Background Hairy cell leukemia (HCL) and hairy cell leukemia variant (HCLv) are rare diseases with overlapping clinicopathological features. Features distinguishing HCL from HCLv include expression of CD25, CD123, CD200, annexin‐A1, and the presence of BRAF V600E mutation. HCLv typically lacks these markers, but they may occur in a subgroup of HCL patients with an aggressive clinical course. We examined CD43, CD81, CD79b, and CD200 expression in HCL and HCLv. Methods Multiparametric flow cytometry (FCM) was performed on blood from 59 HCL and 15 HCLv patients for protocol entry. Mean fluorescent intensity (MFI) of CD43, CD79b, CD81, and CD200 was determined (for CD200, n = 17 and 7, respectively). Results Median MFI of HCL vs HCLv was 545 vs 272 for CD43, 602 vs 2,450 for CD81, 4,962 vs 1,969 for CD79b, and 11,652 vs 1,405 for CD200, respectively. Analysis of the median differences, HCL minus HCLv (and their 95% confidence intervals and P‐values) indicated that CD43 MFI (estimated median difference (95% CI): 212 [72–413; P = 0.0027) and CD200 MFI (9,883 [3,514–13,434]; P < 0.0001) were higher in HCL than in HCLv, while CD81 MFI (−1,858 [−2,604 to −1,365]; P < 0.0001) was lower in HCL than in HCLv. CD79b MFI HCL median was more than double that of HCLv, but the observed difference (1,571 [−739 to 4,417]) was consistent with the null hypothesis of no difference (P = 0.13). Conclusions CD200, CD43, and CD81 are likely differentially expressed between HCL and HCLv, reflecting their differing disease biology. Inclusion of these markers in FCM is potentially informative. © 2019 International Clinical Cytometry Society

We used a liposome lysis assay to measure antibodies against a panel of glycolipids. Antibodies to one or more compounds were detected in 34 of 46 patients with multiple sclerosis, 19 of 31 patients with systemic lupus erythematosus (SLE), and in the majority of patients with cranial trauma or cerebrovascular accidents. Antibodies against ganglioside GM1 and asialo GM1 were found most commonly, and they were frequently present in the same sera. The specificity of the antibodies was tested in four sera that contained antibodies to both glycolipids. The anti-GM1 antibodies cross-reacted with asialo GM1, but the converse was not true. Among patients whose sera contained antibodies to glycolipids, anti-asialo GM1 alone was more common in patients with SLE (7 of 17) than in multiple sclerosis (2 of 34; p = 0.004). Anti-GM1 alone was found in 9 of 34 patients with multiple sclerosis and 1 of 17 patients with SLE, a difference that was not statistically significant (0.135). No correlation was observed between the presence of anti-glycolipid antibodies and symptoms related to the nervous system in patients with SLE. Because of our inability to detect these antibodies by a solid phase immunoassay (ELISA), a comparison was made of the titers obtained with three monoclonal anti-glycolipid antibodies in the liposome lysis assay and ELISA. The ELISA was less sensitive in all instances, requiring from four to 1000 times as much antibody as the liposome lysis assay to give a positive test. We conclude that antibodies to glycolipids occur frequently in patients with multiple sclerosis, SLE, major cranial trauma, and cerebrovascular accidents. Their role in the initiation or perpetuation of inflammatory disease of the central nervous system has yet to be determined.

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