Background and purpose Monitoring of the disease course of patients with chronic inflammatory demyelinating polyneuropathy (CIDP) remains challenging because nerve conduction studies do not adequately correlate with functional disability. The prognostic value of pathological spontaneous activity (PSA) in needle electromyography (EMG) in different CIDP subgroups in a longitudinal context has, to date, not been analysed. We aimed to determine whether PSA was a prognostic marker or a marker of disease activity in a cohort of patients with CIDP. Methods A total of 127 patients with CIDP spectrum disorder were retrospectively analysed over 57 ± 47 months regarding the occurrence of PSA (fibrillations and positive sharp waves). The presence of PSA at diagnosis, newly occurring PSA, and continuously present PSA were longitudinally correlated with clinical disability using the Inflammatory Neuropathy Cause and Treatment Overall Disability Sum Score (INCAT‐ODSS) and CIDP subtype. Results Pathological spontaneous activity occurred in 49.6% of all CIDP patients at first diagnosis. More frequent evidence of PSA was significantly associated with a higher INCAT‐ODSS at the last follow‐up. Continuous and new occurrence of PSA were associated with higher degree of disability at the last follow‐up. The majority of patients with sustained evidence of PSA were characterized by an atypical phenotype, higher degree of disability, and the need for escalation of treatment. Conclusions Pathological spontaneous activity was associated with a higher degree of disability and occurred more frequently in atypical CIDP variants according to the longitudinal data of a large cohort of patients with CIDP. Our results showed that EMG examination was an adequate marker for disease progression and should be evaluated during the disease course.
Background and purpose Monitoring of patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is challenging in daily medical practice because the interrelationship between clinical disability, CIDP subtype, and neuronal degeneration is still elusive. The aim of this prospective cohort study was to investigate the role of different electrophysiological variables in CIDP monitoring. Methods Comprehensive bilateral nerve conduction studies (NCS) and structured clinical examinations were performed in 95 patients with typical CIDP and CIDP variants (age at inclusion 58.6 ± 11.6 years; median [range] inflammatory neuropathy cause and treatment overall disability score (INCAT‐ODSS) 3 [0–9]), at time of first diagnosis in 25 of these patients (based on data from the prospective Immune‐mediated Neuropathies Biobank registry). After 12 months, 33 patients underwent follow‐up examination. Typical CIDP patients and patients with CIDP variants were characterized electrophysiologically and each individual NCS variable and the overall sum score for axonal damage and demyelination were then correlated to clinical disability scores (INCAT‐ODSS, modified Medical Research Council (MRS) sum score, and INCAT sensory score). Results As opposed to demyelination markers, the NCS axonal damage variable correlated strongly with disability at both first diagnosis and advanced disease stages in cross‐sectional and longitudinal analyses. Distal compound muscle action potential amplitudes of the upper limbs were found to have the strongest correlation with overall clinical function. Typical and atypical CIDP variants had distinct electrophysiological characteristics but, in typical CIDP, axonal degeneration markers were more strongly associated with clinical disability. Conclusions Total disability is largely determined by the degree of axonal damage, especially in typical CIDP. Although most patients have symptoms predominantly in the legs, NCS of the upper limbs are essential for the monitoring of patients with CIDP and CIDP variants.
BackgroundIt is reported that subclinic intestinal inflammation may occur in Ankylosing spondylitis (AS) patients, besides, using NSAIDs cause peptic and duedenal ulcers. %50–60 of AS patients have asymptomatic ileal and colonic mucosal inflammation. It is reported that inflammatory bowel disease (IBD) is found in 5–10% of AS patients and 4–10% of IBD patients have concomittant findings with AS. These conditions may cause iron deficiency anemia (IDA).ObjectivesIt is well known that chronic disease anemia is a frequent finding in AS patients. But there is no study in the literature about relationship between AS patients and IDA. In this particular study we aimed to asses frequency of IDA in AS patients and to investigate the etiologies of IDA.MethodsNinety four consecutive AS patients who meet 2012 ASAS/EULAR criteria, who were followed Çukurova University Romatology Clinic, were icluded. We investigated the etiologies of IDA in anemic patients. Twenty six AS patients were diagnosed as IDA. Twenty six patients without anemia were assigned as a control group. Hepcidin, soluble transferrin receptor1 (sTfR1) and anemia parameters were tested in both groups. Findings were anayzed with SPSS version 23.ResultsTwenty six of 94 AS patients were diagnosed as IDA (%27). Frequency of IDA in our AS patients was higher when compared to the IDA prevalence in the society (%1–2). Endoscopy and colonoscopy were performed for searching etiology of IDA. Mucosal inflammation was found in 62% of patients by endoscopy and 11% of patients by colonoscopy. One patient was diagnosed as Crohn's disease and one patient was diagnosed as Coeliac disease histopathologically. Hepcidin was found to be significantly lower in IDA patients (p<0.01). We found sTfR1 levels significantly higher in IDA patients (p<0,01). BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) and sedimentation values were found to be higher in IDA patients statistically (p<0.01and p=0.01 respectively). Although we found C- reactive protein (CRP) values were higher when compared to the non- anemic patients; however it was not statistically significant (p>0.05).ConclusionsWe found higher frequency of IDA when compared to the normal population. We found that AS was more active in patients who were diagnosed as IDA. We suggest that AS activitiy may cause mucosal inflammation and subsequently may result as IDA. Also we found that mucosal inflammation in AS patients is not related to NSAIDs because there was no difference about mucosal lesions between NSAID taking and non-NSAID taking group. No study was met in the literature concerning AS and IDA. Our findings should be supported by further studies.References Rudwaleit M, Baeten D. Ankylosing spondylitis and bowel disease. Best Pract Res Clin Rheumatol 2006; 20(3):451–71.Lanas A, Boers M, Nuevo J. Gastrointestinal events in at-risk patients starting non-steroidal anti-inflammatory drugs (NSAIDs) for rheumatic diseases: the EVIDENCE study of European routine practice. Ann Rheum Dis. 2015;74(4):675–81.Niccoli L, Nannini C, ...
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