Ovotesticular disorder of sexual development due to 47,XYY/46,XY/45,X mixed gonadal dysgenesis in a phenotypic male presenting as cyclical haematuria: clinical presentation and assessment of long-term outcomes

Andrologia ◽  
2012 ◽  
Vol 46 (2) ◽  
pp. 191-193 ◽  
Author(s):  
D. Dutta ◽  
K. S. Shivaprasad ◽  
R. N. Das ◽  
S. Ghosh ◽  
U. Chatterjee ◽  
...  
Keyword(s):  
Sexual Development ◽  
Gonadal Dysgenesis ◽  
Clinical Presentation ◽  
Long Term Outcomes ◽  
Mixed Gonadal Dysgenesis ◽  
Disorder Of Sexual Development ◽  
Phenotypic Male

scholarly journals Long-term outcomes of sigmoid vaginoplasty in patients with disorder of sexual development – our experience

2018 ◽  
Vol 10 (2) ◽  
pp. 185 ◽  
Author(s):  
Ved Bhaskar ◽  
RahulJ Sinha ◽  
Seema Mehrotra ◽  
CN Mehrotra ◽  
Vishwajeet Singh
Keyword(s):  
Sexual Development ◽  
Long Term Outcomes ◽  
Disorder Of Sexual Development ◽  
Sigmoid Vaginoplasty

scholarly journals Clinical presentation and long‐term outcomes of infantile hypertrophic cardiomyopathy: a European multicentre study

2021 ◽  
Author(s):  
Gabrielle Norrish ◽  
Gali Kolt ◽  
Elena Cervi ◽  
Ella Field ◽  
Kathleen Dady ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Multicentre Study ◽  
Clinical Presentation ◽  
Long Term Outcomes

scholarly journals Erratum to “Clinical Presentation and Long-Term Outcomes of Systemic Sclerosis Portuguese Patients from a Single Centre Cohort: A EUSTAR Registration Initiative”

2018 ◽  
Vol 31 (9) ◽  
pp. 520
Author(s):  
Carolina Vidal ◽  
Carina Ruano ◽  
Vera Bernardino ◽  
Pedro Lavado Carreira ◽  
Ana Lladó ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Clinical Presentation ◽  
Long Term Outcomes ◽  
Single Centre ◽  
Espírito Santo ◽  
Espirito Santo ◽  
De Medicina

Article published with errors: https://www.actamedicaportuguesa.com/revista/index.php/amp/article/view/10658On page 312, where the authors’ line reads as:Carolina VIDAL1, Carina RUANO2, Vera BERNARDINO3, Pedro LAVADO CARREIRA3, Ana LLADÓ3, Maria Céu SANTOS4, Heidi GRUNER3, António PANARRA3, Nuno RISO3, Maria Francisca MORAES-FONTESAC,1It should read:Carolina VIDAL1,2, Carina RUANO3, Vera BERNARDINO1, Pedro LAVADO CARREIRA1, Ana LLADÓ1, Maria Céu SANTOS4, Heidi GRUNER1, António PANARRA1, Nuno RISO1, Maria Francisca MORAES-FONTESAC,1 On the same page, where the authors’ affiliation on the footer reads as:Serviço de Medicina Interna. Hospital do Divino Espírito Santo de Ponta Delgada. São Miguel. Portugal.Serviço de Radiologia. Hospital de Santa Marta. Centro Hospitalar de Lisboa Central. Lisboa. Portugal.Unidade de Doenças Auto-Imunes/Serviço Medicina 7.2. Hospital de Curry Cabral. Centro Hospitalar de Lisboa Central. Lisboa. Portugal.Laboratório de Imunologia. Centro Hospitalar de Lisboa Central. Lisboa. Portugal. It should read:Unidade de Doenças Auto-Imunes/Serviço Medicina 7.2. Hospital de Curry Cabral. Centro Hospitalar de Lisboa Central. Lisboa. Portugal.Serviço de Medicina Interna. Hospital do Divino Espírito Santo de Ponta Delgada. São Miguel. Portugal.Serviço de Radiologia. Hospital de Santa Marta. Centro Hospitalar de Lisboa Central. Lisboa. Portugal.Laboratório de Imunologia. Centro Hospitalar de Lisboa Central. Lisboa. Portugal.  

scholarly journals The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis

2021 ◽  
Vol 22 (22) ◽  
pp. 12386
Author(s):  
Ludovico De Stefano ◽  
Bernardo D’Onofrio ◽  
Antonio Manzo ◽  
Carlomaurizio Montecucco ◽  
Serena Bugatti
Keyword(s):  
Rheumatoid Arthritis ◽  
Clinical Presentation ◽  
Adaptive Immune System ◽  
Response To Treatment ◽  
Targeted Intervention ◽  
Long Term Outcomes ◽  
Inflammatory Cascade ◽  
Adaptive Immune ◽  
Disease Subtypes

Differences in clinical presentation, response to treatment, and long-term outcomes between autoantibody-positive and -negative rheumatoid arthritis (RA) highlight the need for a better comprehension of the immunopathogenic events underlying the two disease subtypes. Whilst the drivers and perpetuators of autoimmunity in autoantibody-positive RA have started to be disclosed, autoantibody-negative RA remains puzzling, also due its wide phenotypic heterogeneity and its possible misdiagnosis. Genetic susceptibility appears to mostly rely on class I HLA genes and a number of yet unidentified non-HLA loci. On the background of such variable genetic predisposition, multiple exogeneous, endogenous, and stochastic factors, some of which are not shared with autoantibody-positive RA, contribute to the onset of the inflammatory cascade. In a proportion of the patients, the immunopathology of synovitis, at least in the initial stages, appears largely myeloid driven, with abundant production of proinflammatory cytokines and only minor involvement of cells of the adaptive immune system. Better understanding of the complexity of autoantibody-negative RA is still needed in order to open new avenues for targeted intervention and improve clinical outcomes.

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