scholarly journals Atheroma: links with antiphospholipid antibodies, Hughes syndrome and lupus

QJM ◽  
1999 ◽  
Vol 92 (1) ◽  
pp. 57-59 ◽  
Author(s):  
D. Harats
Lupus ◽  
2016 ◽  
Vol 25 (13) ◽  
pp. 1397-1411 ◽  
Author(s):  
M H A Noureldine ◽  
G Harifi ◽  
A Berjawi ◽  
A A Haydar ◽  
M Nader ◽  
...  

2022 ◽  
pp. 1-2
Author(s):  
João Almeida e Melo ◽  
João Gama Marques

Abstract After reading an article in the journal, regarding affective disorders in patients with rare illnesses, the authors would like to discuss a case of non-affective psychosis, presenting with olfactory reference and Truman symptoms, in a patient with three unusual conditions: Gilbert disease, Hughes syndrome and Lyme neuroborreliosis.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2908 ◽  
Author(s):  
Maria Laura Bertolaccini ◽  
Giovanni Sanna

Antiphospholipid syndrome (APS), also known as Hughes Syndrome, is a systemic autoimmune disease characterized by thrombosis and/or pregnancy morbidity in the presence of persistently positive antiphospholipid antibodies. A patient with APS must meet at least one of two clinical criteria (vascular thrombosis or complications of pregnancy) and at least one of two laboratory criteria including the persistent presence of lupus anticoagulant (LA), anticardiolipin antibodies (aCL), and/or anti-b2 glycoprotein I (anti-b2GPI) antibodies of IgG or IgM isotype at medium to high titres in patient’s plasma. However, several other autoantibodies targeting other coagulation cascade proteins (i.e. prothrombin) or their complex with phospholipids (i.e. phosphatidylserine/prothrombin complex), or to some domains of β2GPI, have been proposed to be also relevant to APS. In fact, the value of testing for new aPL specificities in the identification of APS in thrombosis and/or pregnancy morbidity patients is currently being investigated.


Lupus ◽  
2010 ◽  
Vol 19 (4) ◽  
pp. 343-346 ◽  
Author(s):  
GRV Hughes

This year in Galveston, Texas, Silvia Pierangeli hosts the 13th International Congress on Antiphospholipid Antibodies. Twenty-six years after the first antiphospholipid syndrome meeting, the number of interested colleagues has multiplied, and the subject has become more scientifically understood. So also has the clinical picture. In this short contribution, I will highlight a number of clinical observations which may, or may not, contribute to our understanding of antiphospholipid syndrome.


2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Manoel Tavares Neves Junior ◽  
Carlos Ewerton Maia Rodrigues ◽  
Jozelio Freire de Carvalho

The relationship between prolactin (PRL) and the immune system has been demonstrated in the last two decades and has opened new windows in the field of immunoendocrinology. However, there are scarce reports about PRL in primary antiphospholipid syndrome (pAPS). The objective of this study was to evaluate PRL levels in patients with pAPS compared to healthy controls and to investigate their possible clinical associations. Fifty-five pAPS patients according to Sapporo criteria were age- and sex-matched with 41 healthy subjects. Individuals with secondary causes of hyperprolactinemia (HPRL) were excluded; demographic, biometric, and clinical data, PRL levels, antiphospholipid antibodies, inflammatory markers, and other routine laboratory findings were analyzed. PRL levels were similar between pAPS and healthy controls (8.94±7.02versus8.71±6.73 ng/mL,P=.876). Nine percent of the pAPS patients and 12.1% of the control subjects presented HPRL (P=.740). Comparison between the pAPS patients with hyper- and normoprolactinemia revealed no significant differences related to anthropometrics, clinical manifestations, medications, smoking, and antiphospholipid antibodies (P>.05). This study showed that HPRL does not seem to play a role in clinical manifestations of the pAPS, differently from other autoimmune rheumatic diseases.


Rheumatology ◽  
1995 ◽  
Vol 34 (6) ◽  
pp. 493-494 ◽  
Author(s):  
M. A. KHAMASHTHA ◽  
R. A. ASHERSON

Lupus ◽  
1996 ◽  
Vol 5 (5) ◽  
pp. 343-344 ◽  
Author(s):  
AE Gharavi ◽  
WA Wilson

aPL-associated thrombosis (Hughes syndrome) is widely recognized as a major cause of organ damage in autoimmune diseases. Beginning with the first symposium in 1984, international aPL symposia have facilitated research on aPL antibodies, and the clinical standardization of aPL tests. It is hoped that the present symposium will continue this tradition, because much remains to be learnt about the origin and pathogenicity of aPL antibodies. In addition, new insights are needed for more effective therapies to be developed.


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