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Introduction: mothers with newborn children became an easy target of the COVID-19 pandemic, their lives today revolve around avoiding its contagion and spread due to the confinement in which they live. Objective: determine the impact of COVID-19 on the relationship between lifestyle and the bond of mother-newborn attachment in a Hospital in Peru. Methods: an explanatory, descriptive-correlational, cross-sectional design was carried out, with a population of 1020 puerperal women and a sample of 103 puerperal women. The sampling was stratified by the presence or absence of COVID-19 in puerperal women. The variables were lifestyles, described by: practice of physical activity, quality of life, rest and sleep, physical health and social integrity, and bonding mother-newborn. Spearman's correlation, discriminant analysis and Wilcoxon's test were used. Results: in both groups of puerperal women made up of 51 with COVID-19 and 52 without COVID-19, the lifestyles were regular (66.7% and 55.8 %), good bonding mother-newborn (64.7%) and regular (55.8 %), intense (62.7 %) and moderate (61.5 %) physical activity, healthy diet (84.3% and 69.2 %), adequate rest and sleep (54, 9 % and 75.0 %), good (62.7 %) and fair (63.5 %) mental health and self-esteem, and high (68.6 %) and medium (67.3 %) social integration. Conclusions: COVID-19 had a significant impact (p

Con el objetivo de determinar la influencia de la interculturalidad, equidad de género y derechos humanos en la calidad de atención Obstétrica del Hospital de Apoyo Chepén, 2016, se desarrolló una investigación descriptiva de relación causal y diseño transversal, en la que participaron 242 usuarias en situación de parto, encontrándose que la interculturalidad es Baja (53,3%), el respeto a los derechos humanos Medio (55,8%) y; la equidad de género Media (56,2%) y la calidad de la atención obstétrica Regular en todos sus elementos (acceso, comunicación, respeto/cortesía, credibilidad, responsabilidad y tangibilidad), a excepción de la competencia técnica que es Buena (52,5%). Se concluye que la interculturalidad influye significativamente (p

Introducción: La morbilidad materna neonatal y la depresión posparto con la calidad de vida no solo un problema medico social y psicológico que afecta a la mujer durante el posparto, sino que deja secuelas de daño permanente en la salud de la madre. Objetivo: Determinar la relación entre l_a morbilidad materna neonatal con la depresión y calidad de vida posparto en mujeres atendidas en la Micro Red Materno Infantil de Cachicadán, 2017. Metodología: Se realizó una investigación descriptiva transversal en 72 puérperas. Se recolectaron datos sobre la morbilidad materna neonatal de Historias Clínicas Perinatales y se aplicaron dos cuestionarios: Escala de Edimburgo y el Cuestionario de Calidad de Vida SF-36. Resultado: Se encontró que la morbilidad materna es: hemorragias (mayormente Atonía Uterina con 36,1%), infecciones (principalmente del Tracto Urinario con 61,1%), lesiones de periné (principalmente Desgarro I con 41,7%), dolor (principalmente intenso con 97,2%), uso analgesia (5,6%) y visitas a urgencias tras el alta materna (80,6%). La morbilidad neonatal es: distrés respiratorio (2,8%), infecciones a las 48 horas (2,8%), ingreso a la unidad de neonatos (2,8%), bajo peso al nacer (8,3%), edad gestacional pos término (16,7%) y visitas a urgencias tras el alta (80,6%). Conclusión: que la depresión posparto (mayormente Moderada con 58,3%) se relaciona con las lesiones de periné y las visitas a urgencias tras el alta materna (p0,05) y si con la edad gestacional del neonato (p

The Rituximab vs. Placebo in Polyneuropathy Associated With Anti-MAG IgM Monoclonal Gammopathy (RIMAG) study showed no improvement using the inflammatory neuropathy cause and treatment sensory score (ISS) as primary outcome in patients with IgM anti-myelin-associated glycoprotein neuropathy (IgM anti-MAG neuropathy) treated with rituximab, when compared with placebo. However, some secondary outcomes seemed to improve in the per protocol analysis. Patients from one participating center in the RIMAG study underwent a new evaluation after a median follow-up of 6 (interquartile range (IQR) 4.9; 6.5) years, using the same outcome measures used in the original study. Data were recorded in seven rituximab patients (group 1) and in eight placebo patients (group 2). In group 2, six of eight patients received immunotherapy during follow-up, while only two of seven did in group 1. No significant change was observed in either the ISS or the secondary outcomes in both groups, with the exception of worsening in the 10-m walk time in group 2 (p = 0.016). The RIMAG follow-up study failed to find any significant change in most outcome measures in patients from the RIMAG study, some of them having received new immunotherapies. This study stresses the lack of useful clinical scales sensitive enough to capture small, even meaningful, improvement in IgM anti-MAG neuropathy.

International audience; Background/purpose: In anti-myelin associated glycoprotein (anti-MAG) neuropathies, there is evidence that anti-MAG antibodies are pathogenic but numerous studies report the absence or a weak correlation between the titers of these antibodies and disease course. In this study we assessed the relationships between MAG and glycosylated moieties located on Fc fragment of IgM anti-MAG.Material and methods: IgM were extracted from the serum of 8 patients with anti-MAG neuropathy and in 2 patients with anti-MAG antibodies without anti-MAG neuropathy. Anti-MAG activity was performed with pre- and post-deglycosylated IgM extracts using indirect immunofluorescence (IIF) and ELISA. Sera from 49 patients with IgM monoclonal gammopathy without neurological disease were tested as control group (CG). Results were compared to clinical scores. For 4 patients the affinity constant of IgM with MAG was analyzed pre- and post-deglycosylated, using surface plasmon resonance technology (SPR).Results: The relationships between MAG and glycosylated moieties of IgM anti-MAG were confirmed by kinetic and immunological assays. Deglycosylation resulted in a decrease in anti-MAG titers. Post-deglycosylation anti-MAG titers trended with changes in IgM titers and allowed quantifying anti-MAG antibodies without a saturation of the testing method. After deglycosylation, the titers better represented pathogenic activity and help to follow a given patient's clinical status prospectively. Six patients from CG (12.2%) had anti-MAG antibody titers over positive threshold: 1000 Bühlmann-Titer-Units (BTU) supporting the hypothesis of neutral intermolecular interactions between IgM and MAG. Deglycosylation allowed distinguishing infra clinical forms from neutral relationships forms, when the titers are weak but this assay remains essentially a diagnostic tool.

Between October, 2013, and April, 2014, French Polynesia experienced the largest Zika virus outbreak ever described at that time. During the same period, an increase in Guillain-Barré syndrome was reported, suggesting a possible association between Zika virus and Guillain-Barré syndrome. We aimed to assess the role of Zika virus and dengue virus infection in developing Guillain-Barré syndrome.In this case-control study, cases were patients with Guillain-Barré syndrome diagnosed at the Centre Hospitalier de Polynésie Française (Papeete, Tahiti, French Polynesia) during the outbreak period. Controls were age-matched, sex-matched, and residence-matched patients who presented at the hospital with a non-febrile illness (control group 1; n=98) and age-matched patients with acute Zika virus disease and no neurological symptoms (control group 2; n=70). Virological investigations included RT-PCR for Zika virus, and both microsphere immunofluorescent and seroneutralisation assays for Zika virus and dengue virus. Anti-glycolipid reactivity was studied in patients with Guillain-Barré syndrome using both ELISA and combinatorial microarrays.42 patients were diagnosed with Guillain-Barré syndrome during the study period. 41 (98%) patients with Guillain-Barré syndrome had anti-Zika virus IgM or IgG, and all (100%) had neutralising antibodies against Zika virus compared with 54 (56%) of 98 in control group 1 (p0.0001). 39 (93%) patients with Guillain-Barré syndrome had Zika virus IgM and 37 (88%) had experienced a transient illness in a median of 6 days (IQR 4-10) before the onset of neurological symptoms, suggesting recent Zika virus infection. Patients with Guillain-Barré syndrome had electrophysiological findings compatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disease (median duration of the installation and plateau phases was 6 [IQR 4-9] and 4 days [3-10], respectively). 12 (29%) patients required respiratory assistance. No patients died. Anti-glycolipid antibody activity was found in 13 (31%) patients, and notably against GA1 in eight (19%) patients, by ELISA and 19 (46%) of 41 by glycoarray at admission. The typical AMAN-associated anti-ganglioside antibodies were rarely present. Past dengue virus history did not differ significantly between patients with Guillain-Barré syndrome and those in the two control groups (95%, 89%, and 83%, respectively).This is the first study providing evidence for Zika virus infection causing Guillain-Barré syndrome. Because Zika virus is spreading rapidly across the Americas, at risk countries need to prepare for adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome.Labex Integrative Biology of Emerging Infectious Diseases, EU 7th framework program PREDEMICS. and Wellcome Trust.

Background Guillain–Barre syndrome (GBS) is considered as an acute, immune-mediated polyradiculoneuropathy with different clinical phenotypes arising after viral or bacterial infections, vaccination or surgery. However, in 40% of GBS patients the aetiology remains unknown. In this manuscript, we report the occurrence of GBS in a patient bitten by a snake (Vipera aspis) for which a cross-reaction was shown between GM2 ganglioside and glycosidic epitopes of venom proteins. Methods The venom of the snake implied in the patient's envenomation was collected. Its composition was characterised by ELISA and SELDI-TOF MS. Cross-reactivities between venom proteins and GM2 gangliosides were identified by Western blot after immunoabsorption of patient's serum with increasing amounts of purified GM2. Enzymatic deglycosylation of the venom was performed to determine the specificity of the patient's serum cross-reaction. Findings We proved the absence of neurotoxicity of the viper venom. The patient's serum presented specific cross-reactions with several glycosylated venom proteins. After deglycolysation of these proteins, the patient's serum cross-reactivity was abolished. Furthermore, we compared the immune response to venom proteins of sera from two groups of patients. The first group showed IgM reactivity against GM2 ganglioside associated with GBS, and cross-reacted with venom proteins. The second group presented an IgM reactivity against CMV, without neurological disorders, and reacted with neither venom proteins nor gangliosides. Interpretation Our study proved the auto-immunological aetiology of GBS in our patient based on molecular mimicry mechanisms between venom proteins and GM2 ganglioside.

Background and purpose: Some patients within the spectrum of chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) have distal acquired demyelinating symmetric (DADS) neuropathy, usually associated with anti-myelin-associated-glycoprotein (MAG) IgM monoclonal gammopathy. The aim of this retrospective study was to investigate patients with DADS neuropathy without anti-MAG antibodies, and study their response to immunotherapy. Methods: Patients were selected on the basis of (i) ‘Definite CIDP’ according to the EFNS/PNS Guideline criteria, (ii) The presence of disproportionately prolonged motor latencies resulting in a terminal latency index (TLI) ≤0.25 in at least two motor nerves and (iii) The absence of anti-MAG antibodies on ELISA. Response to immunotherapy was defined as persistent improvement by at least one point on the INCAT disability score. Results: Data from 146 CIDP patients were analysed, and 10 patients were included. Six had clinically pure sensory neuropathy, and four had sensorimotor neuropathy. Ataxia was present in nine patients, generalized areflexia in seven and postural tremor in two. Five of the 10 patients had abnormal sensory potentials only in the upper limbs. An associated condition was found in nine patients: two chronic lymphocytic leukaemias, four IgG monoclonal gammopathies (one associated with non-Hodgkin’s lymphoma) and two IgM monoclonal gammopathies of unknown significance. Patients were mostly improved with intravenous immunoglobulin (IVIg), corticosteroids, plasma exchanges, or a combination thereof. Conclusion: DADS neuropathy without anti-MAG antibodies is more likely to be considered a variant of CIDP. In addition, such patients should be systematically investigated for an associated haematological or immunological condition.

RESUME La recherche d’une cause, en particulier accessible a un traitement, est la preoccupation majeure du neurologue confronte au diagnostic de neuropathie peripherique. Dans cette demarche, la mise en evidence d’anomalies immunologiques dans le serum et plus rarement le liquide cephalo-rachidien, peut etre d’une aide determinante pour le diagnostic etiologique, mais peut aussi constituer une fausse piste, a l’origine de decisions therapeutiques inadaptees. La recherche d’une gammapathie monoclonale doit donc etre pratiquee et interpretee de preference dans les centres specialises dans le diagnostic etiologique des neuropathies peripheriques, en particulier dysimmunitaires, parallelement a d’autres recherches telles qu’une cryoglobulinemie et d’auto-anticorps seriques. La mise en evidence d’une gammapathie monoclonale, en particulier s’il s’agit d’une gammapathie monoclonale de signification indeterminee, implique la confrontation de cette donnee immunologique avec les autres signes de la neuropathie peripherique, en particulier cliniques, electrophysiologiques et le cas echeant neuropathologiques obtenus par biopsie nerveuse. Cette confrontation est d’une aide decisive pour la prise en charge diagnostique et therapeutique dans un nombre limite de correlations considerees comme pertinentes.

Lewis-Sumner syndrome (LSS) is a dysimmune peripheral nerve disorder, characterized by a predominantly distal, asymmetric weakness mostly affecting the upper limbs with sensory impairment, and by the presence of multifocal persistent conduction blocks. The nosological position of this neuropathy in relation to multifocal motor neuropathy (MMN) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is still debated. We report the clinical, biological and electrophysiological features, the course and the response to treatment in 23 LSS patients. The initial symptoms started in the distal part of an upper limb in 70% of patients. They were sensorimotor in 65% and purely sensory in 35% of patients. A cranial nerve involvement was observed in 26% of patients and a distal limb amyotrophy in 52%. The CSF protein level was normal in 67% of patients and mildly elevated in the remainder. None had serum anti-GM1 antibodies. There were multiple motor conduction blocks (average of 2.87/patient), predominantly located in the forearm, whereas demyelinating features outside the blocked nerves were rare. Abnormal distal sensory potentials were found in 87% of patients. The electrophysiological pattern suggests a very focal motor fibre demyelination sparing the nerve endings, whereas sensory fibre involvement was widespread. The course was chronic progressive in 71% of patients and relapsing-remitting in the others. During the follow-up study (median duration of 4 years), half of the patients progressed with a multifocal pattern and the distribution of the motor deficit remained similar to the initial presentation. The other patients showed a progression to the other limbs, suggesting a more diffuse process. Fifty-four percent of the patients treated with intravenous immunoglobulin showed an improvement, compared with 33% of the patients treated with oral steroids. Overall, 73% of patients had a positive response to immune-mediated therapy. LSS may be distinguished from MMN by the presence of sensory involvement, the absence of serum anti-GM1 antibodies and, in some cases, a positive response to steroids. In some of the patients in our study, LSS evolved into a more diffuse neuropathy sharing similarities with CIDP. Others had a clinical course characterized by a striking multifocal neuropathy, which suggests underlying mechanisms different from CIDP. Overall, whatever the clinical course, LSS responded to immune-mediated treatment in a manner similar to CIDP.

Neuropathy in Waldenstrom's macroglobulinemia (WM) is very heterogeneous. We retrospectively studied 40 patients with WM and neuropathy to analyze the different presentations and mechanisms encountered and to propose a diagnostic strategy. Twenty-five patients (62.5%) had axonal neuropathy, related to the following mechanisms: amyloid neuropathy (n = 5), cryoglobulinemic neuropathy (n = 5), neuropathy associated with tumoral infiltration (n = 2), vasculitic neuropathy (n = 2), a clinical motor neuropathy possibly of dysimmune origin (n = 6), or an unclassified mechanism (n = 5). A demyelinating pattern was observed in 15 patients, 10 having anti-myelin-associated glycoprotein (anti-MAG) antibodies and 5 having neuropathy related to chronic inflammatory demyelinating polyradiculoneuropathy. On the basis of these results, we propose a diagnostic strategy combining: (1) an EMG to distinguish between a demyelinating and an axonal pattern; (2) measurement of anti-MAG and anti-ganglioside antibodies; (3) screening for "red flag" features to orientate further investigations. This strategy may help clinicians to identify the mechanism of neuropathy in order to adapt the therapeutic strategy.

Since the first report of a high prevalence of monoclonal gammapathy (MG) in patients with peripheral neuropathy (PN), some 25 years ago, a large number of such associations have been described. Neuropathies associated with MG have heterogeneous clinical, neurophysiological, neuropathological, and hematological features. The most pertinent relationship seems to be that between distal acquired demyelinating sensory (DADS) neuropathy associated with IgM MG of unknown significance (MGUS) and the presence of serum autoantibodies reacting with myelin-associated glycoprotein (MAG). Other interesting correlations were recently reported in CANOMAD (chronic ataxic neuropathy with ophthalmoplegia, M-protein and anti-disialosyl antibodies). Patients with demyelinating neuropathy (DNP) associated with MG should be screened for malignant plasma cell dyscrasia. MG is more likely to be responsible for the neuropathy if it consists of IgM, if autoantibodies (mainly directed to MAG) are found in serum or on nerve biopsy, and if the clinical manifestations correspond to chronic distal sensory neuropathy. DNP associated with IgM MGUS sometimes responds to immunotherapy but the potential benefits must be considered in view of possible adverse effects. Rituximab, an anti-CD20 monoclonal antibody, has shown promise in this setting. DNP associated with IgG or IgA MGUS may be indistinguishable from chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), in terms of clinical and electrophysiological features and the treatment response. In the POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes), appropriate treatment can lead to a drastic improvement in the neuropathy. Patients with chronic axonal polyneuropathy associated with IgG MG should be screened for Al amyloidosis. However, most axonal polyneuropathies associated with IgG or IgM MGUS are indistinguishable from chronic idiopathic axonal polyneuropathies.

Introduction. les polyradiculonevrites sensitives sont considerees comme une variante clinique des polyradiculoneuropathies inflammatoires et demyelinisantes (PiDC). Classiquement, leur frequence varie entre 5 et 15 %. Les symptomes peuvent etre aspecifiques tels que paresthesies distales, hypoesthesie, ataxie, ou douleur neuropathique. leur retentissement est variable avec des formes paucysymptomatiques et d’autres severes avec handicap marque. Alors qu’il s’agit de formes purement sensitives, l’etude de la conduction motrice en eMg montre, dans certains cas, des anomalies de conduction suggerant une demyelinisation qui conduisent au diagnostic. Recemment, une forme ataxique avec eMg normal, liee a une atteinte proximale des racines sensitives diagnostiquee sur les PeS, l’iRM et l’existence d’une hyperproteinorachie a ete decrite (Sinnreich et al., 2004). une autre presentation avec peu d’anomalies eMg ressemblant a des neuropathies axonales cryptogeniques, diagnostiquees par une biopsie nerveuse a ete egalement recemment rapportee (Chin et al., 2004 ; vallat et al., 2003). la frequence de patients atteints de PiDC sensitives echappant aux criteres electrophysiologiques de demyelinisation habituels n’est pas connue, mais un point important est que ces formes semblent accessibles aux traitements immunomodulateurs. Aussi, malgre l’absence de signes suggerant une demyelinisation sur l’eMg, il est important d’identifier ces formes, afin de pouvoir faire beneficier les patients d’un traitement potentiellement efficace. Recemment, le groupe d’etude francais des PiDC a propose une strategie diagnostique pour ne pas meconnaitre les formes atypiques de PiDC, notamment celle echappant aux criteres electrophysiologiques. en pratique, en l’absence de signe eMg evident de demyelinisation, la situation est bien souvent celle d’un patient ou l’on pourrait conclure a une neuropathie axonale d’origine indeterminee, puisque le bilan etiologique demeure negatif. Neanmoins, le groupe d’etude francais des PiDC a propose une serie de signes cliniques qui ne sont pas compatibles avec une origine axonale longueur dependante, et qui doivent faire alors evoquer le diagnostic de PiDC atypiques. la demarche diagnostique s’appuie alors sur d’autres examens tels que l’etude de la ponction lombaire, les potentiels evoques somesthesiques, la biopsie nerveuse ou l’iRM des racines nerveuses. les objectifs de cette etude sont d’analyser : la frequence de PiDC sensitives et leur presentation ; • les elements permettant leur diagnostic ; • leur pronostic et leur reponse aux traitements. •

Abstract 3951 Background: Polyneuropathy is the most frequent neurological complication in Waldenstrom macroglobulinemia (WM). Most patients have an insidiously progressive distal symmetric sensorimotor and ataxic neuropathy due to a monoclonal immunoglobulin M anti-myelin-associated glycoprotein (MAG). There is still no treatment reference today. Recent studies underline the interest of Rituximab (RTX) but its efficacy is not yet proven. In order to identify the interest of immunotherapy, we performed a retrospective study in 61 patients with anti-MAG over a period of 12 years. Methods: All patients underwent neurological, biological (anti-MAG antibodies, IgM serum) and electrophysiological examination before and after each treatment. Clinically, patients were considered to be improved if they had a decrease of at least two points on the INCAT sensory sum score and/or a decrease of 20 mm on the visual analogue scale and/or motor strength improvement by at least two MRC points in the ankle dorsiflexor. Biologically, response anti-MAG antibodies and IgM serum were considered to be improved if their level was diminished by half. Electrophysiological studies were performed using standard procedures. Results: A total of 61 patients were analyzed. The median age at onset was 64 years (range 33–84), median serum IgM concentration 4.6 g/L (0-17), median anti-MAG antibodies 49900 BTU (23000>70000), RANKIN score 1 (35 patients), 2(20 patients), 3(6 patients). Twenty-five patients had WM with lymphoplasmacytic cells bone marrow infiltration. None of the patients had criteria for therapy initiation according to the 2th international workshop except symptomatic or evolving neuropathy. In first line, 45 patients were treated with Chlorambucil (CBL) (8 improved, 28 were stabilised, 9 worsened), 16 patients were treated with RTX alone (9) or in combination (7) (11 improved, 2 were stabilised, 3 worsened). RTX gave a significant higher response rate compared with CBL (p=2×10-4). With a median follow up of 96 months, 15 patients treated with CBL relapsed. Only one patient treated with RTX relapsed but the median follow up was not reached (60 months follow up). In the CBL group, 15 patients were treated at relapse with RTX and 11 improved, 3 were stabilised, 1 worsened. The average time follow up of the 2nd response was 48 months. Twelve patients in failure were treated with RTX: 8 improved, 1 was stabilised, 3 failed with an average follow up of 48 months. There was no significant difference between anti-MAG antibodies level before and after treatment (p=0.64) in patients in response but a low IgM level was associated with response to treatment (p Conclusion: In first line, RTX alone or in combination is associated with a higher response rate than CBL. For patients who relapsed after CHL, patients favourably responded to RTX with an average time follow up of 48 months. IgM level is a prognosis factor (p Disclosures: Choquet: Roche: Consultancy. Leblond:ROCHE: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; MUNDIPHARMA: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; GENZYME: Membership on an entity's Board of Directors or advisory committees; CELGENE: Membership on an entity's Board of Directors or advisory committees; JANSSEN: Membership on an entity's Board of Directors or advisory committees.