Differences between acute-onset chronic inflammatory demyelinating polyneuropathy and acute inflammatory demyelinating polyneuropathy in adult patients
Por:
Alessandro, L, Rueda, JMP, Wilken, M, Querol, L, Marrodan, M, Acosta, JN, Rivero, A, Barroso, F, Farez, MF
Publicada:
1 sep 2018
Resumen:
Acute inflammatory demyelinating polyneuropathy (AIDP) and acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) are conditions presenting overlapping clinical features during early stages (first 4weeks), although the latter may progress after 8 weeks. The aim of this study was to identify predictive factors contributing to their differential diagnosis. Clinical records of adult patients with AIDP or A-CIDP diagnosed at our institution between January 2006 and July 2017 were retrospectively reviewed. Demographic characteristics, clinical manifestations, cerebrospinal-fluid (CSF) findings, treatment and clinical evolution were analyzed. Nerve conduction studies were performed in all patients with at least 12months follow-up. A total of 91 patients were included (AIDP, n=77; A-CIDP, n=14). The median age was 55.5 years in patients with A-CIDP vs 43years in AIDP (P=.07). The history of diabetes mellitus was more frequent in A-CIDP (29% vs 8%, P=.04). No significant differences between groups were observed with respect to: human immunodeficiency virus (HIV) status, presence of auto-immune disorder or oncologic disease. Cranial, motor and autonomic nerve involvement rates were similar in both groups. Patients in the A-CIDP group showed higher frequency of proprioceptive disturbances (83% vs 28%; P <.001), sensory ataxia (46% vs 16%; P=.01), and the use of combined immunotherapy with corticoids (29% vs 3%; P=.005). There were no significant differences in CSF findings, intensive care unit (ICU) admission, or mortality rates. During the first 8 weeks both entities are practically indistinguishable. Alterations in proprioception could suggest A-CIDP. Searching for markers that allow early differentiation could favor the onset of corticotherapy without delay.
Filiaciones:
Alessandro, L:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Rueda, JMP:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Wilken, M:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Querol, L:
Hosp Santa Creu & Sant Pau, Dept Neurol, Barcelona, Spain
Marrodan, M:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Acosta, JN:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Rivero, A:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Barroso, F:
Raul Carrea Inst Neurol Res FLENI, Dept Neurol, Buenos Aires, DF, Argentina
Farez, MF:
Raul Carrea Inst Neurol Res FLENI, Ctr Res Neuroimmunol Dis CIEN, Buenos Aires, DF, Argentina
Raul Carrea Inst Neurol Res FLENI, Ctr Epidemiol Biostat & Publ Hlth CEBES, Buenos Aires, DF, Argentina
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