Contribution of histological, serological, and genetic factors to the clinical heterogeneity of adult-onset coeliac disease

2009 ◽  
Vol 44 (9) ◽  
pp. 1076-1083 ◽  
Author(s):  
Harry J. Thomas ◽  
Tariq Ahmad ◽  
Chandima Rajaguru ◽  
Martin Barnardo ◽  
Bryan F. Warren ◽  
...  
2009 ◽  
Vol 136 (5) ◽  
pp. A-263
Author(s):  
Harry J. Thomas ◽  
Chandima S. Rajaguru ◽  
Bryan F. Warren ◽  
Derek P. Jewell ◽  
Tariq Ahmad

2015 ◽  
Vol 2015 ◽  
pp. 1-19 ◽  
Author(s):  
Pinja Ilmarinen ◽  
Leena E. Tuomisto ◽  
Hannu Kankaanranta

Asthma is a heterogeneous disease with many phenotypes, and age at disease onset is an important factor in separating the phenotypes. Genetic factors, atopy, and early respiratory tract infections are well-recognized factors predisposing to childhood-onset asthma. Adult-onset asthma is more often associated with obesity, smoking, depression, or other life-style or environmental factors, even though genetic factors and respiratory tract infections may also play a role in adult-onset disease. Adult-onset asthma is characterized by absence of atopy and is often severe requiring treatment with high dose of inhaled and/or oral steroids. Variety of risk factors and nonatopic nature of adult-onset disease suggest that variety of mechanisms is involved in the disease pathogenesis and that these mechanisms differ from the pathobiology of childhood-onset asthma with prevailing Th2 airway inflammation. Recognition of the mechanisms and mediators that drive the adult-onset disease helps to develop novel strategies for the treatment. The aim of this review was to summarize the current knowledge on the pathogenesis of adult-onset asthma and to concentrate on the mechanisms and mediators involved in establishing adult-onset asthma in response to specific risk factors. We also discuss the involvement of these mechanisms in the currently recognized phenotypes of adult-onset asthma.


Diabetes Care ◽  
2002 ◽  
Vol 25 (12) ◽  
pp. 2363-2364 ◽  
Author(s):  
M. Fukui ◽  
Y. Kitagawa ◽  
N. Nakamura ◽  
T. Yoshikawa

2015 ◽  
Vol 52 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Affifa FARRUKH ◽  
John Francis MAYBERRY

Central and South America offer an opportunity to resolve some of the current controversies that surround the epidemiology of celiac disease. Through a concerted action which brings together clinicians, researchers and patients there is an opportunity to establish robust data sets which will allow detailed analysis of environmental and genetic factors. In this review available data from the continent together with data from Spain and Italy are drawn together to give a current picture in the hope that it will stimulate further research.


Author(s):  
Begoña Diosdado ◽  
Erica van Oort ◽  
Cisca Wijmenga

AbstractCoeliac disease (CD) is an inflammatory disorder of the small intestine characterised by a permanent intolerance to gluten-derived peptides. When gluten-derived peptides reach the lamina propria in CD patients, they provoke specific changes in the mucosa of their small intestine. Although the susceptibility to CD is strongly determined by environmental gluten, it is clearly a common genetic disorder. Important genetic factors for CD are the


The Lancet ◽  
1991 ◽  
Vol 337 (8754) ◽  
pp. 1373-1374 ◽  
Author(s):  
D.H. Wright ◽  
D.B. Jones ◽  
H. Clark ◽  
G.M. Mead ◽  
E. Hodges ◽  
...  

2005 ◽  
Vol 40 (5) ◽  
pp. 637-638
Author(s):  
F Pereira ◽  
A Ferreira ◽  
M Tavares ◽  
P Canedo ◽  
E Trindade ◽  
...  

1993 ◽  
Vol 38 (2) ◽  
pp. 51-52 ◽  
Author(s):  
P.J. Mckay ◽  
D.B. Kennedy ◽  
N.P. Lucie

The risk of overwhelming septicaemia, most commonly due to encapsulated organisms, is well recognised post-splenectomy. Although a similar risk is documented in hyposplenic patients, many physicians do not routinely give prophylaxis here. We report the case of a 41 year old woman with adult onset coeliac disease who developed pneumococcal meningitis resulting in severe residual disability and suggest that prophylaxis should be given to such individuals who have evidence of reduced splenic function.


2000 ◽  
Vol 15 (2) ◽  
pp. 123-128 ◽  
Author(s):  
F. Limosin ◽  
J. Adès ◽  
P. Gorwood

SummaryGenetic factors explain a non-negligible part of the vulnerability to alcohol dependence, the genetic influence in males being estimated at around 60%. The search for gene(s) potentially implicated in alcoholism is counteracted by the clinical heterogeneity of alcoholism, but also by heterogeneity of the etiologic factors involved. It is thus necessary to redefine more specific phenotypes with more simple determinism, and to focus on more specific subsets of candidate genes. In this view, the existence of co-occurrence (presence at the same time, whatever the cause) between antisocial personality and alcoholism is frequently reported. Three hypotheses have been previously proposed to explain this co-occurrence. Firstly, it could be a pure artefact or contamination, due to common items in diagnostic manuals widely used, such as the DSM or ICD. Secondly, antisocial personality and alcoholism could share common etiologic factor(s), and determine a ‘real’ co-morbidity. Finally, common genetic factors between these two disorders may exist, with the observation of a co-transmission of both disorders more often than expected by chance alone, meaning the existence of co-aggregation. Each of these three hypotheses will be reviewed and discussed.


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