Academic literature on the topic 'Aldosteronism'

Red blood cells (RBCs) are a-nucleated cells particularly exposed to different stimuli, among which circulating hormones and intra/extra-cellular derivatives from oxidization processes. In addition, our previous studies showed that in the case of inflammatory diseases with GSH content alterations, RBCs were much more sensitive to diamide, a mild oxidant able to trigger tyrosine-phosphorylation (Tyr-P) of membrane proteins, mainly band 3. Aldosterone (Aldo), mineralocorticoid hormone, has been shown to induce many effects other than the common diuretic process regulation and involving the expression and activation of the superoxide generating enzyme NADPH oxidase, thus potentially explaining the increased plasma markers of oxidative stress (OS) like isoprostanes in primary aldosteronism (PA), disease characterized by excessive Aldo secretion. This well-known Aldo action is mediated by the activation of a cytosolic specific receptor, the mineralocorticoid receptor (MR), in the so called genomic pathway, which distinguishes from the direct effect of Aldo on many proteins and enzymes in the second mechanism, also known as non-genomic pathway. Starting from these evidences, if a direct Aldo involvement in the triggering of inflammatory-related oxidative status of the cells was evolving, RBCs were the eligible cells for the investigation of the non-genomic Aldo pathway. The study involved PA patients and healthy control (HC) and consisted with three phases: i) a first approach was carried out to evidence potential alterations in PA RBCs followed by an in vitro deepening to assess the effective direct/indirect involvement of Aldo in these alterations; ii) once identified as responsible of the RBCs alterations found in PA, Aldo pathway within HC RBCs cytosol was investigated; iii) at last, Aldo-related pathway in RBCs was studied with particular attention to the mechanism leading to membrane band 3 alterations starting from Aldo induced receptor activation. In the first part, PA RBCs were showed to have oxidative-like alterations such as band 3 protein increase of both Tyr-P level and clustering, thus suggesting that PA could be linked to other inflammatory diseases. The effects of Aldo, cortisol (Cort) and canrenone (Can) (added as agonist and inhibitor, respectively) were compared and Aldo was confirmed as the only responsible of the alterations previously observed in PA RBCs. Furthermore, Aldo was shown to trigger RBCs membrane alterations leading to autologous IgG binding in a sort of premature ageing of the cells. The second part of the study analyzed the mechanism of Aldo action: for the first time MR was identified in RBCs cytosol as a soluble multi-protein complex, differently regulated by the effector utilized. In facts, in the presence of Aldo, MR broke away from the complex to form dimers which were promptly proteolysed in a sort of turn off signaling. Can or Cort were not able to trigger similar events, thus explaining the different alterations found on RBCs membranes. However, since to now no direct evidence was found about the possibility that Aldo induced an increase of oxidation status in RBCs, oxidization level in both membranes and cytosol was addressed in the third and last part of the study. Results showed no difference in GSH and GSSP contents and carbonic anhydrase (CA) monomerization and activity between HC and PA RBCs. In contrast, preliminary data would confirm a sort of oxidative-related increase of band 3 disulfide bond formation, thus suggesting a new intriguing mechanism leading to band 3 increased oxidative status without changing the common anti-oxidative cellular defenses. Further investigations addressing this mechanism are in progress. In conclusion, we found that in PA RBCs Aldo is responsible for the membrane alterations leading to a potential premature removal of the cells from circulation. Aldo exerts its effect through the activation of the soluble MR complex, which participates in the modulation of the Aldo signaling through the possibility of being differently affected by other steroids or Aldo inhibitors (Can). Further studies are in progress to explore both nature and potential mediators of the Aldo-induced alterations in the band 3 dimer formation.
Gli eritrociti (RBCs) sono cellule non nucleate particolarmente esposte a differenti stimoli, tra i quali l’effetto degli ormoni circolanti nel sangue e i derivati dei processi di ossidazione intra o extracellulari. Studi precedenti condotti nel nostro laboratorio hanno dimostrato che, nel caso di malattie infiammatorie con alterazione del contenuto di GSH rispetto ai controlli, gli eritrociti erano molto più sensibili alla diamide, un blando ossidante in grado di innescare la tirosin-fosforilazione (Tyr-P) delle proteine di membrana, principalmente della proteina banda 3. L’aldosterone (Aldo), ormone mineralocorticoide, oltre alla sua classica azione regolatoria dei processi diuretici, è in grado di indurre molti altri effetti tra i quali l’espressione e l’attivazione dell’enzima NADPH ossidasi, generatore di anione superossido. Questo fatto potrebbe potenzialmente spiegare l’incremento di marker plasmatici di stress ossidativo (OS) come gli isoprostani, nell’aldosteronismo primitivo (PA), patologia caratterizzata da un’eccessiva secrezione di Aldo. Partendo da queste evidenze, gli RBCs erano cellule ottimali per studiare se l’Aldo potesse indurre un aumentato stato di ossidazione determinato da una sua azione diretta sui processi infiammatori. Infatti, in queste cellule non nucleate, un eventuale coinvolgimento dell’Aldo nei meccanismi infiammatori, mediante un’azione non-genomica, sarebbe stato univocamente dimostrato. Lo studio ha coinvolto sia pazienti con PA che controlli sani (HC) e si è svolto in tre fasi: i) in un approccio iniziale abbiamo valutato se esistessero potenziali alterazioni negli RBCs dei pazienti, procedendo, poi, con un approfondimento in vitro condotto sugli RBCs di HC per confermare o meno un diretto coinvolgimento dell’Aldo nell’indurre queste alterazioni; ii) una volta identificato come responsabile effettivo delle alterazioni riscontrate, abbiamo cercato di chiarire il meccanismo di azione dell’Aldo a livello citosolico; iii) infine, partendo dall’evidenza che l’azione dell’Aldo veniva mediata dall’attivazione del recettore citosolico, abbiamo cercato di capire il meccanismo attraverso cui questa attivazione si trasmettesse, a livello delle membrane. Nella prima parte, abbiano dimostrato che negli RBCs dei pazienti erano presenti delle alterazioni quali un incremento sia della Tyr-P della banda 3 che una sua aggregazione, suggerendo, così, che la patologia potesse essere correlata ad uno stress ossidativo come dimostrato in altre malattie infiammatorie. Inoltre, dopo aver comparato gli effetti di Aldo, cortisolo (Cort) e canrenone (Can) (aggiunti rispettivamente come agonista ed inibitore), abbiamo confermato che era proprio l’Aldo il diretto responsabile delle alterazione che, in ultima, portavano ad un aumento della quantità degli anticorpi autologhi legati alla membrana, rispecchiando una prematuro invecchiamento cellulare. Nella seconda parte dello studio, abbiamo dimostrato, per la prima volta, la presenza a livello citosolico del recettore dei mineralocorticoidi (MR), che risulta essere presente in un complesso multi-proteico di elevato peso molecolare. Inoltre, abbiamo evidenziato come solo l’Aldo inducesse la liberazione dell’MR dal complesso a formare dimeri prontamente proteolizzati in una sorta di spegnimento del segnale. Al contrario, né Cort né Can erano in grado di indurre l’attivazione del recettore. Tuttavia, poiché finora non è mai stato dimostrato se l’Aldo potesse indurre un aumento delle stato ossidativo dell’eritrocita, nella terza parte dello studio abbiamo analizzato alcuni markers di ossidazione sia a livello di membrana che di citosol. I nostri risultati indicano che nessuna modifica del contenuto di GSH o di proteine glutationilate (GSSP) era presente nei pazienti rispetto ai controlli, come nessuna alterazione nella monomerizzazione e attivazione della anidrasi carbonica (CA), nuovo parametro nella valutazione di un aumentato stato di ossidazione. Tuttavia, i nostri risultati mostrano che la proteina banda 3 risulta effettivamente sottoposta ad uno stress ossidativo che ne induce l’aggregazione attraverso la formazione di ponti disolfuro. Risultato, questo, che merita ulteriori indagini ed approfondimenti. In conclusione, abbiamo trovato che negli RBCs dei pazienti con PA l’Aldo è responsabile di alterazioni di membrana che portano ad una potenziale prematura rimozione delle cellule dalla circolazione. L’azione dell’Aldo viene mediata a livello citosolico dall’MR, ma non dal Cort. Ulteriori studi sono in corso per esplorare sia la natura che il meccanismo di potenziali mediatori dell’effetto dell’Aldo-MR a livello delle membrane eritrocitarie.

Objective: Due to its unique expression of aldosterone synthase cytocromo P450 (CYP11B2), the enzyme required for the final steps of aldosterone biosynthesis aldosterone is exclusively expressed in the adrenalcortical zona glomerulosa cell. Some studies suggested that the CYP11B2 gene expression can be higher in APAs than in normal adrenocortical tissues, leading to postulate a transcriptional modulation of aldosterone overproduction in these tumors but antibodies capable to identify this protein do not exist. Thus we performed studies of in-situ hybridization (ISH) to analyze CYP11B2 localization. Another aim of our study is to understand whether the occurrence of micronodularity peripheral to the main adenomatous mass in some of our patient could be involved in the pathophysiology of the adenoma. Our hypothesis is that a similar humoral stimulating factor could play a role in the genesis of APA. Method: We developed a novel non radioactive in-situ hybridization technique based on use of a CYP11B2 specific oligo probe to localize the specific transcripts of the CYP11B2. Adrenocortical tissue from patients was studied. As housekeeping gene, we used PBGD, (NM_000190) probe labeled with Digoxigenin. The oligonucleotide probe for the CYP11B2 was 5' conjugated with DIG. Negative controls was detected with probe not labeled. The second approach was measuring of serum auto-antibodies anti AT1 in patients with APA and their localization on adrenal gland tissue by IHC. Results: At hystopathology intensely labeled areas called "nodules producing aldosterone" and negative areas were detected in the APA analyzed. ISH showed specific staining of all nodules. The staining was predominantly nuclear, a finding consistent with a good preservation of the transcript at this level. The AAbodies' anti AT1 presence has been demonstrated with ELISA test but the tissue localization still did not show appreciable results. Conclusion: this novel non radioactive ISH technique unequivocally demostrated the presence of aldosterone-producing microsatellites. High levels of AutoAntibodies in the serum of patients with APA allow us to hypothesize that this adrenal gland disorder is autoimmune.
Obiettivo: Alcuni studi hanno suggerito che l'espressione genica CYP11B2 è più elevata in pazienti con APA rispetto ai soggetti normali, tuttavia non esistono anticorpi in grado di identificare questa proteina. Quindi abbiamo deciso di effettuare studi di ibridazione in situ (ISH) per localizzare CYP11B2 a livello tessutale. Un altro obiettivo del nostro studio è quello di capire se la presenza di micronoduli possa influire sulla fisiopatologia dell'adenoma. La nostra ipotesi è che un fattore umorale stimolante potrebbe svolgere un ruolo nella genesi di APA. Metodo: Abbiamo sviluppato un metodo non radioattivo basato sull'uso di uno specifica sonda oligo per localizzare CYP11B2. Per la rilevazione dell'housekeeping gene, abbiamo utilizzato una sonda a doppio filamento per il gene PBGD, (NM_000190). Entrambe le sonde sono state marcate con Digoxigenin. Abbiamo inoltre misurato i livelli di anticorpi anti-AT1 nel siero di pazienti con APA e la loro localizzazione tessutale tramite IHC nella ghiandola surrenalica. Risultati: all'istopatologia si sono evidenziati noduli satelliti che presentavano lèespressione del CYP11B2. L'ISH ha mostrato una colorazione specifica di tutti i noduli a livello prevalentemente nucleare. La presenza di Auto anticorpi anti AT1 è stata dimostrata con test ELISA nel siero, ma la localizzazione nel tessuto non ha ancora mostrato risultati apprezzabili. Conclusione: questa tecnica non radioattiva di ISH dimostra in modo inequivocabile la presenza di micro satelliti producenti aldosterone. Elevati livelli di autoanticorpi nel siero dei pazienti con APA ci permettono di ipotizzare che questo disordine della ghiandola surrenale possa essere di origine autoimmune.

After the elucidation of the underlying genetic cause in many Mendellian diseases molecular medicine has turned its attention to the more common polygenic disorders. High blood pressure is one such complex trait which has been the subject of much interest in recent years. A number of candidate loci have been found to different groups to influence blood pressure and have been implicated in the aetiology of essential hypertension although the most significant discoveries have been in the single gene causes of high blood pressure. Glucocorticoid remediable aldosteronism (GRA) is an autosomal dominant cause of high blood pressure and primary aldosteronism caused by a chimaeric 11- hydroxylase/aldosterone synthase gene. The presence of this chimaeric gene causes aldosterone to be produced in response to adrenocorticotrophic hormone (ACTH) which results in primary aldosteronism and hypertension. GRA is characterised by the normalisation of both blood pressure and serum biochemistry by the administration of dexamethasone. Following screening of 356 individuals from the hypertension clinic in Aberdeen we identified 5 families with the chimaeric gene characteristic of GRA. These patients were initially diagnosed on the basis of an RFLP for the restriction endonuclease BamHI. We show that a long PCR technique can be used reliably to identify patients with the chimaeric gene and that cloning and sequencing of the chimaeric long PCR product can identify the point of crossing over in these families. Members of each of the 5 kindreds were then tested for some of the other candidate gene polymorphisms implicated in the aetiology of essential hypertension to investigate the possibility that these variants could influence the level of blood pressure in GRA patients.

Primary aldosteronism (PA) is a common form of secondary hypertension with an international prevalence rates between 5 and 10 %. It is characterized by a high autonomous aldosterone production that causes cardiovascular damage, renin suppression, hypertension, sodium retention, potassium excretion and hypokalemia. The screening of PA is a simple test measuring aldosterone to renin ratio (ARR) with immunoassay method. This test is currently considered as the most reliable screening tool for PA.     The main objective of the study was to evaluate an ELISA-method, for detection of aldosterone and renin in blood plasma, to be used for routine analysis in the laboratory. The second aim was to investigate the effect of refreezing samples, considering that cryoactivation of prorenin might occur.     One hundred blood samples were analysed, in regard to aldosterone and renin, by using two commercial ELISA assays (DRG ELISA from DRG Diagnostics, Germany) on a Dynex DS2 instrument. In addition, the accuracy and precision of the methods were calculated. The effect of refreezing was investigated with a series of eight samples, which were analyzed twice on the same instrument.     Both assays performed well. The resulting data showed good precision and accuracy. The correlation between the original and refreezed samples was good, r = 0.989 and r = 1.0 for aldosterone and renin respectively. Considering that the study only included eight samples, further investigation is recommended.     Evaluation showed that both immunoassays are reliable in diagnostic use and the ELISA-method is suitable to implement in the laboratory for routine analysis.

Background Primary aldosteronism (PA) is the most common cause of arterial hypertension characterized by high levels of aldosterone, resulting in excessive mineralocorticoid receptor (MR) stimulation, and extensive hypertensive-mediated organ damage (HMOD). Current guidelines recommend one or more exclusion tests in patients performed the screening test with the measurement of aldosterone-to-renin ratio (ARR) to avoid further lateralization procedures in those who tested false-positive. To date the diagnostic gain provided by these exclusion tests over the ARR was examined only in few studies, and, therefore, stands on a weak level of evidence. Moreover, growing experimental evidence has shown that immune system, especially T cells is involved in aldosterone-induced HOMD through MR activation. MR activation in animal models of hyperaldosteronism promoted T cells differentiation to the pro-inflammatory T helper 17 (Th17) subsets while decreasing the number of anti-inflammatory T regulatory (Tregs). Alteration of the balance between Th17 and Tregs contributed to the pathogenesis of hypertension and the associated complications. Furthermore, our previous work provided proof on the MR gene expression and protein expression in both human CD4+ and CD8+ T cells by Droplet Digital PCR and immunoblotting, respectively. However, up to now, there was no relevant research focused on the function of Th17 and Tregs in PA patients, and evaluate the effect of MR antagonists and surgery on these cells in patients with PA. Aims - To meta-analyze available studies of exclusion tests to furnish a more accurate picture of their diagnostic accuracy and gain in the work-up of PA with a higher level of confidence. - To investigate the levels of circulating Th17 and Tregs in PA patients and evaluate the effect of MR antagonists and surgery on these cells in PA patients. Materials and methods - Eligible studies reported on the diagnostic performance of the ARR and the exclusion tests for identifying unilateral PA (uPA) were selected using the “gold” standard (biochemical cure after adrenalectomy), or, whenever unavailable, a “golden” standard (adrenal imaging and/or AVS) as reference. Then, pooled sensitivity, specificity, the summary receiver operating characteristic (sROC) curve, and corresponding area under the curve (sAUC) were examined. - Blood samples from PA patients were obtained at 3-time points: before surgery, when patients had high PAC and were not treated with MR antagonists (T0); before surgery when patients had high PAC and were treated with MR antagonists (T1); one month after surgery when patients had normal PAC (T2). Immunologic markers on Th17 (CD4+IL17+), pathogenic IL-23-dependent Th17 (CD4+IL17+IL23R+), and Tregs (CD4+CD25+FoxP3+) were analyzed by multicolor flow cytometry. Results - By increasing the overall sample size of the patients studied by these tests and comprising the experience gained in multiple centers, we found that two most popluar exclusion tests, captopril challenge test (CCT) and saline infusion test (SIT), had no diagnostic gain over ARR for diagnosing uPA. - The percentage of circulating Th17 in PA patients was significantly lower after treatment of MR antagonists and post-surgery biochemical cure; meanwhile, there was a decrease in pathogenic Th17 one month after surgery. Although there were no differences in the percentage of Tregs at these 3-time points, Th17/Tregs ratio was markedly decreased after treatment with MR antagonists and post-surgically cure of the hyperaldosteronism. Conclusions This meta-analysis revealed that the use of exclusion tests in patients with a high post-test probability of uPA, as identified by ARR values, could be unnecessary, if not confounding. Meanwhile, our current study showed that treatment with MR antagonists and post-surgery biochemical cure can decrease the percentage of circulating Th17 and the ratio of Th17/Tregs in PA patients.
Background Primary aldosteronism (PA) is the most common cause of arterial hypertension characterized by high levels of aldosterone, resulting in excessive mineralocorticoid receptor (MR) stimulation, and extensive hypertensive-mediated organ damage (HMOD). Current guidelines recommend one or more exclusion tests in patients performed the screening test with the measurement of aldosterone-to-renin ratio (ARR) to avoid further lateralization procedures in those who tested false-positive. To date the diagnostic gain provided by these exclusion tests over the ARR was examined only in few studies, and, therefore, stands on a weak level of evidence. Moreover, growing experimental evidence has shown that immune system, especially T cells is involved in aldosterone-induced HOMD through MR activation. MR activation in animal models of hyperaldosteronism promoted T cells differentiation to the pro-inflammatory T helper 17 (Th17) subsets while decreasing the number of anti-inflammatory T regulatory (Tregs). Alteration of the balance between Th17 and Tregs contributed to the pathogenesis of hypertension and the associated complications. Furthermore, our previous work provided proof on the MR gene expression and protein expression in both human CD4+ and CD8+ T cells by Droplet Digital PCR and immunoblotting, respectively. However, up to now, there was no relevant research focused on the function of Th17 and Tregs in PA patients, and evaluate the effect of MR antagonists and surgery on these cells in patients with PA. Aims - To meta-analyze available studies of exclusion tests to furnish a more accurate picture of their diagnostic accuracy and gain in the work-up of PA with a higher level of confidence. - To investigate the levels of circulating Th17 and Tregs in PA patients and evaluate the effect of MR antagonists and surgery on these cells in PA patients. Materials and methods - Eligible studies reported on the diagnostic performance of the ARR and the exclusion tests for identifying unilateral PA (uPA) were selected using the “gold” standard (biochemical cure after adrenalectomy), or, whenever unavailable, a “golden” standard (adrenal imaging and/or AVS) as reference. Then, pooled sensitivity, specificity, the summary receiver operating characteristic (sROC) curve, and corresponding area under the curve (sAUC) were examined. - Blood samples from PA patients were obtained at 3-time points: before surgery, when patients had high PAC and were not treated with MR antagonists (T0); before surgery when patients had high PAC and were treated with MR antagonists (T1); one month after surgery when patients had normal PAC (T2). Immunologic markers on Th17 (CD4+IL17+), pathogenic IL-23-dependent Th17 (CD4+IL17+IL23R+), and Tregs (CD4+CD25+FoxP3+) were analyzed by multicolor flow cytometry. Results - By increasing the overall sample size of the patients studied by these tests and comprising the experience gained in multiple centers, we found that two most popluar exclusion tests, captopril challenge test (CCT) and saline infusion test (SIT), had no diagnostic gain over ARR for diagnosing uPA. - The percentage of circulating Th17 in PA patients was significantly lower after treatment of MR antagonists and post-surgery biochemical cure; meanwhile, there was a decrease in pathogenic Th17 one month after surgery. Although there were no differences in the percentage of Tregs at these 3-time points, Th17/Tregs ratio was markedly decreased after treatment with MR antagonists and post-surgically cure of the hyperaldosteronism. Conclusions This meta-analysis revealed that the use of exclusion tests in patients with a high post-test probability of uPA, as identified by ARR values, could be unnecessary, if not confounding. Meanwhile, our current study showed that treatment with MR antagonists and post-surgery biochemical cure can decrease the percentage of circulating Th17 and the ratio of Th17/Tregs in PA patients.

Background. Previous studies reported that primary aldosteronism (PA) is associated with an increased prevalence of anxiety, depression and subnormal quality of life (QoL) scores that may be improved after surgical treatment. Aim of the Study. The aim of the study was to assess the impact of surgery on health-related QoL and depression status of patients suffering from PA, comparing the results with a control group of patients undergoing surgery for a non-secreting adrenal tumor. Materials and Methods. Data on QoL and depression status were prospectively collected, from January 2014 to October 2016, before, early after surgery (at 1 month) and at long term (at least 6 months) in patients with unilateral PA and in a control group of patients with non-secreting adrenal tumor submitted to unilateral transperitoneal laparoscopic adrenalectomy. QoL was assessed using the Short Form 36 (SF-36) Health Survey for Physical (PCS) and Mental Component (MCS); the depression status by a 20-item depression scale (DS) questionnaire. Results. Twenty-six PA patients and 15 controls were recruited. Biochemical cure of the disease was achieved following surgery in all PA patients; hypertension was cured in 31% of cases and improved in the remaining 69% of cases. No morbidity occurred in both groups. There were no significant differences between PA patients and controls concerning demographics, preoperative PCS, MCS and DS values. In patients with PA, MCS values improved at early (42.72±13.68 vs 51.56±9.03, p=0.0005) and long term follow up (42.72±13.68 vs 51.81±7.04, p<0.0001); also DS values improved at early (15.92±11.98 vs 8.3±8.8, p=0.0002) and long term follow up (15.92±11.98 vs 4.57± 6.11, p<0.0001). In PA patients PCS values significantly improved at long term follow up (51.02±8.04 vs 55.85±5.1, p=0.013). Also in controls an improvement of MCS and DS scores was found at early and long term follow up compared to preoperative values, while no significant differences in PCS were found. Conclusions. Both PA and non-secreting adrenal tumors affect health-related QoL, worsening MCS and DS scores. Adrenalectomy is effective in curing PA, and improving MCS and DS scores at early and long-term follow-up, in patients with PA and non-secreting adrenal tumors. In PA patient surgery also significantly improves PCS at long term follow up.
Presupposti dello studio. Studi precedenti hanno descritto che l’iperaldosteronismo primario (PA) è associato ad un aumento della prevalenza di ansia, depressione e peggioramento della qualità di vita (QoL), con miglioramento significativo dopo il trattamento chirurgico. Scopo dello studio. Lo scopo dello studio è quello di indagare l’impatto della chirurgia sulla qualità di vita dei pazienti con PA, comparando i risultati con un gruppo di controllo costituito da pazienti sottoposti a surrenectomia per tumori surrenalici non secernenti. Materiali e Metodi. I dati sulla qualità di vita e lo stato di depressione sono stati raccolti prospetticamente, da Gennaio 2014 a Ottobre 2016, preoperatoriamente, dopo 1 mese e dopo almeno 6 mesi dall’intervento chirurgico di surrenectomia laparoscopica transperitoneale in pazienti con PA lateralizzato e in un gruppo di controllo costituito da pazienti con tumori non-secernenti del surrene. La QoL è stata valutata utilizzando il questionario SF-36, per valutazione della componente fisica (PCS) e mentale (MCS); lo stato depressivo è stato quantificato utilizzando un questionario di valutazione della depressione (DS) costituito da 20 domande. Risultati. Sono stati reclutati 26 pazienti con PA e 15 controlli. La cura biochimica della malattia è stata ottenuta in tutti i pazienti con PA; l'ipertensione è stata curata nel 31% dei casi ed è migliorata nel 69% dei casi. Non si sono verificate complicanze chirurgiche in entrambi i gruppi. Non sono state rilevate differenze statisticamente significative tra i pazienti con PA e i controlli per quanto riguarda i dati demografici e i valori preoperatori di PCS, MCS e DS. Nei pazienti con PA, i valori di MCS sono migliorati sia a 1 mese dall’intervento (42.72 ± 13.68 vs 51.56 ± 9.03, p = 0,0005) che a distanza (42,72 ± 13.68 vs 51.81 ± 7.04, p <0,0001). Nei pazienti affetti da PA anche i valori di DS sono migliorati sia a breve (15.92 ± 11.98 vs 8.3 ± 8.8, p = 0,0002) che a lungo termine (15,92 ± 11.98 vs 4.57 ± 6.11, p <0,0001); i valori di PCS sono migliorati significativamente solo a distanza dall’intervento (51.02 ± 8.04 vs 55.85 ± 5.1, p = 0,013). Anche nel gruppo di controllo i valori di MCS e DS sono migliorati sia a breve dopo l’intervento che a distanza; in questi pazienti non sono state rilevate variazioni significative nei valori di PCS dopo l’intervento. Conclusioni. I pazienti affetti da PA e tumori surrenalici non-secernenti sono caratterizzati da una QoL peggiore rispetto alla popolazione normale. La surrenectomia è efficace nella cura del PA, e nel migliorare i punteggi di MCS e DS sia a 1 mese dall’intervento che a lungo termine, sia nei pazienti con PA che nel gruppo di controllo. Nei pazienti con PA, i valor di PCS migliorano significativamente solo a lungo termine.

The causes of secondary hypertension and their therapy are discussed. Considered conditions are secondary hypertension, renovascular hypertension, renal parenchymal disease, primary aldosteronism, phaeochromocytoma, adrenal incidentaloma, and other causes of secondary hypertension.

This chapter reviews the clinical features, diagnosis, and treatment of three adrenal diseases: adrenal insufficiency, primary aldosteronism (hyperaldosteronism), and phaeochromocytoma. Adrenal insufficiency is a disorder characterized by impaired adrenocortical function. In primary adrenal insufficiency, destruction of the adrenal cortex results in a decreased production of glucocorticoids, mineralocorticoids, and/or androgens. Secondary adrenal insufficiency is due to disordered pituitary and hypothalamic function resulting in decreased secretion of adrenocorticotropic hormone or corticotrophin-releasing hormone, with consequent reduction in glucocorticoid and/or androgen secretion. Aldosterone is produced in the zona glomerulosa of the adrenal cortex. Abnormal overproduction of aldosterone results in autonomous primary hyperaldosteronism, leading to hypertension and hypokalaemia. Phaeochromocytomas are rare tumours of the adrenal medulla, arising from chromaffin cells, and produce catecholamines. Tumours arising from extra-adrenal ganglia, both sympathetic and parasympathetic, are called paragangliomas. As the majority of sympathetic paragangliomas secrete catecholamines, they are also called extra-adrenal phaeochromocytomas.