May a lymphocytic infiltration have a pathogenic role in an aldosterone-producing adrenal tumor?

Cugini, P; Lucia, P; Letizia, Claudio; Murano, G; Pièche, S.

doi:10.1016/0306-9877(85)90017-9

Cited by 4 publications

(4 citation statements)

References 13 publications

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“…Interestingly, the finding of lymphocytic infiltration of adrenal tissue in patients with APA may represent another sign of an organ‐specific inflammation, autoimmunity, or both. Autoimmune diseases sometimes tend to aggregate in a patient to combine an autoimmune polyendocrine syndrome (APS) .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of angiotensin II type‐1 receptor antibodies in primary aldosteronism and further considerations about their possible pathogenetic role

Sabbadin

Ceccato

Ragazzi

et al. 2018

J of Clinical Hypertension

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Angiotensin II type-1 receptor autoantibodies (AT1RAb) have been involved in the genesis of primary aldosteronism (PA), both in aldosterone-producing adenoma (APA) and in idiopathic hyperaldosteronism (IHA). In this study, we evaluated the titer of AT1RAb in 44 PA patients (15 with APA and 29 with IHA) compared with 18 normotensive healthy controls who were matched for gender and age. In 17 PA patients (6 APA and 11 IHA) the titer was evaluated under mineralocorticoid receptor (MR) antagonist treatment. We found that PA patients had a significantly higher titer of AT1RAb compared with controls (median values 33 [IQR 15.6] IU/mL vs 17.5 [IQR 10.8] IU/mL, respectively; P < 0.0001). No significant difference of the AT1RAb titer was reported among PA patients, subdivided according to the subtypes and the concomitant MR antagonist therapy. No significant correlation was detected between age, gender, BMI, blood pressure values, baseline aldosterone, ARR, and the AT1RAb titer of all patients enrolled. Our data confirm an increased titer of AT1RAb in both subtypes of PA, independently from the concomitant use of MR antagonists and clinical/biochemical characteristics of PA patients. The small sample of patients and the relatively short time of treatment could have influenced these results. Moreover, the ELISA assay fails to evaluate the bioactivity of AT1RAb. Further studies should evaluate if the subtype, the clinical/biochemical recovery of PA, or both, influence the pathogenetic role of AT1RAb. The possible autoimmune pathogenesis and reversal effect with AT1R blocker treatment in PA patients with AT1RAb positivity is intriguing and requires further study.

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Section: Discussionmentioning

confidence: 99%

Evaluation of angiotensin II type‐1 receptor antibodies in primary aldosteronism and further considerations about their possible pathogenetic role

Sabbadin

Ceccato

Ragazzi

et al. 2018

J of Clinical Hypertension

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“…Cytokines It has long been postulated that lymphocytic infiltration of steroid-secreting adrenocortical neoplasms may play a role in the physiopathology of tumor development and hypersecretion through local release of various cytokines (149,150). In agreement with this hypothesis, lymphocytic infiltrate in a cortisol-secreting adenoma was found to be associated with abnormal expression of IL1 receptors by adenoma cells (66).…”

Section: Factorsmentioning

confidence: 76%

MECHANISMS IN ENDOCRINOLOGY: Autocrine/paracrine regulatory mechanisms in adrenocortical neoplasms responsible for primary adrenal hypercorticism

Lefebvre

Prévost

Louiset

2013

European Journal of Endocrinology

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A wide variety of autocrine/paracrine bioactive signals are able to modulate corticosteroid secretion in the human adrenal gland. These regulatory factors, released in the vicinity of adrenocortical cells by diverse cell types comprising chromaffin cells, nerve terminals, cells of the immune system, endothelial cells, and adipocytes, include neuropeptides, biogenic amines, and cytokines. A growing body of evidence now suggests that paracrine mechanisms may also play an important role in the physiopathology of adrenocortical hyperplasias and tumors responsible for primary adrenal steroid excess. These intra-adrenal regulatory systems, although globally involving the same actors as those observed in the normal gland, display alterations at different levels, which reinforce the capacity of paracrine factors to stimulate the activity of adrenocortical cells. The main modifications in the adrenal local control systems reported by now include hyperplasia of cells producing the paracrine factors and abnormal expression of the latter and their receptors. Because steroid-secreting adrenal neoplasms are independent of the classical endocrine regulatory factors angiotensin II and ACTH, which are respectively suppressed by hyperaldosteronism and hypercortisolism, these lesions have long been considered as autonomous tissues. However, the presence of stimulatory substances within the neoplastic tissues suggests that steroid hypersecretion is driven by autocrine/paracrine loops that should be regarded as promising targets for pharmacological treatments of primary adrenal disorders. This new potential therapeutic approach may constitute an alternative to surgical removal of the lesions that is classically recommended in order to cure steroid excess.European Journal of Endocrinology 169 R115-R138

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“…RANTES known to expressed and secreted by activated and normal T cell 23 , IP-10 attracting activated T, and CXCL9 involving in T cell migration 24,25 , were all showing the close relationship with T cells, and those cytokines were strongly associated with CD8 + T-cell infiltration in solid tumors [26][27][28] . Early researches have detected the abundant lymphocytic infiltration in adrenocortical tumor, and recent single cell sequencing studies have further detected the CD8 + T cells with highest proportion in normal adrenal glands 7,29,30 , therefore we speculated that these inflammatory factors might play a role in unilateral PA formation.…”

Section: Discussionmentioning

confidence: 89%

Diagnostic accuracy of using multiple cytokines to predict aldosterone-producing adenoma

Qin

Wen

Zhong

et al. 2023

Sci Rep

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Here, we aimed to study the important cytokines in plasma to identify the aldosterone-producing adenoma (APA). 19 unilateral primary aldosteronism (UPA) patients and 19 healthy people were divided into UPA group and Control group, and the serum of bilateral adrenal veins and inferior vena cava collected by adrenal blood sampling (AVS) in UPA patients and the serum from the healthy subjects were all used to detect multiple cytokines by Luminex immunoassays. Additionally, The UPA patients subjected to laparoscopic adrenalectomy were divided into different groups by pathological results for further study. According our results, IP-10, CXCL9 and RANTES were significantly higher in UPA group compared with control group, and the combination of the three cytokines have significant predictive power for predicting UPA, while the correlational analyses demonstrated that IP-10 and CXCL9 were positively correlated with BP and HR, while EGF was positively correlated with HDL. Additionally, IL-1b was suggested to be the most potential diagnostic biomarker to discriminate the APA and unilateral adrenal hyperplasia (UAH). The present findings might suggest a possibility of IP-10, CXCL9 and RANTES served as a sign to help UPA diagnosis and finally used to assist the diagnosis of APA, while IL-1b was suggested to be the most potential diagnostic biomarker to identify the APA from the UAH patients.

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May a lymphocytic infiltration have a pathogenic role in an aldosterone-producing adrenal tumor?

Cited by 4 publications

References 13 publications

Evaluation of angiotensin II type‐1 receptor antibodies in primary aldosteronism and further considerations about their possible pathogenetic role

Evaluation of angiotensin II type‐1 receptor antibodies in primary aldosteronism and further considerations about their possible pathogenetic role

MECHANISMS IN ENDOCRINOLOGY: Autocrine/paracrine regulatory mechanisms in adrenocortical neoplasms responsible for primary adrenal hypercorticism

Diagnostic accuracy of using multiple cytokines to predict aldosterone-producing adenoma

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