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This is an old revision of this page, as edited by Schaffm (talk | contribs) at 17:21, 9 February 2016 (Added a draft of a new lead section for the article, as well as a plan for improving other sections). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.
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seriously poor quality

This article needs urgent refresh. Most of the information is inaccurate (20-30 subtypes, not 150; pathophysiology not correctly characterised; subtypes not helpfully identified; signs and symptoms should be separated from diagnostic critters) and/or uncited. DavidWaldock (talk) 16:47, 19 August 2011 (UTC)[reply]

Comments

The article presently neglects to mention whether the ID is cellular, humoral or both. There could also be a bit more about the research so far - clearly several subtypes can be mentioned now. JFW | T@lk 15:28, 27 October 2005 (UTC)[reply]

I've tried to find an easily accessible review article on this condition. Most are not available in free fulltext, apart from a Brazilian one[1]. There are a lot of disease associations and phenomena, such as granulomatous disease, autoimmune diseases, malignancies and others. To get this article up-to-date we need a few good sources. JFW | T@lk 23:12, 27 October 2005 (UTC)[reply]
Interesting addition about the CA, and not something I've come across. I shall consult other patients to find out what their experiences are in relation to it. DavidWaldock 07:39, 28 October 2005 (UTC)[reply]

Informal research

The article states that EBV is implicated in the pathogenesis of some types of CVID "by some informal research"... what is informal research? Is is a euphemism for alternative quakery? --211.30.119.171 11:48, 17 May 2006 (UTC)[reply]

Currently there is no reference for transient hypogammaglobulinemia of infancy or THI. User: gatos 02:34, 31 March 2007

Subtypes

doi:10.1182/blood-2007-06-091744 - might there be subtypes of CVID? JFW | T@lk 16:47, 23 December 2007 (UTC)[reply]

doi:10.1182/blood-2007-11-124545 - there might indeed. JFW | T@lk 21:07, 7 July 2008 (UTC)[reply]

doi:10.1016/S0140-6736(08)61199-X - recent Lancet review. This page is now a real candidate for updating. JFW | T@lk 20:27, 27 August 2008 (UTC)[reply]

doi:10.1111/j.1365-2141.2009.07669.x - Br J Haem review. Even more important that we hack at this page at some point. JFW | T@lk 23:10, 3 June 2009 (UTC)[reply]


New Lead Section

This is a draft of a new lead section for the CVID page. I plan on updating information in the rest of existing article, specifically focusing on the epidemiology, history, and research sections, which contain very minimal information. I also plan to add relevant pictures (for example, of B cells, inflammed gut, picture of diseased lung).

Common Variable Immunodeficiency (CVID) is an immune disorder characterized by recurrent infections and low antibody levels, specifically in immunoglobulin (Ig) types IgG, IgM and IgA.[1] It is thought to infect between 1 in 25,000 to 1 in 50,000 people worldwide. CVID is a rare primary immunodeficiency, and can take many forms due to the diverse ways in which antibody production can be impaired.[2] Generally, CVID symptoms include high susceptibility to foreign invaders, chronic lung disease, and inflammation and infection of the gastrointestinal tract.[1] However, symptoms vary greatly, making the disease not only phenotypically heterogeneous, but also hard to diagnose, taking on average 6-7 years after onset.[3] [2]

CVID is a lifelong disease, but its origin is poorly understood. Current research points to particular genetic markers, like deletions in the CD19, CD20, CD21, and CD80 genes, as likely sources of the disease.[2] Additionally, the disease is defined by T cell defects, namely reduced proliferative capacity.[4] CVID is formally diagnosed by levels of IgG and IgA less than two standard deviations from the mean for age and no other cause for hypogammaglobulinemia, an abnormally low level of immunoglobulins in the blood.

CVID was first diagnosed over 60 years ago, and since has emerged as the predominant class of primary antibody deficiencies. Treatment options are limited, and usually include life-long immunoglobulin replacement therapy.[3] This therapy is thought to help reduce bacterial infections. This treatment alone is not wholly effective, and many patients still experience inflammatory symptoms and the potential to develop cancer. Current research is aimed at studying large cohorts of CVID patients in an attempt to better understand age of onset, as well as mechanism, genetic factors, and progression of the disease.[2]


Potential Sources

Some creditable sources to help improve this article:

Source list for Common Variable Immunodeficiency

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[6]

[7]

[8]

  1. ^ a b "Common Variable Immune Deficiency". Genetics Home Reference. Retrieved 8 February 2016.
  2. ^ a b c d Abbott, Jordan K.; Gelfand, Erwin W. (2015). "Common Variable Immunodeficiency: Diagnosis, Management, and Treatment". Immunol Allergy Clin N Am. 35: 637–658. Retrieved 8 February 2016.
  3. ^ a b Resnick, Elena S.; Cunningham-Rundles, Charlotte (2012). "The many faces of the clinical picture of common variable immune deficiency". Current Opinion. 12 (6): 595–601.
  4. ^ Stober, Warren; Chua, Kevin (2000). "Common Variable Immunodeficiency". Clinical Reviews in Allergy and Immunology. 19: 157–181. {{cite journal}}: |access-date= requires |url= (help)
  5. ^ Strober, Warren; Chua, Kevin (2000). "Common Variable Immunodeficiency". Clinical Reviews in Allergy and Immunology. 19 (2): 157–181. Retrieved 30 January 2016.
  6. ^ "Common variable immune deficiency". Genetics Home Reference. Retrieved 30 January 2016.
  7. ^ Schwartz, Robert A; Modak, Rohit M; Modak, Prema. "Common Variable Immunodeficiency". Medscape. Retrieved 30 January 2016.
  8. ^ Yazdani, Reza; Fatholahi, Maryam; Ganjalikhani-Hakemi, Mazdak; Abolhassani, Hassan; Azizi, Gholamreza; Hamid, Kabir Magaji; Rezaei, Nima; Aghamohammadi, Asghar (2015). "Role of apoptosis in common variable immunodeficiency and selective immunoglobulin A deficiency". Molecular Immunology. 71 (2016): 1–9. doi:10.1016/j.molimm.2015.12.016.