Herpes zoster myelitis occurring during treatment for systemic lupus erythematosus.

A woman with systemic lupus erythematosus (SLE) presented with a zoster eruption. Transverse myelitis developed at the site of the dermatomal distribution of the rash. SLE and varicella zoster virus (VZV) can both cause myelitis, and are difficult to differentiate. The topographic association between the cutaneous and the neurological involvement suggesting VZV myelitis was confirmed by polymerase chain reaction (PCR) for VZV in the cerebrospinal fluid. This case illustrates the potential role of the selective amplification of VZV DNA in cerebrospinal fluid to diagnose central neurological complications associated with VZV. The value of magnetic resonance imaging of the spinal cord in the evaluation of patients with myelitis is emphasized.

Expression of CD5 and CD23 on B cells of patients with rheumatoid arthritis, systemic lupus erythematosus and Sjögren's syndrome. Relationship with disease activity and treatment.

CD5+ and CD23+ lymphocytes were determined in peripheral blood of patients with rheumatoid arthritis (RA) (n = 56), systemic lupus erythematosus (SLE) (n = 20) and primary Sjögren's syndrome (pSS) (n = 21). No definite correlation between the numbers of CD5+ or CD23+ cells and most of the parameters of disease activity was found. A significant correlation (r = 0.59, p = 0.005) between rheumatoid factor levels and numbers of CD23+ cells was found in RA patients not taking disease modifying agents. For SLE and pSS no signification associations with autoantibody production were found. In conclusion, although CD5+ and CD23+ B cells might be important in the pathogenesis of autoimmune diseases, determination of these subsets in peripheral blood of RA, SLE or pSS patients provides no clear useful clinical information for the individual patient.

Significantly increased expression of T-cell activation markers (interleukin-2 and HLA-DR) in depression: further evidence for an inflammatory process during that illness.

1. Recently, the authors have reported that severe depression may be accompanied by a systemic immune activation with an increase in the number of T cells expressing activation receptors. 2. The present large-scale study examines specific T (CD2+HLADR+ and CD7+CD25+) and B (CD7-CD25+) cell activation markers in depressed inpatients and normal volunteers together with the number of leukocytes and monocytes. 3. The authors have established that depression is characterized by a significantly increased expression of T cell activation receptors (CD7+CD25+) and by the appearance of previously unexpressed T cell surface markers (CD2+HLADR+). There was a significant and positive correlation between the number of CD7+CD25+ cells and monocytes, with the expression of the HLADR and CD25 T cell activation markers being significantly and positively correlated. Up to 64% of all depressed subjects exhibit an increased expression of these activation markers with a specificity of 91%. 4. The normal control group and the depressive sample constitute two discrete classes (i.e., qualitatively distinct groups) with respect to the expression of these activation markers and leukocytosis. 5. It is concluded that our results are compatible with the presence of T-cell activation in a considerable number of depressed patients.

Leukocytosis, monocytosis and neutrophilia: hallmarks of severe depression.

To date, there has been a small number of reports that severe depression is accompanied by disturbances in total white blood cell (i.e. leukocytosis) and leukocyte subset (i.e. neutrophilia, monocytosis, lymphopenia) counts. These results, however, have not yet been validated in a large-scale, well-controlled study. To this end, we have counted the number of leukocytes, monocytes, lymphocytes and granulocytes (neutrophils, eosinophils, basophils) in 22 healthy controls and in 109 depressed inpatients. We noted leukocytosis in major depressed patients compared with normal subjects, whilst minor depressives manifested intermediate findings. Leukocytosis was significantly more pronounced in major depressed males compared with major depressed females. Major depression related leukocytosis appears to be characterized by neutrophilia and monocytosis. There was a significant positive relationship between the overall severity of illness on one hand, and the degrees of leukocytosis, neutrophilia and monocytosis on the other. The total number of both phagocytic cell populations (i.e. monocytes and neutrophils) was significantly and positively related. Our results might point to the existence of an inflammatory process in major depressed subjects, particularly in males.

A significantly increased number and percentage of B cells in depressed subjects: results of flow cytometric measurements.

Recently, there have been some reports that depression may be accompanied by indices of polyclonal B cell proliferation. In order to examine whether depression is characterized by an altered B cell subset profile we determined the number and percentage of the following B cells: HLADR+, CD19+, CD20+, and CD21+. We found a significantly increased number of HLADR+ and CD19+ B cells in depressed subjects compared with normal controls. Depressed patients exhibited a significantly higher percentage of HLADR+ and CD21+ B cells than normal controls. The number of CD21+ cells and the percentage of CD19+ cells were higher in melancholics than in normal controls. The increase in the number of the various B cells was highly sensitive (63%) and specific (94%) for melancholia. Our results may indicate B cell proliferation in depression, and particularly in melancholia.