Chronic inflammatory demyelinating polyneuropathy associated with diabetes: a European multicentre comparative reappraisal

Rajabally, Yusuf A.; Perić, Stojan; Cobeljic, Mina; Afzal, Samina; Božović, Ivo; Palibrk, Aleksa; Basta, Ivana

doi:10.1136/jnnp-2020-322971

Cited by 25 publications

(27 citation statements)

References 23 publications

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“…Furthermore, the mean HbA1c of our diabetic patients was relatively low (6.8%), indicating a relatively good glycemic control, a finding which should prompt a clinician to further investigate the presence of another cause of neuropathy even in the clinical context of established diabetic neuropathy when new progressive/relapsing symptoms arise. Our patients with diabetes were in average older than non‐diabetics and had relatively higher disability, characteristics comparable with findings of previous studies 22,24 . NCS showed slightly less accentuated signs of demyelination in diabetics, but only the difference in mean CMAP duration was statistically significant.…”

Section: Discussionsupporting

confidence: 90%

“…Our patients with diabetes were in average older than non-diabetics and had relatively higher disability, characteristics comparable with findings of previous studies. 22,24 NCS showed slightly less accentuated signs of demyelination in diabetics, but only the difference in mean CMAP duration was statistically significant. The most important finding was that fulfillment of the EFNS/PNS criteria as well as treatment response did not differ significantly, so that a substantial proportion of the diabetics benefited from immunotherapy.…”

mentioning

confidence: 71%

“…There is great controversy and debate on the association of diabetes with CIDP, 13,14,22,23 especially since diabetic neuropathy can present with demyelinating characteristics and there is no clear‐cut method of distinguishing this from CIDP. Recent studies have shown evidence to support an increased prevalence of CIDP in diabetics 13,24 . As our study represents a real‐world situation, we chose to include these patients with previously known diabetes who the clinicians considered having comorbid CIDP.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown evidence to support an increased prevalence of CIDP in diabetics. 13,24 As our study represents a real-world situation, we chose to include these patients with previously known diabetes who the clinicians considered having comorbid CIDP. We find that the prevalence of diabetes in the cohort (17.7%) is not exceptionally high, considering the mean age and male predominance, and it is compatible with the estimated prevalence of diabetes in the German population of this age group.…”

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confidence: 99%

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Evaluation of the EFNS/PNS diagnostic criteria in a cohort of CIDP patients

Athanasopoulos

Motte

Grüter

et al. 2021

Ann Clin Transl Neurol

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Objective To evaluate the European Federation of Neurological Societies (EFNS)/Peripheral Nerve Society (PNS) diagnostic criteria for chronic inflammatory demyelinating polyneuropathy (CIDP) in a cohort of patients diagnosed and treated for CIDP in a tertiary university hospital. Methods In a monocentric retrospective study of 203 CIDP patients, diagnosed according to expert opinion, we evaluated the EFNS/PNS diagnostic criteria. Clinical course and nerve conduction studies (NCS) over 1 year from first referral were studied. Secondarily, we compared the clinical and paraclinical characteristics, including nerve ultrasound, of patients who failed with those who fulfilled the criteria in order to identify clinically relevant differences. Results At 1 year, 182 (89.7%) patients fulfilled the criteria (156/76.9% definite, 22/10.8% probable, and 4/2% possible). Twenty‐one (10.3%) patients did not because the electrodiagnostic criteria remained negative. These still showed signs of demyelination but did not reach the cut‐off values. They also presented typical, albeit less pronounced, multifocal nerve enlargement in ultrasonography. Mean disability at presentation and 1 year after was significantly lower. Most importantly, a relevant proportion of these patients also responded to therapy (6/21 = 28.6% vs. 82/182 = 45.3% of those fulfilling the criteria). Interpretation CIDP diagnosis could be established for 89.7% of patients over the course of 1 year using EFNS/PNS criteria. The remaining patients (10.3%) presented with milder disability, less accentuated demyelination, but otherwise similar characteristics and still considerable probability of treatment response. Failure to fulfill diagnostic criteria should not automatically preclude treatment. Nerve ultrasound should be considered as a complementary diagnostic tool to detect signs of inflammation in CIDP.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Evaluation of the EFNS/PNS diagnostic criteria in a cohort of CIDP patients

Athanasopoulos

Motte

Grüter

et al. 2021

Ann Clin Transl Neurol

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“… 6 Diabetes mellitus (DM) has been discussed controversially as a risk factor in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and has lately been confirmed in multicenter studies. 7 We previously described DM as a comorbidity in patients with antiparanodal antibodies. 5 However, little is known about the frequency of DM in nodo-paranodopathy.…”

mentioning

confidence: 99%

Diabetes Mellitus Is a Possible Risk Factor for Nodo-paranodopathy With Antiparanodal Autoantibodies

Appeltshauser

Messinger

Starz

et al. 2022

Neurol Neuroimmunol Neuroinflamm

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Background and ObjectivesNodo-paranodopathies are peripheral neuropathies with dysfunction of the node of Ranvier. Affected patients who are seropositive for antibodies against adhesion molecules like contactin-1 and neurofascin show distinct clinical features and a disruption of the paranodal complex. An axoglial dysjunction is also a characteristic finding of diabetic neuropathy. Here, we aim to investigate a possible association of antibody-mediated nodo-paranodopathy and diabetes mellitus (DM).MethodsWe retrospectively analyzed clinical data of 227 patients with chronic inflammatory demyelinating polyradiculoneuropathy and Guillain-Barré syndrome from multiple centers in Germany who had undergone diagnostic testing for antiparanodal antibodies targeting neurofascin-155, pan-neurofascin, contactin-1–associated protein 1, and contactin-1. To study possible direct pathogenic effects of antiparanodal antibodies, we performed immunofluorescence binding assays on human pancreatic tissue sections.ResultsThe frequency of DM was 33.3% in seropositive patients and thus higher compared with seronegative patients (14.1%, OR = 3.04, 95% CI = 1.31–6.80). The relative risk of DM in seropositive patients was 3.4-fold higher compared with the general German population. Seropositive patients with DM most frequently harbored anti–contactin-1 antibodies and had higher antibody titers than seropositive patients without DM. The diagnosis of DM preceded the onset of neuropathy in seropositive patients. No immunoreactivity of antiparanodal antibodies against pancreatic tissue was detected.DiscussionWe report an association of nodo-paranodopathy and DM. Our results suggest that DM may be a potential risk factor for predisposing to developing nodo-paranodopathy and argue against DM being induced by the autoantibodies. Our findings set the basis for further research investigating underlying immunopathogenetic connections.

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