Active psoriasis and profound CD4<sup>+</sup>
 lymphocytopenia

Hardman, Catherine; Baker, Barbara S.; Lortan, J.; Breuer, Judith; Surentheran, T.; Powles, A.V.; Fry, Lionel

doi:10.1046/j.1365-2133.1997.01802.x

Cited by 11 publications

(2 citation statements)

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“…Only English language papers were reviewed. We found 258 cases diagnosed with ICL in 143 published papers[134567891011121314151617181920212223242526272829303132333435363738394041424344454647484950515253545556575859606162636465666768697071727374757677787980818283848586878889909192939495969798…”

Section: Methodsmentioning

confidence: 99%

Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections, malignancies, and autoimmune diseases

2013

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Idiopathic CD4 lymphocytopenia (ICL) was first defined in 1992 by the US Centers for Disease Control and Prevention (CDC) as the repeated presence of a CD4+ T lymphocyte count of fewer than 300 cells per cubic millimeter or of less than 20% of total T cells with no evidence of human immunodeficiency virus (HIV) infection and no condition that might cause depressed CD4 counts. Most of our knowledge about ICL comes from scattered case reports. The aim of this study was to collect comprehensive data from the previously published cases to understand the characteristics of this rare condition. We searched the PubMed database and Science Direct for case reports since 1989 for Idiopathic CD4 lymphocytopenia cases. We found 258 cases diagnosed with ICL in 143 published papers. We collected data about age, sex, pathogens, site of infections, CD4 count, CD8 count, CD4:CD8 ratio, presence of HIV risk factors, malignancies, autoimmune diseases and whether the patients survived or died. The mean age at diagnosis of first opportunistic infection (or ICL if no opportunistic infection reported) was 40.7 ± 19.2 years (standard deviation), with a range of 1 to 85. One-sixty (62%) patients were males, 91 (35.2%) were females, and 7 (2.7%) patients were not identified whether males or females. Risk factors for HIV were documented in 36 (13.9%) patients. The mean initial CD4 count was 142.6 ± 103.9/mm3 (standard deviation). The mean initial CD8 count was 295 ± 273.6/mm3 (standard deviation). The mean initial CD4:CD8 ratio was 0.6 ± 0.7 (standard deviation). The mean lowest CD4 count was 115.4 ± 87.1/mm3 (standard deviation). The majority of patients 226 (87.6%) had at least one infection. Cryptococcal infections were the most prevalent infections in ICL patients (26.6%), followed by mycobacterial infections (17%), candidal infections (16.2%), and VZV infections (13.1%). Malignancies were reported in 47 (18.1%) patients. Autoimmune diseases were reported in 37 (14.2%) patients.

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Section: Methodsmentioning

confidence: 99%

Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections, malignancies, and autoimmune diseases

2013

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“…Psoriasis and PsA are known to occur despite a deficiency in CD4 T cells undermining a pivotal pathogenic role for CD8 lymphocytes. In fact, active chronic plaque psoriasis has been reported in a patient with profound CD4 lymphocytopenia [41] and psoriasis and PsA also occur with greater frequency and severity in HIV-positive patients [42]. The development of Koebner-induced psoriatic lesions correlated with invasion of CD8 T cells into the epidermis [43].…”

Section: Psoriatic Arthritismentioning

confidence: 97%

T-cell studies in the spondyloarthropathies

Märker‐Hermann

Schwab

2000

Curr Rheumatol Rep

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A growing body of evidence suggests that T lymphocytes play an important role in initiating and maintaining the inflammatory process characteristic of the human leukocyte antigen (HLA)-B27-associated spondyloarthropathies. T cells seem to be involved in the primary defense reaction against arthritis-triggering gram-negative bacteria at the site of extra-articular infection, in determining the systemic cytokine pattern, in the recirculation process between gut mucosa and the joint, and in mediating secondary autoimmune joint inflammation. The factors involved in disease chronicity (namely in ankylosing spondylitis and psoriatic arthritis) are still unknown. Autoreactive T cells may contribute to this process by recognition of cross-reactive self-epitopes (ie, molecular mimicry between bacterial and self-antigens). Autoreactive T cells may as well be inappropriately upregulated by bacterial superantigens, or by local inflammatory reactions leading to the uncovering of former cryptic self-epitopes. In this paper, we review recent studies on peripheral blood and synovial T cells in patients with reactive arthritis, enteropathic spondyloarthropathy, psoriatic arthritis, and ankylosing spondylitis.

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