ATTENTION! Starting from October 2021, a new medical center will open for you at the address: Dmitrovskoye Shosse, 81 (5 min. walk from the Selegerskaya metro station), where you can receive a wide range of medical services, including CT (computer tomography).
- home
- Analyzes
- Autoimmune analysis
Systemic diseases are illnesses that affect the entire body. Such diseases, as a rule, are autoimmune in nature, which is why they are called systemic autoimmune diseases.
Autoimmune diseases are a consequence of improper functioning of the human immune system. The immune system, by its nature, is the protector of our body; when cells in the body become infected or modified, becoming a threat to health, the immune system must destroy the threat that has arisen. However, it happens that a malfunction occurs in the body, and the immune system does not recognize healthy cells and begins to destroy them, considering them dangerous. The process of self-destruction begins, which becomes the cause of many autoimmune diseases.
Description
Synonyms (rus): Antifilaggrin antibodies, AFA, antiperinuclear factor, ACE.
Synonyms (eng): Anti-filaggrin antibodies, AFA, antiperinuclear factor, APF.
Biomaterial: Venous blood
Indicator(s): Antifilaggrin autoantibodies to stratified squamous epithelium of the rat esophagus
Method(s): Indirect immunofluorescence reaction
Container type and preanalytical features: Biochemical tube with coagulation activator, 6 ml (red or brown cap)
Antiperinuclear factor (ACE) is one of the autoantibodies directed against citrullinated proteins. ACEs, like antikeratin antibodies, bind filaggrin, or rather its predecessor, profilaggrin. Citrullinated profilaggrin is part of keratin during the assembly process. Citrullinated proteins are recognized as antigens by the human immune system. Normally, citrulline is not present in proteins, and the citrullination reaction is necessary for cell differentiation and apoptosis. It is likely that in rheumatoid arthritis (RA), normal apoptotic processes are disrupted and citrulline accumulates in the synovium. ACE is detected by the reaction of indirect immunofluorescence in keratohyaline granules around the cell nuclei of the human cheek epithelium, and the luminescence of characteristic perinuclear (3-8 per cell) granules is determined.
What does a comprehensive range of diagnostics provide?
Getting tested for autoimmune diseases in our clinic means getting the following benefits:
- the presence of autoantibodies in the body, since their occurrence is associated with the degree of the disease. This stage allows you to make a prognosis for the patient and find out the likely clinical manifestations;
- assess immunity and determine a further treatment program;
- determine the appearance of subsequent autoantibodies;
- receive professional advice and a program for a course of treatment;
- determine the amount of various antibodies (reactive protein, which may indicate infection, malignancy, inflammatory processes or allergies, rheumatoid factor, an increased level of which may be an indicator of arthritis, viral infections and other diseases;
Tests for autoimmune diseases also determine the amount and ratio of other antibodies, which make it possible to make a diagnosis, identify the cause of a particular disease and prescribe the most effective treatment. There are a lot of autoimmune diseases, so the process of deciphering and recognizing analysis results is work that should be entrusted exclusively to qualified, experienced and responsible specialists. After all, the patient’s life depends on the quality of the procedure performed, the experience and professionalism of the specialist, namely, the accuracy of the results and the ability to create an effective treatment program for autoimmune diseases with an individual approach. KDS Clinic - help from real professionals and new generation techniques.
Interpretation
The detection of ACE correlates with the severity of RA disease. Thus, in the presence of ACE, the disease activity is higher, the course is more aggressive, articular syndrome and resistance to therapy are more pronounced. The incidence of ACE in RA varies, according to various sources, from 30 to 80%, but the specificity is quite high and can reach 90%. In addition, antifilaggrin antibodies are used as an independent serological marker of RA, since its titer does not correlate with the concentration of other antibodies in RA. A positive test result highly likely suggests the possibility of RA, but cannot be assessed separately from the clinical picture, since in rare cases (no more than 10%) it can be found in clinically healthy people, as well as in patients suffering from other autoimmune pathologies. A negative test result does not exclude the diagnosis of RA.
Angiotensin Converting Enzyme (ACE)
Angiotensin-converting enzyme (ACE) is normally produced in the epithelial cells of the lungs and is detected in small quantities in the blood vessels and kidneys. It promotes the conversion of angiotensin I into the powerful vasoconstrictor angiotensin II, which constricts blood vessels, which causes an increase in blood pressure.
In sarcoidosis, the level of ACE in the blood increases significantly and correlates with the activity of the pathological process. It is believed that in this case, ACE is produced in increased quantities by epithelioid cells of nodular inflammatory formations - granulomas.
Sarcoidosis is a systemic disease of unknown etiology, the characteristic feature of which is the formation of granulomas in various organs and tissues. The lymph nodes, lungs, liver, skin, and eyes are mainly affected. The disease is observed more often at the age of 20-40 years and is often asymptomatic, being detected during a preventive X-ray examination of the lungs.
The clinical picture of sarcoidosis depends on the duration of the process, the location and extent of the lesion, and the activity of the granulomatous process. Symptoms are often nonspecific: fever, malaise, weight loss, swollen lymph nodes, joint pain. When the lungs are affected, shortness of breath, dry cough, and chest pain occur. Nodular and diffuse-infiltrative changes are possible on the skin. When the eyes are affected - uveitis - there is redness and a burning sensation in the eyes, and photosensitivity. Considering the possible multiple organ damage in sarcoidosis and the similarity of the clinical picture with many diseases of various etiologies (tuberculosis, neoplasms, bacterial and some fungal infections, pneumoconiosis, systemic autoimmune diseases), correct differential diagnosis is very important in making an accurate diagnosis.
Abnormal secretion of ACE leads to an increase in its concentration not only in the blood, but also in the cerebrospinal fluid and bronchoalveolar lavage.
An increase in serum ACE level by more than 60% has diagnostic significance. This parameter may correlate with the total number of granulomas in the patient’s body. The specificity of this test is more than 90%, sensitivity is 55-60%. During the active phase of sarcoidosis, ACE levels may more than double. ACE remains at a normal level in other diseases with lung lesions (tuberculosis, lymphogranulomatosis). During dynamic observation, a decrease in ACE levels during treatment indicates the effectiveness of therapy and is a good prognostic sign. What is the research used for:
- Diagnosis of sarcoidosis.
- Differential diagnosis of diseases clinically similar to sarcoidosis.
- Assessment of disease activity.
- Monitoring the course of sarcoidosis.
- Evaluation of the effectiveness of treatment for sarcoidosis.
When a study is ordered:
- If there are clinical signs of probable sarcoidosis in patients aged 20-40 years: granulomas in organs and tissues, chronic dry cough, red eyes, joint pain, fever, weight loss, enlarged lymph nodes.
- If changes in the structure of the lungs, similar to sarcoidosis, are detected during an x-ray examination.
- When monitoring the course of the disease.
- In the treatment of sarcoidosis.
What can influence the result:
- In children, adolescents and young adults under 20 years of age, ACE levels are normally elevated. In 5% of healthy adults, enzyme activity in the blood can be increased without any signs of disease.
- Medicines that increase the level of ACE in the blood: nicardipine, triiodothyronine (T3).
- Medicines that reduce the level of ACE in the blood: ACE inhibitors (benazepril, captopril, lisinopril, perindopril, ramipril, fosinopril, cilazapril, enalapril), magnesium sulfate, prednisolone, propranolol.
Important Notes:
- ACE is not a particularly specific marker of sarcoidosis. An increase in ACE levels without other signs of sarcoidosis activity cannot be a criterion for initiating treatment. Also, a separate increase in ACE is not a reliable sign of sarcoidosis. A normal ACE level in the presence of granulomas in tissues does not exclude sarcoidosis.
- The final diagnosis is established based on taking into account all the data from the clinical, laboratory and instrumental examination and the results of pathohistological examination of the granuloma biopsy.
Bibliography
- Maslyansky A.L., Lapin S.V., Ilivanova E.P., Mazurov V.I., Totolyan A.A. Antikeratin antibodies and antiperinuclear factor are markers of the aggressive course of rheumatoid arthritis, St. Petersburg PO RAAKI, Medical Immunology, 2003; 5-6(5), p559-608
- Abedian Z, Sagafi M, Kenari SA, Abedian F. Anti-perinuclear Factor as Diagnostic Marker in Rheumatoid Arthritis. J Clin Diagnosis Res. 2015;9(9):OC13–OC16.
- Paimela L, Gripenberg M, Kurki P, Leirisalo-Repo M. Antikeratin antibodies: diagnostic and prognostic markers for early rheumatoid arthritis. Ann Rheum Dis. 1992 Jun;51(6):743-746.
- Sebbag M, Simon M, Vincent C, Masson-Bessière C, Girbal E, Durieux JJ, Serre G. The antiperinuclear factor and the so-called antikeratin antibodies are the same rheumatoidarthritis-specific autoantibodies. J Clin Invest. 1995 Jun;95(6):2672-9.
- Aletaha D. et al. 2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/EuropeanLeague Against Rheumatism collaborative initiative. Ann Rheum Dis. 2010 Sep;69(9):1580-8.
- Lapin S.V. Totolyan A.A. Immunological laboratory diagnostics of autoimmune diseases / Publishing house "Man", St. Petersburg - 2010.
- 7.. Nasonov E.L., Aleksandrova E.N. Modern standards of laboratory diagnosis of rheumatic diseases. Clinical recommendations / BHM, M - 2006.
Price for autoimmune tests
MARKERS OF AUTOIMMUNE DISEASES | price, rub. |
Systemic rheumatic diseases | |
Antinuclear factor on the HEp-2 cell line (ANF) | 1890 |
Antibodies to extractable nuclear antigen (ENA/ENA-screen) | 1890 |
Antibodies to nuclear antigens (ANA) | 1215 |
Antibodies to double-stranded DNA (native, a-dsDNA) | 1080 |
Antibodies to single-stranded DNA (a-ssDNA) | 1080 |
Antinuclear antibodies, immunoblot (IgG autoantibodies to 14 different antigens: nRNP/Sm, Sm, SS-A (SS-A native and Ro-52), SS-B, Scl-70, Jo-1, PM-Scl, protein B centromere, PCNA, dsDNA, nucleosomes, histones, ribosomal protein P, AMA-M2) | 4860 |
Antibodies for polymyositis, immunoblot (Mi-2, Ku, Pm-Scl100, Pm-Scl75, SPR, Ro-52, Jo-1, PL-7, PL-12, EJ, OJ) | 5400 |
Detailed serological examination for polymyositis (ANF on Hep-2 cells, ENA-screen, immunoblot of autoantibodies for polymyositis) | 8100 |
Autoimmune neurological diseases | |
Antibodies to myelin | 2700 |
Anti-skeletal muscle antibodies (ASM) | 2862 |
Antibodies to aquaporin -4 | 4590 |
Antibodies to acetylcholine receptors (AChR) | 7560 |
Antibodies to NMDA-type glutamate receptor | 4590 |
Antibodies for paraneoplastic syndromes, immunoblot (to Yo-1, Hu, Ri, CV2, Ma2, amphiphysin) | 10665 |
Antiphospholipid syndrome (APS) | |
Antibodies to phospholipids (cardiolipin, phosphatidylserine, phosphatidylinositol, phosphatidylic acid), total | 1215 |
Antibodies of the IgM class to phospholipids (cardiolipin, phosphatidylserine, phosphatidylinositol, phosphatidylic acid) | 1296 |
IgG antibodies to phospholipids (cardiolipin, phosphatidylserine, phosphatidylinositol, phosphatidylic acid) | 1296 |
Antibodies to cardiolipin (total) | 1080 |
Antibodies to cardiolipin, IgM | 1134 |
Antibodies to cardiolipin, IgG | 1134 |
Antibodies to beta2-glycoprotein | 1215 |
Antibodies to beta-2-glycoprotein, IgM | 1215 |
Antibodies to beta-2-glycoprotein, IgG | 1215 |
Antibodies to phosphatidylserine-prothrombin, total (IgM, G) | 1620 |
Antibodies to annexin V class IgM | 2430 |
Annexin V IgG antibodies | 2430 |
Antibodies to platelets, IgG class | 1998 |
Diagnosis of arthritis | |
Antibodies to cyclic citrullinated peptide (ACCP, anti-CCP) | 1350 |
Anti-citrullinated vimentin antibodies (anti-MCV) | 1701 |
Antikeratin antibodies (AKA) | 2430 |
Autoimmune kidney damage and vasculitis | |
Antibodies to glomerular basement membrane (GBM) | 2160 |
Antineutrophil cytoplasmic antibodies, IgG (ANCA), Combi 6 | 1755 |
Antibodies to vascular endothelial cells (HUVEC) | 1755 |
Antibodies to complement factor C1q | 1620 |
Autoimmune liver lesions | |
Antibodies to mitochondria | 1188 |
Antismooth muscle antibodies (ASMA) | 1620 |
Antibodies to the microsomal fraction of the liver and kidneys (anti-LKM) | 1215 |
Antibodies to liver antigens, immunoblot (IgG autoantibodies to 4 different antigens: pyruvate dehydrogenase complex (M2), liver and kidney microsomes (LKM-1), cytosolic liver antigen type 1 (LC-1), soluble liver antigen/liver and pancreas antigen glands (SLA/LP)) | 2160 |
Autoimmune lesions of the gastrointestinal tract and celiac disease | |
Antibodies to gastric parietal cells (APCC) | 2430 |
Determination of antibodies to f.Kastla - internal factor (AVF) | 1890 |
Determination of IgG4 subclass content | 2160 |
Antibodies to intestinal goblet cells (GBC) | 2700 |
Antibodies to the yeast Saccharomyces cerevisiae (ASCA), IgA | 1418 |
Antibodies to the yeast Saccharomyces cerevisiae (ASCA), IgG | 1418 |
Antibodies to gliadin, IgA | 1256 |
Antibodies to gliadin, IgG | 1256 |
Antibodies to deaminated alpha-gliadin peptides IgA (AAG) | 2295 |
Antibodies to deaminated alpha-gliadin IgG peptides (AAG) | 2295 |
Antibodies to tissue transglutaminase, IgA | 2025 |
Antibodies to tissue transglutaminase, IgG | 2025 |
Antibodies to endomysium, IgA (AEA) | 1895 |
Antireticulin antibodies (APA) | 1418 |
Autoimmune diseases of the lungs and heart | |
Diagnosis of sarcoidosis (angiotensin-converting enzyme (ACE) activity) | 3537 |
Antibodies to myocardium (Mio) | 2295 |
Antibodies to skin desmosomes | 3915 |
Antibodies to the basement membrane of the skin (AMB) | 2835 |
Autoimmune endocrinopathies and autoimmune infertility | |
Anti-islet cell antibodies (ICA) | 2565 |
Antibodies to glutamate decarboxylase (GAD) | 3780 |
Insulin Antibodies (IAA) | 2025 |
Antibodies to steroid-producing adrenal cells (ASPCs) | 1701 |
Antibodies to steroid-producing ovarian cells (ASCP-Ovary) | 2430 |
Antisperm antibodies | 1215 |
Eli tests | |
ELI-B-Test-6 (antibodies to ds-DNA, beta2-glycoprotein 1, Fc-lg, collagen, interferon alpha, interferon gamma) | 2565 |
ELI-APS-hCG-Test-6 (antibodies to hCG, beta2-glycoprotein 1, Fc-lg, ds-DNA, collagen, total to phospholipids) | 2835 |
ELI-P-Complex-12 | 6750 |
ELI-Viscero-Test-24 (antibodies to 24 antigens of the main human organs and systems) | 12150 |
Paraproteinemias and immunofixation | |
Screening for paraproteins in serum (immunofixation) | 3375 |
Screening for Bence Jones protein in spot urine (immunofixation) | 1755 |
Typing of paraprotein in blood serum (using immunofixation with a panel of IgG, IgA, IgM, kappa, lambda antisera) | 6210 |
Immunofixation of Bence Jones protein with a panel of antisera | 5130 |
KDS Clinic is a modern, comprehensive medical center that provides comprehensive diagnostics of systemic and autoimmune diseases, including autoimmune analysis. Our specialists have extensive experience, have new technological research methods and have new, modern equipment for accurate and high-quality diagnostics.