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Granulomatous Conditions of the Nose
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Granulomatosis with polyangiitis (GPA; formerly Wegener's granulomatosis) classically involves a triad of upper airway, lung and renal disease, but limited or localized forms of the condition occur in up to 30%. It is thought to be an autoimmune disease, associated with cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCAs) which are specific for proteinase-3 (PR3). Any part of the body may be affected and in generalized disease there is often malaise disproportionate to the clinical findings.
Immunologic Mechanisms in Renal Disease
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Brian D. Schreiber, Gerald C. Groggel
Recently a new, soluble mediator of glomerular immune injury has been identified in humans. This is a group of autoantibodies referred to as antineutrophil cytoplasmic antibodies (ANCA) (Falk and Jennette, 1988). These autoantibodies react with neutrophil azurophilic granules and monocyte lysosomes (Falk and Jennette, 1991). There are two types of ANCAs as defined by immunofluorescent patterns. One is characterized by a cytoplasmic staining and is reactive with the granule constituent, proteinase 3. The other type manifests a perinuclear pattern and the antigen is usually myeloperoxidase. ANCAs have been found in the serum of patients with vasculitis either involving the kidney alone or other organs as well (Falk and Jennette, 1991).
Diagnostic Approach to Acute Kidney Injury in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Sonali Gupta, Divyansh Bajaj, Sana Idrees, Joseph Mattana
Basic blood testing should include a complete blood count, serum electrolytes and creatinine and blood urea nitrogen (BUN). The rise in serum creatinine is commonly delayed after kidney function decline in the critical care setting, and hence, it is important to remember that creatinine can be a suboptimal marker for AKI in such settings. Other blood testing will depend on the clinical scenario and may include examination of the peripheral smear for the presence of schistocytes, tear cells and rouleaux phenomenon, myoglobin and free hemoglobin levels, creatine kinase levels, serum uric acid, lactate dehydrogenase (LDH), complement levels, antinuclear antibody (ANA), ANCA including anti-myeloperoxidase antibodies and anti-proteinase-3 antibodies, anti-glomerular basement membrane antibodies (anti-GBM), hepatitis B and C virus studies, antistreptolysin (ASO), serum immunofixation, serum free light chains, and prostate-specific antigen (PSA) levels. If sepsis is suspected, a basic septic screen should be performed. A summary of selected laboratory testing used in the assessment of AKI is provided in Table 24.3.
Endocarditis-associated rapidly progressive glomerulonephritis mimicking vasculitis: a diagnostic and treatment challenge
Published in Annals of Medicine, 2022
Sanxi Ai, Jianzhou Liu, Guotao Ma, Wenling Ye, Rongrong Hu, Shangzhu Zhang, Xiaohong Fan, Bingyan Liu, Qi Miao, Yan Qin, Xuemei Li
On review of laboratory studies, abnormalities in haematology were common, including anaemia (100%, 24/24), thrombocytopenia (58%, 14/24) and pancytopenia (13%, 3/24) (Table 1). Various markers usually seen in autoimmune diseases were detected with high frequency (Table 2). ANCA was positive in 45% (10/22) of patients, predominantly proteinase 3 (PR3)-ANCA. The titres of PR3-ANCA ranged from 35 to 819 RU/ml with a median titre of 138 RU/ml (reference range <20 RU/ml in our centre). Six patients showed high titres of PR3-ANCA (>100 RU/ml). One patient (case 9) showed dual positivity for PR3-ANCA (>200 RU/ml) and myeloperoxidase (MPO)-ANCA (34 RU/ml). Anti-nuclear antibody was positive in 54% (13/24) of patients, while only one patient showed positive anti-double strand DNA. Hypocomplementemia and elevated rheumatoid factor were presented in 87% (20/23) and 90% (18/20) of patients, respectively.
Interleukin (IL)-33 immunobiology in asthma and airway inflammatory diseases
Published in Journal of Asthma, 2022
Reversible or irreversible post-translational modifications regulate protein function and expression levels (33). These modifications include phosphorylation, acetylation, ubiquitination, methylation, glutathionylation, citrullination, among others (33). Most known post-translational modifications in IL-33 are related to its proteolytic cleavage leading to diverse functional outcomes. The full-length IL-33 is cleaved by mast cell chymase (34,35), tryptase (35), and neutrophil proteases such as elastase, and cathepsin G (35) to highly active forms. The active full-length form is inactivated by caspase-1, 3 and 7 during apoptosis to reduce or prevent the inflammatory cascade (22). Interestingly, neutrophil-derived proteinase 3 appears to have a dual role in IL-33 processing (36). It cleaves the full length IL-33 to promote bioactivity (35,36), but with prolonged exposure, proteinase 3 decreases IL-33 bioactivity (36) (Figure 1). Others report regulation of IL-33-ST2 axis by ubiquitination processes (37–39). For example, FBXL19 is an ‘orphan’ member of the Skp1-Cullin-F-box family of E3 ubiquitin ligases that selectively binds ST2 leading to its polyubiquitination and proteasomal degradation in a murine model of pneumonia (37), resulting in reduced inflammatory signals.
Orbital apex syndrome on initial presentation of giant cell arteritis: a case report and review of the literature
Published in Scandinavian Journal of Rheumatology, 2022
S Tsuzuki, H Tsuchiya, H Shoda, K Fujio
A 69-year-old woman with a history of chronic sinusitis and recurrent exudative otitis media was referred to our hospital with a persistent headache for 6 months and diminished visual acuity in her left eye. A computed tomography (CT) scan showed no intracranial bleeding or ischaemic lesions. Two months before referral, she had progressive ophthalmalgia and diplopia. In addition, she lost 5 kg over 6 months. She reported no fevers. On admission to our hospital, she had diplopia, ophthalmalgia, exophthalmos, and ocular motility disorder and trismus in the left eye. An otolaryngological examination revealed exudative otitis media in the left ear and no sinusitis. The ophthalmological examination revealed a significant reduction in visual acuity of the left eye and a normal fundus. The review of systems was negative for cough, sputum, chest pain, abdominal pain, bloody stools, rashes, oedema, and peripheral movement and sensory disorders. Physical examination was normal. Laboratory tests revealed the following: white blood cell count 7600 cells/mm3; platelet count 38 000 cells/mm3; haemoglobin 13.8 g/dL; C-reactive protein 2.94 mg/L; erythrocyte sedimentation rate 52 mm/h; normal liver and renal function; normal serum electrolytes; normal urinalysis; and negative anti-nuclear antibody, myeloperoxidase, and proteinase-3 anti-neutrophil cytoplasmic antibodies. Angiotensin-converting enzyme, soluble interleukin-2 receptor, and serum immunoglobulin G4 (IgG4) were within normal limits; and the interferon-γ release assay for tuberculosis was negative.