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ANCA vasculitis: case report A 51-year-old man developed anti neutrophil cytoplasmic antibody (ANCA) associated vasculitis during treatment with propylthiouracil and carbimazole for Grave’s disease [routes, dosages, duration of treatments to reactions onsets not stated; not all outcomes stated]. The man, who had Grave’s disease, had been receiving treatment with carbimazole. During treatment, he developed mood disturbance secondary to carbimazole. His treatment with carbimazole was replaced with propylthiouracil. Three months prior to hospitalisation, he discontinued this treatment without medical consultation. He reported feeling unwell, weight loss, fever, lethargy and worsening goitre. Therefore, his treatment with propylthiouracil was restarted 2 weeks prior to presentation. He presented to hospital with impaired renal function and haematoproteinuria. He had a history of asthma and smoking. He had a family history of renal failure, autoimmune thyroid disease and kidney dysfunction. On arrival, his serum creatinine level was 568 µmol/L compared to 116 µmol/L one year prior. His CRP level was 100 mg/dL. Point of care urinalysis showed 3+ blood and 3+ protein. An ultrasound showed unremarkable renal tract. He felt well and did not have symptoms of systemic illness. He denied visible haematuria, dyspnoea, cough, haemoptysis, arthralgia, rash, oral ulceration or peripheral oedema. There was no change in his urine output. His physical examination was not significant. He was clinically euthyroid and became normotensive. Therefore, he was transferred to the regional renal unit for further investigation. On arrival a renal biopsy showed cellular crescents with little or no organisation in 50% of glomeruli, along with segmental necrosis and moderate chronic damage (40% tubular atrophy). Additionally, widespread lymphoplasmacytic infiltrate associated with tubulitis was noted. The man’s treatment with propylthiouracil was discontinued, and he was started on low dose carbimazole. He was treated with methylprednisolone for 3 days. On the following day, an autoimmune serology revealed positive titres for anti-glomerular basement membrane (GBM), p and c-ANCA, anti-proteinase-3 (PR3) and anti-antibodies against myeloperoxidase (MPO). Based on these findings, he was diagnosed with ANCA vasculitis. His serum creatinine level was 448 µmol/L at the time. Serum protein electrophoresis revealed polyclonal hypergammaglobulinaemia. His immunoglobulin G and A levels were found to be mildly elevated. Considering the triple-positive immunology, histologically confirmed crescentic glomerulonephritis and severe renal dysfunction, a plasma exchange was performed for 8 sessions over consecutive days. At this point, his anti-GBM titre normalised. Additionally, he received induction therapy with cyclophosphamide and unspecified glucocorticoids. Eventually, his creatinine level improved, and he was discharged with two doses of cyclophosphamide. Further treatment with cyclophosphamide was continued due to lower respiratory tract infection.