Work deals with the biological function of TRH-like peptides in different parts of organisms where various mechanisms may serve for realisation of biological function of TRH-like peptides as negative feedback to the pituitary exerted by the TRH-like peptides, the role of pEEPam such as fertilization-promoting peptide, the mechanism influencing the proliferative ability of prostatic tissues, the neuroprotective and antidepressant function of TRH-like peptides in brain and the regulation of thyroid status by TRH-like peptides.

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