How often do nurses suspect violence and domestic violence in local emergency medical communication centre? A cross-sectional study.

OBJECTIVE: To assess the extent of violence that is revealed by screening at first contact with a local out-of-hours emergency medical communication centre (LEMC; Norwegian 'Legevaktsentral'). DESIGN: Cross-sectional study. SETTING: Arendal LEMC, covering 10 municipalities in south-eastern Norway. All contacting patients (telephone or personal attendance) were asked by nurse whether the encounter was related to violence. SUBJECTS: All first patient encounters at Arendal LEMC. MAIN OUTCOME MEASURES: Number and proportion of cases where the nurses suspected violence, both domestic violence and other violence. Incidence rate of violence, age and gender distribution of patients, time of day and reason for encounter. RESULTS: Violence was suspected in 336 of 103,467 first patient encounters (0.3%), of which 132 (0.1%) was domestic violence. Patients were female in 50.6% of all violence cases, and in 79% of domestic violence cases. Incidence rates were 137 per 100,000 person-years for all violence, and 53 for domestic violence. CONCLUSIONS: This study indicates violence may be revealed in three of 1000 first encounters to an LEMC when nurses screen systematically for domestic or other violence.Key points    Violence as underlying reason for encounter with primary care emergency health services is probably often not discovered by health personnel. • We examined how often nurses reveal violence upon first contact when systematically asking all patients. • Violence was suspected in 0.3% of cases, and domestic violence in 0.1%. • Among patients with disclosed domestic violence, 79% were female.

IgG Fc-receptor polymorphisms in Guillain-Barré syndrome.

The authors studied immunoglobulin G (IgG) Fc receptor (FcgammaR) IIA, IIIA, and IIIB polymorphisms in 62 patients with Guillain-Barré syndrome (GBS) and in 89 healthy controls. The FcgammaR genotypes and allele frequencies did not differ significantly between the patients with GBS and the controls. Patients homozygous for the FcgammaRIIIB neutrophil antigen (NA) 1 allele had a significantly less severe disease than patients heterozygous or homozygous for the NA2 allele. The FcgammaRIIIB NA1/NA1 genotype has high affinity for IgG1 and IgG3, and clearance of circulating autoantibodies and immune complexes may therefore be of importance in the pathogenesis of GBS.

IgG allotypes and subclasses in Norwegian patients with multiple sclerosis.

Multiple sclerosis (MS) is a multifactorial disease in which genetic and environmental factors apparently have a major influence on the susceptibility and course of the disease. In the present study we have investigated the genetic basis and subclass levels of IgG in MS. Hundred and thirty-six Norwegian patients with MS and 92 controls were genotyped for IgG allotypes of the GM and KM systems. IgG and IgG subclasses were quantified in sera from 115 MS patients and 20 controls. Neither GM nor KM allo-, haplo- or genotypes were significantly correlated with susceptibility, severity or course of the disease. The G1M (3) (3), G2M (23) (23) and G3M (5) (5) allotypes were significantly correlated with high serum levels of IgG3, whereas high IgG2 levels were correlated with G1M (3) (3) and G2M (23) (23) in both patients and controls. Serum levels of IgG subclasses were not significantly correlated with course or severity of the disease. The results indicate no major role for IgG allotypes or IgG subclass levels in the pathogenesis of MS.

Immunoglobulin G Fc-receptor (FcgammaR) IIA and IIIB polymorphisms related to disability in MS.

OBJECTIVE: MS is immunologically mediated in genetically susceptible individuals. Receptors for the Fc fragment of immunoglobulin G (IgG) (FcgammaR) link the humoral and cellular immune responses by targeting immune complexes to effector cells. Different FcgammaR show variability in their distribution, strength, and capacity of binding different IgG subclasses. METHODS: To investigate the role of FcgammaR in MS, 136 MS patients and 96 matched controls were genotyped for FcgammaRIIA and FcgammaRIIIB gene polymorphisms; the results were correlated to disease susceptibility and severity measured by the Expanded Disability Status Scale (EDSS). RESULTS: The allele frequencies of the FcgammaRIIA and FcgammaRIIIB did not differ significantly between the MS patients and the controls. Patients homozygous for the FcgammaRIIIB neutrophil antigen (NA) 1 allele had a significantly more benign course of MS than patients heterozygous or homozygous for the FcgammaRIIIB NA2 allele. Patients homozygous for the FcgammaRIIA histidine (H) allele also had a more benign course of MS than patients heterozygous or homozygous for the FcgammaRIIA arginine (R) allele. CONCLUSION: The results implicate FcgammaRIIIB and to a lesser extent FcgammaRIIA as disease-modifying genes in MS. FcgammaRIIIB NA1/NA1 and FcgammaRIIA H/H bind more efficient IgG1/IgG3 and IgG2 subclasses, respectively, than FcgammaRIIIB NA2/NA2 and FcgammaRIIA R/R. A more effective processing of circulating immune complexes may be one mechanism for better clinical outcome in MS.

FcgammaRIIA and FcgammaRIIIB polymorphisms in myasthenia gravis.

The Fcgamma receptors, FcgammaRIIA and FcgammaRIIIB contain polymorphisms with different capacity for IgG binding and phagocytosis. Thirty myasthenia gravis (MG) patients and 49 healthy controls were genotyped for the FcgammaRIIA and FcgammaRIIIB polymorphisms using polymerase chain reaction. The frequency of the FcgammaRIIA-H/H genotype was increased in thymoma MG patients compared to other MG patients (P = 0.05) and controls (P = 0.02). The distribution of FcgammaRIIIB alleles in MG patients did not differ from the controls, but MG patients with the NA1/NA1 genotype had the most severe MG (P = 0.01). Levels of AChR-antibodies and frequency of titin or ryanodine receptor antibodies were not associated with the FcgammaRIIA or FcgammaRIIIB genotypes. The results suggest different pathogenetic mechanisms in paraneoplastic and non-paraneoplastic autoimmune MG.