Search Results

You are looking at 11 - 20 of 99 items for

  • Abstract: Autoimmune x
  • Abstract: Inflammation x
  • Abstract: Late effects of cancer treatment x
  • Abstract: Cognition x
Clear All Modify Search
Weiwei He Department of Endocrinology, Affiliated Hospital of Yanan Medical University, Shaanxi, China

Search for other papers by Weiwei He in
Google Scholar
PubMed
Close
,
Bin Wang Department of Endocrinology, Jinshan Hospital of Fudan University, Shanghai, China

Search for other papers by Bin Wang in
Google Scholar
PubMed
Close
,
Kaida Mu Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Search for other papers by Kaida Mu in
Google Scholar
PubMed
Close
,
Jing Zhang Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Search for other papers by Jing Zhang in
Google Scholar
PubMed
Close
,
Yanping Yang Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Search for other papers by Yanping Yang in
Google Scholar
PubMed
Close
,
Wei Yao Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Search for other papers by Wei Yao in
Google Scholar
PubMed
Close
,
Sheli Li Department of Endocrinology, Affiliated Hospital of Yanan Medical University, Shaanxi, China

Search for other papers by Sheli Li in
Google Scholar
PubMed
Close
, and
Jin-an Zhang Department of Endocrinology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Search for other papers by Jin-an Zhang in
Google Scholar
PubMed
Close

Background

Accumulating data have shown that interleukin-27 (IL27) polymorphisms are linked to the susceptibility of some autoimmune diseases. We assessed whether there was an association between three single-nucleotide polymorphisms (SNPs) of IL27 gene and autoimmune thyroid diseases (AITDs).

Methods

Three SNPs (rs153109, rs17855750 and rs181206) of IL27 gene were genotyped by Hi-SNP high-throughput genotyping in 843 patients with AITDs (516 Graves’ disease (GD) and 327 Hashimoto’s thyroiditis (HT)) and 677 healthy controls in Chinese Han population.

Results

Compared with controls, rs153109 displayed significant associations with GD in allele and genotype frequencies (P = 0.002 and P = 0.008, respectively) and rs17855750 displayed significant associations with HT in allele frequencies (P = 0.02), whereas no differences in genotype or allele frequencies were found between AITD patients and controls at rs181206.

Conclusion

Our study, for the first time, showed the significant association of the IL27 gene SNPs with AITD.

Open access
Stavroula A Paschou Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

Search for other papers by Stavroula A Paschou in
Google Scholar
PubMed
Close
,
Nektaria Papadopoulou-Marketou Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

Search for other papers by Nektaria Papadopoulou-Marketou in
Google Scholar
PubMed
Close
,
George P Chrousos Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

Search for other papers by George P Chrousos in
Google Scholar
PubMed
Close
, and
Christina Kanaka-Gantenbein Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, ‘Aghia Sophia’ Children’s Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece

Search for other papers by Christina Kanaka-Gantenbein in
Google Scholar
PubMed
Close

Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of β cells of the endocrine pancreas. Pathogenesis of T1DM is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the β cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy β cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occur after a long latency period, which reflects the large percentage of β cells that need to be destroyed before overt diabetes become evident.

Open access
Nancy J Olsen Division of Rheumatology, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, Milton S Hershey Medical Center, The Pennsylvania State University, Mail Code H044, 500 University Drive, Hershey, Pennsylvania 17033-0850, USA

Search for other papers by Nancy J Olsen in
Google Scholar
PubMed
Close
,
Ann L Benko Division of Rheumatology, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, Milton S Hershey Medical Center, The Pennsylvania State University, Mail Code H044, 500 University Drive, Hershey, Pennsylvania 17033-0850, USA

Search for other papers by Ann L Benko in
Google Scholar
PubMed
Close
, and
William J Kovacs Division of Rheumatology, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, Milton S Hershey Medical Center, The Pennsylvania State University, Mail Code H044, 500 University Drive, Hershey, Pennsylvania 17033-0850, USA

Search for other papers by William J Kovacs in
Google Scholar
PubMed
Close

Clinical and experimental evidence support a role for gonadal steroids in modulating the expression and course of autoimmune diseases such as lupus. Whether or not inherited variation in sensitivity to circulating androgenic hormones could influence the manifestations of such disease is, however, unknown. We sought to determine whether differences in androgen sensitivity conferred by variation in the exon 1 CAG repeat region of the androgen receptor (AR) gene were associated with differences in the clinical or humoral immune manifestations of lupus in a cohort of female subjects. We found that shorter AR CAG repeat lengths in lupus subjects correlated with a higher Systemic Lupus Erythematosus Disease Activity Index score, higher ANA levels, and expression of a broader array of IgG autoantibodies. Our findings of more severe clinical manifestations and more exuberant humoral autoimmunity in women with a shorter AR exon 1 CAG repeat length suggest a role for genetically determined sensitivity to androgens as a modulator of autoimmune processes.

Open access
Aaron Lerner B. Rappaport School of Medicine, Technion-Israel Institute of Technology, Haifa, Israel
AESKU.KIPP Institute, Wendelsheim, Germany

Search for other papers by Aaron Lerner in
Google Scholar
PubMed
Close
,
Patricia Jeremias AESKU.KIPP Institute, Wendelsheim, Germany

Search for other papers by Patricia Jeremias in
Google Scholar
PubMed
Close
, and
Torsten Matthias AESKU.KIPP Institute, Wendelsheim, Germany

Search for other papers by Torsten Matthias in
Google Scholar
PubMed
Close

Autoimmune thyroiditis has an increased prevalence in patients with celiac disease and vice versa. The objective of the current review is to highlight the epidemiological, clinical, serological, pathological, pathophysiological, hormonal, genetic and immunological factors shared between the two entities. They might represent the two ends of the gut-thyroid axis where the cross-talks’ pathways are still unravelled. New observations are reviewed, highlighting some gut-thyroid interrelated pathways that potentially might lead to new therapeutic strategies.

Open access
Charlotte Höybye Patient Area Endocrinology and Nephrology, Infection and Inflammation Theme, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

Search for other papers by Charlotte Höybye in
Google Scholar
PubMed
Close
,
Laia Faseh Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

Search for other papers by Laia Faseh in
Google Scholar
PubMed
Close
,
Christos Himonakos Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden
Department of Medicine, Karlstad Hospital, Karlstad, Sweden

Search for other papers by Christos Himonakos in
Google Scholar
PubMed
Close
,
Tomasz Pielak NUTOPI Sp. z o. o., Poznan, Poland

Search for other papers by Tomasz Pielak in
Google Scholar
PubMed
Close
, and
Jesper Eugen-Olsen Clinical Research Centre, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark

Search for other papers by Jesper Eugen-Olsen in
Google Scholar
PubMed
Close

Growth hormone deficiency (GHD) syndrome is associated with adverse levels of several risk factors for cardiovascular diseases (CVD), including metabolic inflammation. However, the impact of GHD and GH treatment on low-grade inflammation is unknown. The aim of the study was to establish the level of the low-grade inflammation biomarker soluble urokinase plasminogen activator receptor (suPAR) in adults with GHD and the response to long-term GH treatment. Measurements of suPAR and CRP were performed in bio-bank serum samples from 72 adults, 34 males and 38 females, with GHD before and during at least 5 years of GH treatment. Mean age was 52.5 ± 15.5 years, BMI 27.3 ± 5 kg/m2. Clinical evaluations and blood sampling were performed at routine visits. Data on demography, anthropometry, lab results and clinical events were retrieved from post-marketing surveillance study databases and medical records. suPAR and high-sensitive (hs) CRP were analysed using ELISA and immunochemistry, respectively. At baseline blood pressure, lipid profile and fasting glucose were within the normal reference range. Baseline geometric mean and 95% CI of suPAR was 2.9 (2.7–3.3) ng/mL and of CRP 2.3 (0.6–4.0) mg/L. Mean follow-up was 8 ± 2 years. The suPAR levels remained stable during follow-up, although individual increases were seen on occurrence or presence of co-morbidities. In contrast, levels of CRP decreased. In conclusion, the decrease in CRP and indirectly the absence of an expected increase in suPAR over time indicates a favourable effect of GH on low-grade inflammation.

Open access
Wentao Zhou The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China
Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Wentao Zhou in
Google Scholar
PubMed
Close
,
Tiantao Kuang The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Tiantao Kuang in
Google Scholar
PubMed
Close
,
Xu Han Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Xu Han in
Google Scholar
PubMed
Close
,
Wenqi Chen Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Wenqi Chen in
Google Scholar
PubMed
Close
,
Xuefeng Xu The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Xuefeng Xu in
Google Scholar
PubMed
Close
,
Wenhui Lou Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Wenhui Lou in
Google Scholar
PubMed
Close
, and
Dansong Wang The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Dansong Wang in
Google Scholar
PubMed
Close

Objectives

Systemic inflammation markers have been demonstrated to be associated with prognosis in various tumors. In this study, we aimed to assess the value of neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index and the counts of lymphocyte, monocyte and neutrophil in predicting prognosis among patients with resected pancreatic neuroendocrine neoplasms (pNENs).

Methods

A total of 174 patients were included in the study. Univariate and multivariate analyses were performed to evaluate the predictive roles of inflammation markers for relapse-free survival (RFS) and overall survival (OS) in pNEN patients.

Results

The optimal cut-off values of NLR, LMR and lymphocyte count were 1.9, 5.0 and 1.4 × 109/L, respectively, determined by the X-tile software. RFS was found to be significantly longer in patients with NLR ≤1.9 (P = 0.041), LMR >5.0 (P < 0.001) and lymphocyte count >1.4 × 109/L (P = 0.002) in comparison to those with NLR >1.9, LMR ≤5.0 and lymphocyte count ≤1.4 × 109/L, respectively. Multivariate analysis revealed that LMR (hazard ratio 0.30, 95% CI 0.11–0.85, P = 0.023) was an independent predictor for RFS, but not NLR or lymphocyte count. For long-term survival analysis, patients with NLR ≤1.9 (P = 0.016) were found to be associated with favorable OS, but NLR was not an independent factor validated by multivariate analysis.

Conclusions

Preoperative LMR is an independent systemic inflammation marker to predict relapses in pNEN patients who underwent curative resections, whose clinical value needs to be verified in further large sample-based prospective studies.

Open access
Frederique Van de Velde Department of Endocrinology, Ghent University Hospital, Ghent, Belgium

Search for other papers by Frederique Van de Velde in
Google Scholar
PubMed
Close
,
Marlies Bekaert Department of Endocrinology, Ghent University Hospital, Ghent, Belgium

Search for other papers by Marlies Bekaert in
Google Scholar
PubMed
Close
,
Anja Geerts Department of Hepatology, Ghent University Hospital, Ghent, Belgium

Search for other papers by Anja Geerts in
Google Scholar
PubMed
Close
,
Anne Hoorens Department of Pathology, Ghent University Hospital

Search for other papers by Anne Hoorens in
Google Scholar
PubMed
Close
,
Arsène-Hélène Batens Department of Endocrinology, Ghent University Hospital, Ghent, Belgium

Search for other papers by Arsène-Hélène Batens in
Google Scholar
PubMed
Close
,
Samyah Shadid Department of Endocrinology, Ghent University Hospital, Ghent, Belgium

Search for other papers by Samyah Shadid in
Google Scholar
PubMed
Close
,
Margriet Ouwens Department of Endocrinology, Ghent University Hospital, Ghent, Belgium
Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Duesseldorf, Germany
German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany

Search for other papers by Margriet Ouwens in
Google Scholar
PubMed
Close
,
Yves Van Nieuwenhove Department of Gastrointestinal Surgery, Ghent University Hospital, Ghent, Belgium

Search for other papers by Yves Van Nieuwenhove in
Google Scholar
PubMed
Close
, and
Bruno Lapauw Department of Endocrinology, Ghent University Hospital, Ghent, Belgium

Search for other papers by Bruno Lapauw in
Google Scholar
PubMed
Close

Purpose

Obese subjects with nonalcoholic fatty liver disease (NAFLD) are more prone to develop additional metabolic disturbances such as systemic insulin resistance (IR) and type 2 diabetes. NAFLD is defined by hepatic steatosis, lobular inflammation, ballooning and stage of fibrosis, but it is unclear if and which components could contribute to IR.

Objective

To assess which histological components of NAFLD associate with IR in subjects with obesity, and if so, to what extent.

Methods

This cross-sectional study included 78 obese subjects (mean age 46 ± 11 years; BMI 42.2 ± 4.7 kg/m2). Glucose levels were analysed by hexokinase method and insulin levels with electrochemiluminescence. Homeostasis model assessment-estimated insulin resistance (HOMA-IR) was calculated. Liver biopsies were evaluated for histological components of NAFLD.

Results

A positive association between overall NAFLD Activity Score and HOMA-IR was found (r s = 0.259, P = 0.022). As per individual components, lobular inflammation and fibrosis stage were positively associated with HOMA-IR, glucose and insulin levels (P < 0.05), and HOMA-IR was higher in patients with more inflammatory foci or higher stage of fibrosis. These findings were independent of age, BMI, triglyceride levels, diabetes status and sex (all P < 0.043). In a combined model, lobular inflammation, but not fibrosis, remained associated with HOMA-IR.

Conclusion

In this group of obese subjects, a major contributing histological component of NAFLD to the relation between NAFLD severity and IR seems to be the grade of hepatic lobular inflammation. Although no causal relationship was assessed, preventing or mitigating this inflammatory response in obesity might be of importance in controlling obesity-related metabolic disturbances.

Open access
Zhiwei Zhang Department of Obstetrics and Gynecology, Liaocheng People’s Hospital, Liaocheng, Shandong, China

Search for other papers by Zhiwei Zhang in
Google Scholar
PubMed
Close
,
Hui Zhao Department of Obstetrics and Gynecology, Liaocheng People’s Hospital, Liaocheng, Shandong, China

Search for other papers by Hui Zhao in
Google Scholar
PubMed
Close
, and
Aixia Wang Department of Obstetrics and Gynecology, Liaocheng People’s Hospital, Liaocheng, Shandong, China

Search for other papers by Aixia Wang in
Google Scholar
PubMed
Close

Background

Gestational diabetes mellitus (GDM) has a high incidence rate among pregnant women. The objective of the study was to assess the effect of plant-derived oleuropein in attenuating inflammatory and oxidative stress of GDM.

Methods

Oleuropein was administered to GDM mice at the doses of 5 or 10 mg/kg/day. Body weight, blood glucose, insulin and hepatic glycogen levels were recorded. To evaluate the effect of oleuropein in reducing oxidative stress, ELISA was used to measure the hepatic oxidative stress markers. The inflammation levels of GDM mice were evaluated by measuring serum levels of IL-6 and TNF-α by ELISA and mRNA levels of IL-1β, TNF-α and IL-6 by real-time PCR (RT-PCR). The AMP-activated protein kinase (AMPK) signaling pathway was assessed by Western blot. Gestational outcome was analyzed through comparing litter size and birth weight.

Results

Oleuropein attenuated the elevated body weight of GDM mice and efficiently reduced blood glucose, insulin and hepatic glycogen levels. Oxidative stress and inflammation were alleviated by oleuropein treatment. The AMPK signaling was activated by oleuropein in GDM mice. Gestational outcome was markedly improved by oleuropein treatment.

Conclusions

Our study suggests that oleuropein is effective in alleviating symptoms of GDM and improving gestational outcome in the mouse model. This effect is achieved by attenuating oxidative stress and inflammation, which is mediated by the activation of the AMPK signaling pathway.

Open access
Shaomin Shi Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

Search for other papers by Shaomin Shi in
Google Scholar
PubMed
Close
,
Xinghua Chen Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Xinghua Chen in
Google Scholar
PubMed
Close
,
Wen Yu Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China

Search for other papers by Wen Yu in
Google Scholar
PubMed
Close
,
Xiaolan Ke Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

Search for other papers by Xiaolan Ke in
Google Scholar
PubMed
Close
, and
Tean Ma Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

Search for other papers by Tean Ma in
Google Scholar
PubMed
Close

Protection of podocytes is one of the important means to delay the progression of diabetic nephropathy (DN), and glucagon-like peptide-1 (GLP-1) has been shown to have a protective effect on the kidney in DN models, but whether it has a protective effect on podocytes and the potential mechanisms of action remain largely unknown. In the present study, we established a type 2 diabetes mellitus (T2DM) mouse model by high-fat diet feeding combined with streptozotocin (STZ) induction and administered the intervention for 14 weeks. We found that liraglutide significantly ameliorated podocyte injury in DN mice. Mechanistically, we detected glucagon-like peptide-1 receptor (GLP-1R) protein expression levels in kidney tissues by immunohistochemical staining, immunofluorescence staining, and western blotting and found that podocytes could express GLP-1R and liraglutide treatment could restore GLP-1R expression in the kidney tissues of DN mice. Furthermore, we found that NLRP3-induced inflammation and pyroptosis were positively correlated with podocyte injury in DN mice, and liraglutide inhibited the expression of NLRP3-induced inflammation and pyroptosis-related proteins. Our results suggest that liraglutide protects DN mouse podocytes by regulating GLP-1R in renal tissues and by regulating NLRP3-induced inflammation and pyroptosis.

Open access
Lia Ferreira Department of Endocrinology, Centro Hospitalar do Porto, Porto, Portugal

Search for other papers by Lia Ferreira in
Google Scholar
PubMed
Close
,
João Silva Department of Endocrinology, Hospital das Forças Armadas, Lisboa, Portugal

Search for other papers by João Silva in
Google Scholar
PubMed
Close
,
Susana Garrido Department of Endocrinology, Centro Hospitalar Tâmega e Sousa, Porto, Portugal

Search for other papers by Susana Garrido in
Google Scholar
PubMed
Close
,
Carlos Bello Department of Endocrinology, Centro Hospitalar Lisboa Ocidental, Lisboa, Portugal

Search for other papers by Carlos Bello in
Google Scholar
PubMed
Close
,
Diana Oliveira Department of Endocrinology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal

Search for other papers by Diana Oliveira in
Google Scholar
PubMed
Close
,
Hélder Simões Department of Endocrinology, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

Search for other papers by Hélder Simões in
Google Scholar
PubMed
Close
,
Isabel Paiva Department of Endocrinology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal

Search for other papers by Isabel Paiva in
Google Scholar
PubMed
Close
,
Joana Guimarães Department of Endocrinology, Centro Hospitalar do Baixo Vouga, Aveiro, Portugal

Search for other papers by Joana Guimarães in
Google Scholar
PubMed
Close
,
Marta Ferreira Department of Endocrinology, Centro Hospitalar de Leiria, Leiria, Portugal

Search for other papers by Marta Ferreira in
Google Scholar
PubMed
Close
,
Teresa Pereira Department of Endocrinology, Centro Hospitalar de Leiria, Leiria, Portugal

Search for other papers by Teresa Pereira in
Google Scholar
PubMed
Close
,
Rita Bettencourt-Silva Department of Endocrinology, Centro Hospitalar de São João, Porto, Portugal

Search for other papers by Rita Bettencourt-Silva in
Google Scholar
PubMed
Close
,
Ana Filipa Martins Department of Endocrinology, Centro Hospitalar Lisboa Norte, Lisboa, Portugal

Search for other papers by Ana Filipa Martins in
Google Scholar
PubMed
Close
,
Tiago Silva Department of Endocrinology, Hospital Garcia da Orta, Lisboa, Portugal

Search for other papers by Tiago Silva in
Google Scholar
PubMed
Close
,
Vera Fernandes Department of Endocrinology, Hospital de Braga, Braga, Portugal

Search for other papers by Vera Fernandes in
Google Scholar
PubMed
Close
,
Maria Lopes Pereira Department of Endocrinology, Hospital de Braga, Braga, Portugal

Search for other papers by Maria Lopes Pereira in
Google Scholar
PubMed
Close
, and
Adrenal Tumors Study Group of the Portuguese Society of Endocrinology Department of Endocrinology, Centro Hospitalar do Porto, Porto, Portugal

Search for other papers by Adrenal Tumors Study Group of the Portuguese Society of Endocrinology in
Google Scholar
PubMed
Close

Introduction

Primary adrenal insufficiency (PAI) is a rare but severe and potentially life-threatening condition. No previous studies have characterized Portuguese patients with PAI.

Aims

To characterize the clinical presentation, diagnostic workup, treatment and follow‐up of Portuguese patients with confirmed PAI.

Methods

This multicentre retrospective study examined PAI patients in 12 Portuguese hospitals.

Results

We investigated 278 patients with PAI (55.8% were females), with a mean age of 33.6 ± 19.3 years at diagnosis. The most frequent presenting clinical features were asthenia (60.1%), mucocutaneous hyperpigmentation (55.0%) and weight loss (43.2%); 29.1% of the patients presented with adrenal crisis. Diagnosis was established by high plasma ACTH and low serum cortisol in most patients (43.9%). The most common aetiology of PAI was autoimmune adrenalitis (61.0%). There were 38 idiopathic cases. Autoimmune comorbidities were found in 70% of the patients, the most frequent being autoimmune thyroiditis (60.7%) and type 1 diabetes mellitus (17.3%). Seventy-nine percent were treated with hydrocortisone (mean dose 26.3 ± 8.3 mg/day) mostly in three (57.5%) or two (37.4%) daily doses. The remaining patients were treated with prednisolone (10.1%), dexamethasone (6.2%) and methylprednisolone (0.7%); 66.2% were also on fludrocortisone (median dose of 100 µg/day). Since diagnosis, 33.5% of patients were hospitalized for disease decompensation. In the last appointment, 17.2% of patients had complaints (7.6% asthenia and 6.5% depression) and 9.7% had electrolyte disturbances.

Conclusion

This is the first multicentre Portuguese study regarding PAI. The results emphasize the need for standardization in diagnostic tests and etiological investigation and provide a framework for improving treatment.

Open access