Serum autoantibodies (autoAbs) represent the hallmark of systemic autoimmune rheumatic diseases (SARD) (1), and can be detected years before the development of clinical manifestations and diagnosis (2). Currently, a high number of autoAbs are routinely detected worldwide to assist the clinicians in the diagnosis of SARD and their importance is related to the fact that they correlate with disease phenotype and severity, independently from their frequency. However, some patients are still defined “seronegative” when no known or specific autoAb is detected (3).
Patients affected by SARD can develop various disease manifestations, which share in most cases serum ANA positivity, and they may be diagnosed as systemic sclerosis (SSc), systemic lupus erythematosus (SLE), Sjögren’s syndrome (SjS), polymyositis and dermatomyositis (PM/DM) and mixed connective tissue disease (MCTD). The clinical manifestations of SARD may also overlap in some cases (4), and the identification of serum autoAbs is of major importance not only for SARD diagnosis but also for their prognosis, as they may predict internal organ involvement and/or cancer coexistence, as for anti-TIF1γ/α in inflammatory myositis associated with cancer (5). Moreover, anti-dsDNA and anti-Sm antibodies are classic serological markers of SLE, with increased titers of anti-dsDNA associated with a more active and severe disease such as lupus nephritis (6). Anti-topoisomerase I/Scl-70 and anti-RNA polymerase I/III antibodies are both associated with diffuse scleroderma (dcSSc) with increased mortality rates due to interstitial lung disease (ILD) and renal crisis, while anti-centromere antibodies (ACA) are commonly detected in the limited cutaneous form of SSc (lcSSc), which may be related to the onset of pulmonary arterial hypertension (7).
Myositis-specific antibodies (MSA) include autoAbs directed against tRNA synthetases, anti-SRP, anti-Mi-2, and anti-TIF-1γ. Among the anti-tRNA synthetases antibodies, anti-Jo-1 is the most frequently reported and this class of autoAbs is commonly associated with the occurrence of arthritis, myositis, ILD, Raynaud’s phenomenon (RP), fever and mechanic’s hands (8).
Recently, a novel ANA specificity defined by dense fine speckled (DFS) pattern has been reported but it is now considered the most frequent ANA pattern in healthy individuals, thus it may have a protective role towards the development of SARD (9).
As described, the identification of a specific autoAb is important to define the diagnosis and the prognosis of specific SARDs such as SLE and SSc. However, the diagnosis of SARD might be challenging when clinical manifestations are weak, heterogeneous and uncommon, and in those patients without detectable autoAb, therefore patients do not fulfill classification criteria (10-13). The identification of rare or non-diagnostic serum autoAbs might be challenging as well and in most cases the search for these autoAbs cannot be performed routinely but only by research laboratories in a few centers worldwide. Furthermore, novel rare autoAbs with unknown clinical associations are detected in a small number of patients with CTD, and only few observational studies have addressed these infrequent serological markers and published data that mostly derive from single case reports. Therefore, the diagnostic and prognostic value of these markers, as well as their potential role in monitoring disease activity and predicting specific organ involvement, still remains unknown.
Systematic literature review for the identification of rare autoAbs in rheumatic diseases
Based on the principles described above, we conducted a systematic literature review to identify the prevalence and clinical significance of rare autoAbs in SARD. The systematic review procedures we adopted are in line with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (14). The structured literature research was conducted as of January 20th 2017 in the following databases: The Cochrane Library, PubMed/MEDLINE and EMBASE. Search terms included the medical subject headings (MeSH) or Emtree terms for “systemic sclerosis”, “systemic lupus erythematosus”, “sjögren’s syndrome”, “dermatomyositis”, “polymyositis”, “mixed connective tissue disease”, “connective tissue disease”, “anti-synthetase syndrome”, “autoantibodies”, “rare”, “prevalence”, and “clinical significance”. Titles and abstracts were screened to determine if they met the inclusion criteria and if they were of potential interest, then two independent reviewers (Bianca Palermo and Elena Generali) selected relevant abstracts. Articles of seminal importance were included in the final analysis.
Observational studies, case reports and clinical trials were included.
Articles not concerning SARD, and reviews or editorials in languages different from English, if including children or animals, were excluded to limit the literature review to adults and because no funding was available for translation. The selection process was performed by two authors, based on titles, abstracts and subsequently full text papers. Figure 1 represents the flowchart of the selection process of this systematic literature review.
The year of publication, study design, number of patients and demographic data were recorded. The outcome was defined by the identification of rare autoAbs and their prevalence and clinical significance in SARD. Articles were divided into categories depending on the disease.
Results of the systematic literature review
The literature search allowed us to identify articles (n=116) that are described in the Tables below, that show the prevalence and clinical significance of autoAbs in each specific SARD.
AutoAbs in SLE
SLE is a chronic systemic autoimmune disease characterized by the positivity of specific autoAbs, namely anti-dsDNA and anti-Sm, but several other rare autoAbs have been reported in association with SLE as described in Table 1. The appearance of the autoAbs in SLE has been demonstrated to start years before the clinical onset of the disease, thus autoAbs in SLE patients have are fundamental for early diagnosis and treatment (2).
Among the rare autoAbs identified in SLE patients, anti-RNP antibodies are frequently detected in SLE patients (15,19,20,22-26,28-30) with a prevalence ranging from 9.5% to 30% (15,19,20,22,24,31). They have been reported in association with neuropsychiatric SLE (NPSLE), and in case reports in association with anti-CASPR2 antibodies (32), shrinking lung syndrome (30) and Crohn’s disease (28). Anti-Ku antibodies have been detected in the sera of 18 (11.6%) African American SLE patients, while they were not found in SLE Caucasian patient (25,33). Anti-NKG2A antibodies have been detected in one patient with SLE, in particular in association with vascular involvement and deep venous thrombosis, renal involvement, progressive alveolitis and increased levels of interferon α (17). Anti-replication protein A antibodies (anti-RPA) have been found in 1.4% of SLE patients (and in 2.5% of SjS patients), with a subset of SLE without other autoAbs commonly found in SLE (27). Very high titers of antibodies to glucose-6-phosphate isomerase (anti-GPI) were reported in one patient with SLE with articular involvement (21). Anti-neuronal antibodies are being evaluated in NPSLE, i.e., anti-VGCK, CASPR2, NMDA-R, LGI1, GAD, AMA-R, GABAB-R antibodies; however, Karaaslan et al. found that, in a cohort of eighteen SLE patients with epilepsy, only one female patient had anti-GAD, one female patient with hippocampal sclerosis on magnetic resonance imaging was CASPR-2 antibody positive, whereas four female patients showed hippocampal neutrophil staining reflecting antibodies against unknown neuronal cell surface antigens (18). One case of anti-VGKC positive antibodies in a SLE patient followed by acquired neuromyotonia development was reported (29). Another autoAb described in SLE patients is represented by anti-GW182 autoAbs that have been detected in SLE and SjS patients, mostly female, and interestingly, six patients manifested neurological disease (16).
AutoAbs in SSc
Serological markers of SSc are shown in Table 2. AutoAbs to nucleolar antigens (ANoA) have been reported to occur in 8–47% of sera from patients with SSc (41,43,52), and they include PM-Scl (57), RNA polymerase I (41), Th/To (43,57,58), and small nucleolar RNP particles, such as U3 RNP/fibrillarin (51,52).
The prevalence of anti-U3 RNP/fibrillarin antibodies ranges between 1.1–18% in SSc patients, who are more likely to be African American male patients with dcSSc and younger age at disease onset (35,36,43,46,47,51-53,56,59,60). In contrast, Tormey et al. found a high proportion of Caucasian patients with lcSSc and anti-U3 RNP/fibrillarin positivity (61). In additional reports, anti-U3 RNP/fibrillarin antibodies are associated with higher prevalence of hypo/hyper- skin pigmentation (51,53), calcinosis (51), digital pitting scars and/or ulcers (51,53), digital amputation (62), myositis (47,51,60,61), PAH (51,53,61), pulmonary fibrosis (35,46,52,61), diarrhea and gastric antral vascular ectasia (GAVE) (59,62), cardiac and renal involvement (35,59,61). Arnett et al. found a significant association between anti-U3 RNP/fibrillarin and the HLA class II haplotype DRB1*1302, DQB1*0604; in addition, one or more HLA-DQB1 alleles *0604, *0301, *0602, and/or *0302 were detected in all anti-U3 RNP/fibrillarin positive patients who joined the study (35). Furthermore, anti-U3 RNP/fibrillarin may be more frequently related to the rare occurrence of SSc/ANCA-associated vasculitis (AAV) than the other scleroderma-specific antibodies. Glomerulonephritis, renal arteritis, and pulmonary fibrosis occur more frequently than expected in SSc/AAV overlap (38), and a case of nodular scleroderma with positive anti-U3RNP/fibrillarin antibodies has been reported (63,64).
Anti-RNA polymerase (RNApol) antibodies are directed towards the antigens called RNA polymerase I–III, and anti-RNApolIII antibodies are the most relevant as they have been recently included in the SSc classification criteria (65). Their identification has been possible in the past thanks to a time and labor consuming technique called “immunoprecipitation” until the late 90’s when a specific RNAP ELISA was developed and validated as described by Chang et al. (33). This allowed the large scale and rapid identification of anti-RNApol antibodies in a clinical diagnostic laboratory setting to identify SSc patients who are at risk for developing SSc with these autoAbs (66,67). Anti-RNApol antibodies are found in 1.1% to 15% of SSc patients (33,36,37,40,41,45,47,49,52,54,68) and anti-RNA polymerase I/III positive patients are more likely to develop dcSSc with pulmonary involvement, joint and tendon involvement, myositis, and a significantly increased risk of scleroderma renal crisis (33,37,40,45,47,49,50,52,62). However, patients with anti-RNA polymerase III antibodies have lower risk of gastrointestinal (GI) manifestations and esophageal dysmotility compared to patients with anti-topo I/Scl70 (40,62), as well as a lower incidence of pulmonary disease (40). A subset of anti-RNA polymerase III positive patients may have an atypical clinical presentation with the onset of scleroderma prior to Raynaud’s phenomenon (36). In 2010, Shah et al. (69) ﬁrst reported a possible association of anti-RNA polymerase I/III with the development of malignancy that occurred concomitantly to SSc onset in a small number of US patients. Subsequently, the higher frequency of synchronous cancer cases in SSc patients with anti-RNA polymerase III antibodies has been validated in independent SSc patients of European, Australian and Japanese populations (34,48,50,54).
Autoantibodies to U1RNP are commonly detected in scleroderma overlap syndromes, with frequency ranging from 4.8% to 10.7% in SSc patients (41,47). Specific autoantibodies to U5snRNP represent a rare finding (2.4%) in patients with SSc-PM overlap syndrome (31). Anti-Ku and anti-PM-Scl antibodies, when found in SSc patients (about 1.2–1.8% and 4.0–4.9%, respectively), are often related to overlap syndromes with muscular manifestations, including creatine phosphokinase (CPK) elevation (45). Antibodies to p25/p23 characterize a subset within the ACA-positive SSc patients, which is strongly associated with SjS symptoms (47). A case report of nephrotic syndrome in a patient with lcSSc and anti-ribosomal P antibodies was found (70). The association of anti-HMGCR antibodies and necrotizing autoimmune myositis (NAM) is well-known (71,72). Such autoAbs have been identified in 1.3% of SSc patients; these subjects show significantly lower levels of CPK, a higher frequency of heart involvement and pulmonary hypertension, and no history of statin use (39).
AutoAbs in polymyositis/dermatomyositis (PM/DM) and in the anti-synthetase syndrome
As described in the results shown in Table 3, anti-synthetase antibodies identified in myositis patients have a variable prevalence, and this depends on each single specificity. In particular, anti-Jo-1 antibodies have the highest prevalence ranging from 0.5% to 54.7% (82,88), while other anti-synthetase antibodies have lower prevalence, as for anti-PL-7 0.5–9.3% (82,90), anti-PL-12 1.5–19.2% (82,88), anti-OJ 0.5% (82,88), anti-EJ 1–3% (82,88). Antibodies to asparaginyl-tRNA synthetase (anti-KS) occur in 0.3–0.5% of patients with CTD—especially in Japanese patients (62.5%)—most of them presenting ILD (88%)—while an association with myositis was rarely found, as it was detected in 0% of Japanese subjects with PM/DM and in 25% of all positive patients. Interestingly, cancer history was reported in 25% of anti-KS positive patients (83), thus it may be very important to be able to identify this rare autoAb not only for diagnostic but also for prognostic evaluations. With regard to clinical manifestations, overall anti-synthetase antibodies are more frequent in female patients with diffuse cutaneous involvement similarly to limited SSc, arthralgia, joint deformities, high CK levels (88), and overlap myositis (90). Lung involvement is a common manifestation of anti-synthetase syndrome, and anti-Jo-1 antibodies have been reported in association with ILD (91,92), even though a larger study reported that anti-Jo-1 (+) patients have higher rates of myositis and arthralgia than ILD, as well as higher CK levels compared to anti-PL-12 and PL-7 (+) patients (81). Anti-synthetase antibodies have also been detected in a case of cryptogenic organizing pneumonia (93) and in association with uncommon clinical manifestations such as aphthous-like ulcerations and xerostomia (94). As for their prognostic significance, anti-PL-12 and PL-7 antibodies are related to lower survival rates (81,82), and anti-EJ antibodies have been reported in a case of fatal myocarditis in anti-synthetase syndrome (95).
Rare autoAbs reported in PM/DM patients include anti-Mi-2 (5%) 90), anti-SRP (2.8%) (90), anti-Ku (1–1.7%) (90,96) and anti-HMGCR (3%) (96,97). In particular, anti-Mi-2 and anti-SRP antibodies are more common in female patients affected by DM, while DM skin manifestations are less frequently seen in anti-Ku and anti-SRP positive patients. Anti-SRP antibodies have been associated with higher CK levels (90) in clinically relevant myositis (86), and more severe clinical symptoms, such as rapidly developing muscle weakness and atrophy, dysphagia, ILD complicated by massive pleural effusion and respiratory insufficiency (89,98-100) with poor response to immunosuppressive treatments (101).
Anti-HMGCR antibodies have been reported in several studies (77,78,102-106), in particular in association with necrotizing autoimmune myositis (NAM) (44.9%), followed by PM (4.4%) and DM (1.9%) (107). The titer of anti-HMGCR antibodies seems to correlate with CPK levels (106) and their association with statin therapy is controversial since some studies report that less than 50% of patient have used statins (77,80,97,105), while other reports suggest a strong association in a higher percentage of cases (89,104,107,108). A case of NAM associated with anti-HMGCR antibodies with severe head and neck involvement, resembling a retropharyngeal abscess, has also been reported (71).
As for anti-TIF1γ antibodies, they have been detected mainly in cases of paraneoplastic myositis associated in particular with solid tumors such as breast cancer (109), thus they have not only a diagnostic but also a prognostic value for myositis patients.
When histology is considered, anti-Mi-2 and anti-synthetase antibodies are more frequent in cases with typical DM involvement, while unspecified myositis is the most frequent pathologic finding in patients with anti-Ku antibodies, and NAM is present in 75% of anti-SRP positive subjects (90).
A distinct subset of DM, called clinically amyopathic DM (CADM), has been associated with anti-CADM-140/MDA5 antibodies which are strongly related to rapidly progressive ILD (84) and in cases of anti-CADM-140/MDA5 positive patients with idiopathic pulmonary fibrosis (110).
AutoAbs in MCTD, Sjögren’s syndrome (SjS) and other rheumatic diseases
MCTD is characterized by the overlap of SSc, SLE and RA diagnosis in the presence of autoAbs such as anti-synthetase antibodies, described in previous sections of this review. Other undefined autoAbs directed towards tRNA were identified in about 1.9% of sera from patients with SARD, and nearly all the positive sera belonged to patients affected by either SLE or SjS. Subjects with both anti-tRNA synthetase antibodies and anti-RoSSA/LaSSB (57.1%) develop annular or papulosquamous recurrent erythema in 37.5% of cases (111). Antibodies to NOR 90 were first described in a patient with SSc by Rodriguez-Sanchez et al., who identified a novel 90-kDa protein recognized by autoantibodies that selectively stained the nucleolus-organizing region (NOR) of chromosomes 13, 14, 15, 21, and 22 (112). The 90-kDa autoantigen was later shown to be identical to human upstream-binding factor (hUBF), an RNA polymerase I-specific transcription factor which plays a central role in transcriptional regulation of rRNA (113). In search for the NOR 90 specificity among 254 patients with various autoimmune rheumatic diseases, Rodriguez-Sanchez et al. concluded that anti-NOR 90 antibodies were associated with SSc. By contrast, Kipnis et al. did not detect anti-NOR 90 in sera from 112 patients with SSc (41), while Imai et al. (114) and Dick et al. (115) reported the presence of antibodies to NOR 90 in patients with heterogeneous conditions, including SSc, SLE, RA, SjS, UCTD and other non-rheumatic diseases.
Among patients with SjS, the occurrence of several rare autoAbs and uncommon clinical presentations (such as severe motor-dominant weakness in the lower extremities, depression, cerebellar ataxia) have been described, for example in a patient with anti-neuronal antibodies (116) and in a patient with antibodies to Ma2/Ta with progressive spastic paresis without evidence of cancer over a 4-year follow-up (117). One case of anti-aquaporin 4 antibodies positivity had tetraparesis due to recurrent central nervous system demyelination, together with distal renal tubular acidosis, hypokalemia, medullary nephrocalcinosis, respiratory failure, and secondary anti-phospholipid syndrome (118). Vandergheynst et al. report the occurrence of anti-PM-Scl antibodies in one patient with SjS and ILD, without features of SSc or myositis (99).
AutoAbs against the mitotic apparatus (MA) represent a subtype of ANA rarely detected in sera from patients with SARD. Different MA antigens have been identified so far: mitotic spindle apparatus (MSA), centrosome (CE), midbody (MB/MSA-2), and centromere-F (CENP-F) (119). After the description of anti-MSA antibodies by McCarty et al. in 1981 (120), two major classes were identified: autoAbs against the nuclear mitotic apparatus protein (NuMA) and the kinesin-like protein HsEg5 (121,122). Their prevalence is estimated to be less than 1%, with anti-HsEg5 being less frequently detected than anti-NuMA (123,124). Anti-mitotic spindle apparatus antibodies appear to be primarily associated with SjS, SLE and UCTD (26,121-124), and the most frequent clinical symptoms are arthralgia and sicca syndrome (26).
SARD are characterized by the presence of serum autoAbs directed against cellular components belonging to different tissues and organs, and in this view the first step to recognize the presence of an autoimmune response in a specific clinical setting is the identification of autoAbs. However, autoAbs and serum ANA are not disease specific for rheumatic diseases and they can be present also in a significant proportion of healthy people (3), as well as in other autoimmune conditions, i.e., autoimmune thyroid disease (125). AutoAbs specific for SARD have been identified and described since the 1990s, and albeit the most known (i.e., anti-dsDNA and anti-RoSSA/LaSSB), which are also included in the disease classification criteria (126,127) and easily tested in routine assays (128), many others are rare and they are not available for the routine testing. In this view, rheumatologists treating SARD should know also the prevalence and clinical associations of rare autoAbs, especially for particular rheumatic disease subsets and their possible association with malignancy (129). The results of the present systematic literature summarize the main features of rare serum autoAbs identified in SARD, as described in Tables 1-4, and a few novel findings have been identified. For example, the number of autoAbs targeting the nervous system, as well as the field of neuroimmunology, have enormously increased (131). In the present work, we have retrieved several articles regarding anti-neuronal antibodies in NPSLE (17,18,29,32), however, most of them are case reports or small case series, thus estimating the prevalence of these autoAbs remains difficult. Lastly, we confirm that an autoAb called “anti-DFS70” which stands for diffuse speckled pattern at IIF has been associated negatively with SARD, as it is more frequent in healthy subjects (73-76,132-135) and it is rare in SLE patients (132), thus maybe representing a protective pattern.
We must acknowledge that a large variability is found when searching for rare autoAbs in SARD, and additional unsolved problems are represented by the lack of validation, the small number of cases described with different prevalence in different ethnic groups and the use of different laboratory methods for autoAb identification. Further research is needed to strengthen evidence for the role of such autoAbs in the clinical assessment of specific diseases.
This project has been supported by the contribution of the Italian Ministry of Foreign Affairs (Ministero degli Affari Esteri e della Cooperazione Internazionale, Direzione Generale per la Promozione del Sistema Paese).
Conflicts of Interest: The authors have no conflicts of interest to declare.
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Cite this article as: Ceribelli A, Isailovic N, De Santis M, Generali E, Gorlino C, Palermo B, Selmi C. Clinical significance of rare serum autoantibodies in rheumatic diseases: a systematic literature review. J Lab Precis Med 2018;3:89.