Chronic inflammatory demyelinating polyradiculopathy (CIDP) is an immune-mediated disorder for which specific clinical cerebrospinal fluid (CSF), electrophysiologic and histological criteria have been proposed 1 . CIPD is an uncommon cause of childhood polyneuropathy. Descriptions of children with CIPD are scarce. Therefore, this article intends to report a case about an adolescent with type 1 diabetes mellitus (T1DM) with a satisfactory therapeutic response to immunoglobulin and methylprednisolone.This presentation highlights the importance of investigating diabetic patients, including children, with polyneuropathy in an attempt to identify the ones with demyelinating polyneuropathy, because of the likelihood of these patients to benefit from immumodulatory and/or immunossupressive treatment.
CaSeMale, 14 year-old, with a seven year history of T1DM and one year history of diabetic nephropathy. Under insulinotherapy and captopril with unsatisfactory glycemic control. Nine months before the initial evaluation he presented pain, paresthesia and a progressive, symmetric muscular weakness, in both lower limbs. After five months of therapeutic failure under carbamazepine and amytryptiline, he was referred to our service. The initial evaluation showed a mild and symmetric, proximal and distal lower limb weakness (the upper limbs were not affected). The proximal compromise was worse than distal. There were patellar and Achilles tendon hyporeflexia, with absence of Babinski sign. Pain, vibratory and position stimulus modalities were normal, although tactile sensory tests evidenced paresthesias. Anal and vesical sphincter function and muscular tone were preserved.Complete blood count, erythrocyte sedimentation rate, urea, creatinine, electrolytes, AST, ALT, GGT, alkaline phosphatase, prothrombine time, total proteins, albumin, creatinekynase (CK), CK-MB, thyroid function tests, lipid profile and cerebrospinal fluid evaluation were normal.The first electromyography (EMG), done five months after the beginning of the neurologic symptoms (Nihon Khoden Electromyography, 4 channels), evidenced decreased conduction velocities with normal amplitude in the median, ulnar, left fibular and posterior tibial nerves, except in the deep right fibular nerve, where although the amplitude was 75% of the lower limit of the normal range (LLNR), the conduction study was 80% lower than LLNR. The distal motor latencies of the median, left ulnar, superficial fibular and sural nerves were prolonged (above 120% of the normal range). The F waves presented prolonged latencies in the ulnar and posterior tibial nerves. The examination with monopolar needle showed decrease in the recruitment of action potentials of the motor unit.The patient was initially treated with human immunoglobulin (400 mg/Kg/day, IV, 5 days), improving the sensory symptoms for about a month, with subsequent relapse, in smaller intensity. There was not improvement of the lower limb weakness. A second EMG, performed 2 months after therapy with immunoglobulin, evidenced increment...