Abstract
Guillain-Barre syndrome (GBS) is also known as an acute inflammatory demyelinating polyneuropathy (AIDP). It is an immune-mediated polyneuropathy commonly post-infectious in origin that presents with ascending weakness, loss of sensation and deep tendon reflexes resulting from demyelination of peripheral nerve. Drug-induced neuropathy has been describing before and remains a rare clinical entity. Development GBS after an episode of infections such as Campylobacter Jejuni, Epstein Barr Virus, and Mycoplasma pneumonia has been well described. However, GBS associated with Cyclosporine A (CsA) is rarely reported. Here we report a case of GBS developed two weeks after initiation of CsA in a patient with a known case of primary membranous nephropathy and responded well with cessation of the offending drug.
Highlights
Guillain-Barre syndrome (GBS) is the most common acute polyneuropathy and resembles acute inflammatory demyelinating polyneuropathy (AIDP)
Cyclosporine A (CsA) has been widely used as the immunosuppressive agent in human recipients of kidney, liver, heart, pancreas, lung and bone marrow transplantations
Each of these conditions has its own protocols for doses, frequency, target therapeutic levels as well as the concomitant use of other immunosuppressive agents
Summary
Guillain-Barre syndrome (GBS) is the most common acute polyneuropathy and resembles acute inflammatory demyelinating polyneuropathy (AIDP). She had severe nephrotic syndrome with 24-hours urine protein was 6gm/day, serum albumin 16 g/l and preserved kidney function with a serum creatinine of 86 μmol/L (estimated glomerular filtration rate (eGFR) of 56 ml/kg/1.73m2). Despite 3.0gm cumulative dose of IV CYC over a period of 6 months, her 24-hours urine protein was failed to achieve below nephrotic range, the IV CYC was discontinued and Cyclosporine (CsA) was started at a dose of 75 mg twice daily with her body weight was 72 kg.
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