Background. Gout is an inflammatory arthritis caused by monosodium urate (MSU) deposition. Acute gout is a dramatic painful swelling of the joint; however, MSU can deposit in other tissues as well, including skin, gastrointestinal tract, and bones over time. Disseminated tophi in the skin are a rare presentation of gout known as gout nodulosis. We present a case of gout nodulosis with subcutaneous diffuse miliary nodules in nonarticular areas with concurrent findings suggestive of chronic inflammatory arthritis. Case Presentation. A 39-year-old patient presented with intermittent painful swelling in multiple joints with prolonged morning stiffness. On exam, synovitis was present in multiple proximal interphalangeal joints, wrists, elbows, and knees. Chronic raised pearly nodular rash and swellings on extensor aspects of arms, legs, and anterior abdomen were noticeable. He had negative rheumatoid factor and anti-CCP antibody, C-reactive protein of 0.23 mg/dL, erythrocyte sedimentation rate of 37 mm/hr, and uric acid of 10.6 mg/dL. Hand X-rays revealed severe periarticular osteopenia and joint space narrowing in several joints. Musculoskeletal ultrasound showed a double contour sign at multiple joints and a tophaceous deposit over the olecranon fossa. The biopsy of the nodular rash was consistent with tophi. He was diagnosed with chronic tophaceous gout with skin nodulosis and possible overlap of seronegative rheumatoid arthritis given his X-ray findings. Conclusion. This case discusses one of the rare presentations of gout with disseminated gouty tophi in the skin to raise clinical awareness. The clinical dilemma of the overlap of gout and rheumatoid arthritis posing a diagnostic challenge for clinicians is also highlighted.
Anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) is a class of small vessel vasculitis that includes granulomatosis with polyangiitis (GPA), eosinophilic GPA (EGPA), and microscopic polyangiitis (MPA). Despite extensive research, the mechanisms behind AAV etiology remain obscure. The genetics of AAV is a complex area of investigation because of the rarity of familial cases. However, recent multi-center genome-wide association studies (GWAS) have greatly contributed to our understanding of the genetic basis of AAV. In this study, we report a rare occurrence of GPA in two Caucasian family members who presented with similar clinical symptoms and performed a comprehensive review to study the present literature available regarding the heritability of this disease.
Cardiac tamponade is an uncommon complication of systemic sclerosis (SSc) with a high mortality rate. Here, we report a case of a 58-year-old patient with limited cutaneous systemic sclerosis (lcSSc), gastroesophageal reflux disease (GERD), diabetes mellitus, pulmonary hypertension (PHTN), and COVID-19 infection, which occurred one month ago, presenting with a large hemorrhagic pericardial effusion and early cardiac tamponade. The patient had an acute onset of progressive dyspnea and anasarca. On examination, she was tachypneic, tachycardic, desaturating on room air, and hypotensive. Pitting edema up to thighs and bilateral basilar crackles were also appreciated. Labs were remarkable for negative troponin, chest X-ray with pulmonary congestion, D-dimer at 6.01, CT angiogram negative, brain natriuretic peptide level at 73 pg/mL, C-reactive protein level at 7.64 mg/dL, normal complement levels, and negative COVID-19 test results. Echocardiography showed early tamponade and a large circumferential effusion with chamber collapse. Right heart catheterization was performed finding PHTN at 54 mmHg. Pericardiocentesis drained 500 mL of the hemorrhagic effusion. Fluid analysis showed RBC at 220,000/uL, WBC at 5000/uL, protein 4.8 g/dL, lactate dehydrogenase level of 1275 U/L, and negative cytology. The patient was treated for serositis from lcSSc flare with mycophenolate mofetil and steroids, and responded very well. Hemorrhagic cardiac tamponade is a very rare phenomenon in limited scleroderma. A recent COVID-19 infection could have served as a trigger factor for our patient’s lcSSc in long remission to flare up. Clinicians should maintain a high index of suspicion and a low threshold for intervention when lcSSc patients have an acute onset of cardiac compromise, especially with a history of a recent COVID-19 infection.
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