Angiotensin Converting Enzyme (ACE)

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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

  1. 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
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. Lapin S.V. Totolyan A.A. Immunological laboratory diagnostics of autoimmune diseases / Publishing house "Man", St. Petersburg - 2010.
  7. 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 DISEASESprice, 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 myelin2700
Anti-skeletal muscle antibodies (ASM)2862
Antibodies to aquaporin -44590
Antibodies to acetylcholine receptors (AChR)7560
Antibodies to NMDA-type glutamate receptor4590
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), total1215
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, IgM1134
Antibodies to cardiolipin, IgG1134
Antibodies to beta2-glycoprotein1215
Antibodies to beta-2-glycoprotein, IgM1215
Antibodies to beta-2-glycoprotein, IgG1215
Antibodies to phosphatidylserine-prothrombin, total (IgM, G)1620
Antibodies to annexin V class IgM2430
Annexin V IgG antibodies2430
Antibodies to platelets, IgG class1998
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 61755
Antibodies to vascular endothelial cells (HUVEC)1755
Antibodies to complement factor C1q1620
Autoimmune liver lesions
Antibodies to mitochondria1188
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 content2160
Antibodies to intestinal goblet cells (GBC)2700
Antibodies to the yeast Saccharomyces cerevisiae (ASCA), IgA1418
Antibodies to the yeast Saccharomyces cerevisiae (ASCA), IgG1418
Antibodies to gliadin, IgA1256
Antibodies to gliadin, IgG1256
Antibodies to deaminated alpha-gliadin peptides IgA (AAG)2295
Antibodies to deaminated alpha-gliadin IgG peptides (AAG)2295
Antibodies to tissue transglutaminase, IgA2025
Antibodies to tissue transglutaminase, IgG2025
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 desmosomes3915
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 antibodies1215
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-126750
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 antisera5130

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.

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