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Letters: CD4+ Lymphocytopenia in Systemic Lupus Erythematosus
- Michael Guma, DO; and
- Randal Krakauer, MD
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TO THE EDITOR:
We read with great interest Laurence's review [1] on CD4+ T-lymphocytopenia. We report a case of CD4+ lymphocytopenia in a young woman with systemic lupus erythematosus.
A 35-year-old white woman was seen in 1987 reporting recurrent arthralgias, rash, increased hair loss, and the Raynaud phenomena. Her physical examination showed a malar flush, the presence of herpes zoster along the lateral aspect of her abdomen, and synovitis of her wrists and ankles. Laboratory results included: a positive antinuclear antibody count (1:640 homogeneous), an erythrocyte sedimentation rate of 20 mm/h, a moderately positive double-stranded DNA, a normal C3, and a slightly low C4.
She was given hydroxychloroquine and a gradually tapering dose of prednisone, which she tolerated well. She reported frequent episodes of candidiasis and recurrent herpes zoster attacks with subsequent postherpetic neuralgia. Along with a positive double-stranded DNA, T-cell studies showed a total lymphocyte count of 396/mm3 (6.4%) (normal, 1049/mm3 to 3500/mm3 or 10% to 47%). Her CD3 count was 111/mm3 or 28% (normal, 870/mm3 to 2147/mm3 or 50% to 84%). Her CD4 counts were 20/mm3 or 5% (normal, 536/mm3 to 1571/mm3 or 31% to 59%) and her CD8 counts were 83/mm3 or 21% (normal, 235/mm3 to 753/mm3 or 12% to 3%). Her T4:T8 ratio was.24 (normal, 1.2 to 4.8). Several human immunodeficiency virus (HIV) test results were negative. Recently she presented with a cavitary lung lesion that was shown to be caused by Cryptococcus neoformans. Her CD4+ level (6 years after the initial study) is 40/mm3 and her CD8+ level is 135/mm3. Test results for HIV-1, HIV-2, and human T-cell lymphotropic virus types 1 and 2 remain negative. She continues to deny any risk factors for HIV.
Although many researchers have speculated about the cause or causes of idiopathic CD4+ T-lymphocytopenia [2-4], few have considered autoimmune diseases as a possible cause. Depletion of CD4+ cells by antilymphocytic antibodies has been described [5]. Differences in antilymphocytic antibodies could account for some of the clinical variation found in some patients with this disease.
Michael Guma, DO
Randal Krakauer, MD
Seton Hall University, School of Graduate Medical Education; South Orange, NJ 07079-2689
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
