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Arthritis and Common Musculoskeletal Conditions
Published in K. Rao Poduri, Geriatric Rehabilitation, 2017
Jennifer H. Paul, Katarzyna Iwan, Claudia Ramirez
Lung involvement is common and has many presentations. Rheumatoid arthritis can cause lung disease of different histological and clinical presentations. Pleural disease is common in rheumatoid arthritis and usually presents as pleural thickening or small pleural effusions. Autopsy results identified pleural disease in 38%–73% of patients with rheumatoid arthritis, but only 5%–21% of those affected reported symptoms.20,21 Pleural involvement is most common in chronic disease and in men.22 It coexists with rheumatoid nodules and interstitial lung disease in up to 30% of patients.22 Rheumatoid pleuritis and pleural effusions usually do not require specific treatment and resolve spontaneously or with treatment of joint disease.22 Other manifestations include upper and lower airway obstruction, rheumatoid nodules, drug-induced toxicity due to methotrexate, and infection related to immunosuppression.20,21 Moreover, there is a slightly increased risk of lung cancer than the general population.20 Research has not shown an increased prevalence of pulmonary infections but there is an association with higher morbidity and mortality.23 Patients should be vaccinated against streptococcal pneumonia and influenza on a yearly basis.
Clinical Diagnosis of Pleural Disease
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
The great majority of patients who have granulomas on pleural biopsy have tuberculosis. Nearly 100% of patients with caseous necrosis or positive acid fast bacilli stains have pleural tuberculosis. On rare occasions other entities such as fungus diseases, sarcoidosis, or rheumatoid pleuritis can produce granulomatous pleuritis, and these possibilities should be kept in mind when granulomatous pleuritis is discovered.
Morphological and primary structural consistency of fibrils from different AA patients (common variant)
Published in Amyloid, 2019
Falk Liberta, Matthies Rennegarbe, Reinhild Rösler, Johan Bijzet, Sebastian Wiese, Bouke P.C. Hazenberg, Marcus Fändrich
A 61-year-old man developed proteinuria (approximately 3 g/L, endogenous creatinine clearance unknown) and amyloid was detected in a kidney biopsy. No serum M-protein nor Bence Jones proteinuria were found. Underlying inflammatory disease was a progressively erosive rheumatoid arthritis from the age of 40 and rheumatoid pleuritis from the age of 55. At the age of 62 he suddenly died one week after an acute myocardial infarction. Coronary arterial atherosclerosis and both an old anteroseptal and recent left lateral myocardial infarction were found at autopsy. AA amyloid was found in the arterial walls of the liver and spleen and in the kidneys particularly in all glomeruli, but also in small arterial walls.
Posterior reversible encephalopathy syndrome and microangiopathic haemolytic anaemia developing in a regularly haemodialysed patient with scleroderma renal crisis: a case report
Published in Modern Rheumatology Case Reports, 2019
Yuya Sato, Tomoyuki Ito, Akira Iguchi, Kazuhiro Yoshita, Yumi Ito, Naofumi Imai, Hajime Yamazaki, Takako Saeki, Ichiei Narita
A 69-year-old female patient with limited cutaneous SSc (anti-centromere antibody positive, anti-scl-70 antibody negative, and anti-RNA polymerase III antibody negative) and rheumatoid arthritis had been treated with salazosulfapyridine and methotrexate for several years. She had complained sclerodactyly, Raynaud’s phenomenon and telangiectasia, but had no signs of interstitial pneumonitis, pulmonary arterial hypertension or oesophageal dysfunction, at the time of SSc diagnosis. Although her arthritis disease activity score had been low to medium and her general condition had been stable, she developed rheumatoid pleuritis. Although this was immediately improved by prednisolone at 30 mg daily, she developed acute oliguric renal failure with thrombocytopenia (63,000/µl) and abrupt onset of hypertension (from 110/70 at the baseline to 160/90 mmHg) 2 months after the start of steroid therapy. She had no preceding episode of infection such as diarrhoea or fever and had not been started on any new drug. The complement value was normal. A computed tomography (CT) scan had revealed no evidence of malignancy from the neck to the pelvis. Considering the timing of onset of the condition shortly after the start of steroid therapy, SRC was highly suspected. Therefore, we began treatment with ACEi (enalapril) immediately, and this alone improved platelet count to 177,000/µl. After adequate blood pressure control, we then performed renal biopsy, the findings of which are shown in Figure 1. The diagnosis of SRC was thus confirmed pathologically. Despite the improvements in blood pressure and platelet count, her renal function declined rapidly in the following month, necessitating maintenance haemodialysis. Her systolic blood pressure had been maintained at between 110 and 130 mmHg with enalapril.