scholarly journals Renal Tubular Acidosis Causing Acute Hypokalemic Paralysis in Systemic Lupus Erythematosus: Sjogren’s Syndrome Overlap

Cureus ◽  
2020 ◽  
Author(s):  
Mohammad Ammad Ud Din ◽  
Gaby Razzouk
2017 ◽  
Vol 10 ◽  
pp. 117954411772276 ◽  
Author(s):  
Yelitza Velarde-Mejía ◽  
Rocío Gamboa-Cárdenas ◽  
Manuel Ugarte-Gil ◽  
César Pastor Asurza

Acute hypokalemic paralysis is a rare and potentially fatal condition, with few related causes, one of which highlights distal renal tubular acidosis (dRTA). Distal renal tubular acidosis is a rare complication of several autoimmune diseases such as systemic lupus erythematosus, Sjögren’s syndrome, and Hashimoto thyroiditis. We report a case of a lupic patient who presented rapidly progressive quadriparesis in the context of active renal disease. Research revealed severe refractory hypokalemia, metabolic acidosis, and alkaline urine suggestive of dRTA. We diagnosed Sjögren’s syndrome based on sicca symptoms, an abnormal salivary glands’ nuclear scan and the presence of anti-Ro/SSA and anti-La/SSB. In addition, the finding of thyroid peroxidase, thyroglobulin antibodies, and hypothyroidism led us to the diagnosis of Hashimoto thyroiditis. Due to the active renal involvement on the context of systemic lupus erythematosus and Sjögren’s syndrome, the patient received immunosuppression with rituximab, resulting in a progressive and complete improvement.


2017 ◽  
Vol 30 (3) ◽  
pp. 246 ◽  
Author(s):  
Sofia Silvério Serra ◽  
Teresa Pedrosa ◽  
Sandra Falcão ◽  
Jaime Cunha Branco

Interstitial lung disease occurs in up to 25% of patients with Sjögren’s syndrome and 2% - 8 % of patients with systemic lupus erythematosus. Corticosteroid therapy remains the main treatment for systemic lupus erythematosus. However, it can be associated with several neuropsychiatric disorders especially with prednisolone at a dose of more than 40 mg/day. We present the case of a 51-year-old patient with systemic lupus erythematosus and secondary Sjögren’s syndrome with severe pulmonary involvement four years after the diagnosis. Chest computed tomography revealed neofibrosis and ground glass appearance pattern. After increasing the dose of prednisolone to 60 mg/day, the patient presented a manic episode. There was need of hospitalization and the situation was considered to be secondary to corticosteroids at high doses. Central neurological involvement by organic disease was excluded.We introduced monthly perfusion of cyclophosphamide for six months and later started mycophenolate mofetil 2 g/day, reducing prednisolone to 10 mg/day and maintaining hydroxychloroquine 400 mg/day, with control of disease activity.


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