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| English | English | |
| Previous Nomenclature | None | |
| Description | Discontinuous speckled or granular perinuclear ribbon-like staining with polar distribution in the cytoplasm. e.g. anti-giantin, anti-golgin-245. | |
| Antigen Association | giantin/macrogolgin, golgin-95/GM130, golgin-160, golgin-97, golgin-245 | |
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Clinical Relevance
First level information About Clinical Relevance & List of Abbreviations |
Clinical Relevance
First level information About Clinical Relevance & List of Abbreviations |
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▶ Found in small numbers of patients with a variety of conditions ▶ Antigens recognized include giantin/macrogolgin and distinct golgin molecules; specific immunoassays to detect autoantibodies directed to specific Golgi antigens are currently not commercially available (85) |
| First level information references | First level information references |
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85. Stinton LM, Eystathioy T, Selak S, et al. Autoantibodies to protein transport and messenger RNA processing pathways: endosomes, lysosomes, Golgi complex, proteasomes, assemblyosomes, exosomes, and GW bodies. Clin Immunol 2004;110:30-44. |
85. Stinton LM, Eystathioy T, Selak S, et al. Autoantibodies to protein transport and messenger RNA processing pathways: endosomes, lysosomes, Golgi complex, proteasomes, assemblyosomes, exosomes, and GW bodies. Clin Immunol 2004;110:30-44. |
| Second level information | Second level information |
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None |
▶ The AC-22 pattern has been reported in small numbers of patients with a variety of conditions, including SjS, SLE, RA, MCTD, GPA, idiopathic cerebellar ataxia, paraneoplastic cerebellar degeneration, adult Still’s disease, and viral infections including HIV and EBV (29, 36-38) ▶ Although possibly biased by the referral pattern, one study concluded that the AC-22 pattern is not clinically associated with SARD as there were only 1 SjS and 2 RA diagnoses among their 20 AC-22 positive cases collected over 10-years and a clinical follow-up observation ranging from 0 – 10 years; the remaining cases showed diverse diagnoses including 2 carcinomas (37) ▶ The AC-22 pattern is rare in the general population (39) |
| Second level information references | Second level information references |
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29. Stinton LM, Eystathioy T, Selak S, et al. Autoantibodies to protein transport and messenger RNA processing pathways: endosomes, lysosomes, Golgi complex, proteasomes, assemblyosomes, exosomes, and GW bodies. Clin Immunol 2004;110:30-44. 36. Fritzler MJ, Etherington J, Sokolu, C, et al. Antibodies from patients with autoimmune disease react with a cytoplasmic antigen in the Golgi apparatus. J Immunol 1984;132:2904-8. 37. Vermeersch P, Van den Bergh K, Blockmans D, et al. Anti-Golgi autoantibodies are not clinically associated with systemic autoimmune diseases. Ann Rheum Dis 2011;70:234-5. 38. Staub HL, Souza F, Chan EKL, et al. Anti-Golgi antibodies in adult Still's disease. Clin Exp Rheumatol 2003;21:275-6. 39. Satoh M, Chan EKL, Ho LA, et al. Prevalence and sociodemographic correlates of antinuclear antibodies in the United States. Arthritis Rheum 2012;64:2319-27. |
29. Stinton LM, Eystathioy T, Selak S, et al. Autoantibodies to protein transport and messenger RNA processing pathways: endosomes, lysosomes, Golgi complex, proteasomes, assemblyosomes, exosomes, and GW bodies. Clin Immunol 2004;110:30-44. 36. Fritzler MJ, Etherington J, Sokolu, C, et al. Antibodies from patients with autoimmune disease react with a cytoplasmic antigen in the Golgi apparatus. J Immunol 1984;132:2904-8. 37. Vermeersch P, Van den Bergh K, Blockmans D, et al. Anti-Golgi autoantibodies are not clinically associated with systemic autoimmune diseases. Ann Rheum Dis 2011;70:234-5. 38. Staub HL, Souza F, Chan EKL, et al. Anti-Golgi antibodies in adult Still's disease. Clin Exp Rheumatol 2003;21:275-6. 39. Satoh M, Chan EKL, Ho LA, et al. Prevalence and sociodemographic correlates of antinuclear antibodies in the United States. Arthritis Rheum 2012;64:2319-27. |
| FAQ |
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How to deal with just a “nuclear speckled” IFA report? In my practice I have followed patients with ANA findings, with a nuclear speckled pattern (without specifying whether fine/dense/coarse), in patients with very heterogeneous phenotypes, some with a clinical picture that suggests further investigation of systemic autoimmune disease (one patient with proximal muscle weakness and skin thickening) and others who represent only non-specific findings. In such situations, as a precaution, I request more specific autoantibodies. However, this pattern (nuclear speckled pattern) is not described by the "ICAP" and I am in doubt about which antigenic association it represents, even to guide which autoantibody may be present and which ones to look after. How to interpret this pattern? Does the lab describe it when it is not possible to "refine" such a conclusion? Could this be associated with deficiency in the methodology, sample, interpretation? |