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Rheumatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Autoantibodies: Autoantibodies to nuclear and cytoplasmic antigens may be present (see Table 4.1). The antinuclear antibody (ANA) test is the best screening test for lupus as it is usually positive. Anti-dsDNA antibodies are specific for lupus and may reflect disease activity, while RF is found in 30–50% of patients. Anti-Smith RNA antibodies are also virtually confined to individuals with lupus but are present in less than 20% of such patients.
Rheumatologic diseases and antiphospholipid syndrome
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Thomas J. Santoro, Michiyo Tomita, Alfonse T. Masi
Diagnosis depends upon characteristic clinical manifestations together with confirmation by typical laboratory abnormalities (1–4,93). The antinuclear antibody (ANA) test is positive in essentially all SLE patients. However, it also occurs frequently in other CTD. The ANA has greater diagnostic import when either absent (tending to exclude SLE) or when present in high titers, especially with homogeneous or peripheral-staining nuclear patterns (typical of SLE). An isolated low-titer ANA lacks association with SLE or adverse pregnancy outcome, compared with high-titer ANA or the more specific antibodies that correlate with this disorder. The specific and confirmatory immunologic abnormalities of SLE include anti-native (double-stranded) DNA (nDNA) or anti-Smith (Sm) antibody. Positive lupus erythematosus (LE) cell preparation, a test that is rarely performed today, or chronic (at least 6 months) biologic false-positive test for syphilis supports, but does not confirm the diagnosis, since these serologic findings are typical but are not specific for SLE (1).
AI and Autoimmunity
Published in Louis J. Catania, AI for Immunology, 2021
No single laboratory test can diagnose autoimmune diseases. It requires a physical examination to assess signs and symptoms with a combination of lab tests. The antinuclear antibody test (ANA) is often one of the first tests used when symptoms suggest an autoimmune disease. A positive ANA test suggests the potential presence of autoimmune disease, but it does not confirm exactly which one or even if one is present for certain. Other tests look for specific autoantibodies produced in certain autoimmune diseases. The bottom line is laboratory diagnosis is non-specific and can only assist in the symptoms and other tests to confirm the diagnosis.40
Post-marketing safety surveillance of erenumab: new insight from Eudravigilance
Published in Expert Opinion on Drug Safety, 2022
Antinuclear antibody, C-reactive protein increased, and liver function test increased were identified as signals of disproportional reporting. The antinuclear antibody test is used in clinics to support the diagnosing of autoimmune diseases. Previous studies have described, in a clinical setting, the increase of antinuclear antibody levels in individuals with migraines. Therefore, we cannot exclude that this disproportionality signal is confounded by indication or rather that erenumab is used for migraines and consequently associated with increased biomarkers in migraines [29]. Similarly, positive C-reactive protein is increased in patients with migraines with complex clinical features such as those leading to treatment-resistant migraines requiring second-line treatment such as erenumab [30]. A recent update of the safety information on erenumab highlighted the occurrence of liver injury and increased biomarkers of liver injury [31]. However, in many cases, there was limited information for a proper assessment of the individual causality. This disproportionality signal merit further investigation as pre- and post-marketing clinical trials investigating the safety of erenumab excluded individuals with preexisting liver disorders [32,33]. However, it should also be mentioned that erenumab is not metabolized by the liver and, therefore, the probability of developing erenumab-induced liver injury are quite limited [34].
Intestinal angioedema caused by an acquired C1 esterase inhibitor deficiency associated with underlying splenic marginal zone lymphoma
Published in Baylor University Medical Center Proceedings, 2021
Thanita Thongtan, Anasua Deb, Genanew Bedanie, Mohamed Elmassry, Matthew Soape, Kenneth Nugent
Contrast-enhanced computed tomography (CT) of the abdomen and pelvis showed splenomegaly (16.1 cm) with splenic varices and bowel wall thickening with mucosal enhancement suggestive of enteritis (Figure 1). Small bowel enteroscopy showed jejunal narrowing at 70 cm distal to the pylorus without signs of inflammation; the biopsy result was normal. Colonoscopy was unremarkable. The FibroScan score was 7.7 kPa. A complete blood count showed pancytopenia, with white blood cells 2.89 k/µL, hemoglobin 9.3 g/dL, mean corpuscular volume 84.3 fL, and platelet count 96 k/µL. A peripheral blood smear showed pancytopenia with no atypical cells. The complement component 4 level was low at <6 mg/dL (normal 10–40 mg/dL), C1-INH protein level was low at 4 mg/dL (normal 21–39 mg/dL), and C1-INH protein function was low at 18% (normal ≥68%). An antinuclear antibody test was negative. Peripheral blood flow cytometry revealed a small population (0.1%) of monoclonal B cells with nonchronic lymphocytic lymphoma type, with no evidence of an aberrant T-cell process or increased blasts. Bone marrow biopsy revealed a hypercellular marrow (60%) with megakaryocytic hyperplasia but no evidence of B-cell lymphoma involvement. Fluorescence in situ hybridization was negative for abnormalities of chromosomes 3, 7, 11, 18, rearrangements of BCL6, MALT1, or t(11;14) translocation. The cytogenetic result was normal (46, XX).
Detectable anti-proteinase-3 antibodies precede clinical manifestations in a case of anti-neutrophil cytoplasmic antibody-associated vasculitis
Published in Scandinavian Journal of Rheumatology, 2021
AYS Lee, MJ Nissen, D Beroukas, MJ Ahern, JA Barbara
A 46-year-old female diagnostic laboratory scientist had been using her own serum as a ‘healthy control’, stored at −80°C. She did not have any significant medical history. In August 2004, she developed progressive symmetrical polyarthritis and was treated with celecoxib 100 mg bd with some improvement in symptoms. Investigations revealed normal haematological and biochemical parameters including renal function and urinalysis. Autoimmune serology in August revealed a positive antinuclear antibody (ANA) (1:160, speckled); but negative anti-extractable nuclear antigens, anti-double-stranded DNA antibodies, rheumatoid factor, and anti-cyclic citrullinated peptide. Her cytoplasmic anti-neutrophil cytoplasmic antibody (c-ANCA) was strongly positive, with an associated anti-PR3 of 21 600 units/mL (reference range < 5 units/mL) (Figure 1). Without overt evidence of vasculitis, a decision was made to continue treating symptomatically. Her celecoxib dose was doubled in December 2004 to 200 mg bd.