LETTER N. Giordano Æ B. Lucani Æ A. Amendola Æ S. Geraci C. Santacroce Æ C. Gennari Æ G. Hartini Æ R. Nuti IgG and IgM antiganglioside M1 antibodies in primary Sjogren’s syndrome with and without peripheral neuropathy Received: 5 August 2002 / Accepted: 15 November 2002 Ó Clinical Rheumatology 2003 Introduction Gangliosides are a diverse class of glycolipids (GM1,GD1a, GD1b and GT1b) evidenced in the plasma membrane of mammalian cells and particularly abundant in the cells of the nervous system [1, 2]. Among others, the ganglioside M1 (GM1) is amply represented in neuronal membrane, where it enhances neurite outgrowth and recovery from injury [1]. Serum antiganglioside antibodies (AGA) have been detected in many central and peripheral neurological diseases [1, 2], and in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) [3–5] when complicated by pe- ripheral neuropathy. In these conditions, anti-GM1 AGA seem to play a pathogenic role in the develop- ment of the inflammatory demyelinating process [2]. Although peripheral sensorimotor neuropathy is a rather frequent neurological manifestation of primary Sjogren’s syndrome (pSS) [6], few authors [7, 8] have investigated the possible pathogenetic role of anti-GM1 AGA in this condition: Moreover, these studies inves- tigated IgM isotype anti-GM1 AGA alone. Therefore, we evaluated IgG and IgM isotypes anti-GM1 AGA in 30 outpatients affected by pSS [9], examined consecu- tively in the Department of Internal Medicine of the University of Siena, in a period ranging from 1999 to 2001. Of these 30 pSS patients, 15 were affected by peripheral sensorimotor neuropathy (PN), diagnosed clinically and by electromyography [10]. The patients, correctly informed, expressed their written consent. As a control group, we selected 30 age- and sex-matched subjects from among the paramedical and medical staff of the above-mentioned department. No patient or control manifested signs or symptoms suggestive of other neurological disorders. IgG and IgM anti-GM1 AGA were dosed by a commercial kit based on an enzyme-linked immunosorbent assay technique (anti- GM1 autoantibodies EIA, Buhlmann Laboratories AG, Postfach, CH-4123 Allschwil 1, Switzerland), re- cently validated in the literature [11, 12]. Moreover, erythrocyte sedimentation rate (ESR) (Westergren method), rheumatoid factor (RF) (latex test, positive >1:80), cryoglobulins (serum samples obtained at 37°C, cryoglobulins estimated by centrifugation after incubation at 4°C for 7 days), immunoglobulins, C3 and C4 (nephelometry technique), antinuclear anti- bodies (ANA, positive >1:80) (IFI technique), and anti-Ro (SS-A) and anti-La (SS-B) (counterimmuno- electrophoresis) were evaluated in patients and con- trols. The statistical analysis was performed using Student’s t-test, and Pearson’s correlation coefficient. Table 1 shows: the patients’ and control subjects’ clinical characteristics; serum IgG and IgM anti-GM1 AGA titres; and the other laboratory parameters (both expressed as percentages); and IgG and IgM anti-GM1 AGA serum titres in the different populations. IgG and IgM anti-GM1 AGA appeared increased with respect to normal values in pSS patients, whereas they re- mained normal in controls. IgG anti-GM1 AGA were increased in five (16.6%) of the 30 pSS patients, two (13%) without PN and three (20%) with PN. IgM anti- GM1 AGA were increased in seven (23.3%) of the 30 pSS patients: four (26.6%) without PN and three (20%) with PN. A statistically significant difference (P< 0.001) was found when comparing total anti- GM1 AGA, and IgG and IgM anti-GM1 AGA taken one by one, between the pSS group and the control group. Both IgG and IgM anti-GM1 AGA increased in 12 (40%) of the 30 pSS patients: six (40%) without PN and six (40%) with PN. Comparing both IgG and IgM AGA, and IgG or IgM AGA taken one by one, no significant difference was found between the pSS pa- tients without PN and those with PN. Lastly, no cor- relation was evidenced either between PN on the one Clin Rheumatol (2003) 22: 256–258 DOI 10.1007/s10067-003-0709-2 N. Giordano (&) Æ B. Lucani Æ A. Amendola Æ S. Geraci C. Santacroce Æ C. Gennari Æ G. Hartini Æ R. Nuti Department of Internal Medicine, Viale Bracci 1, 53100 Siena, Italy e-mail: giordanon@unisi.it Tel.: +39577-233383 Fax: + 39577-233446