Exploring culturally competent primary care diabetes services: a single-city survey.

AIMS: To determine the cultural competence of diabetes services delivered to minority ethnic groups in a multicultural UK city with a diabetes prevalence of 4.3%. METHODS: A semi-structured survey comprising 35 questions was carried out across all 66 general practices in Coventry between November 2011 and January 2012. Data were analysed using descriptive statistics. The cultural competence of diabetes services reported in the survey was assessed using a culturally competent assessment tool (CCAT). RESULTS: Thirty-four general practices (52%) responded and six important findings emerged across those practices. (1) Ninety-four per cent of general practices reported the ethnicity of their populations. (2) One in three people with diabetes was from a minority ethnic group. (3) Nine (26.5%) practices reported a diabetes prevalence of between 55% and 96% in minority ethnic groups. (4) The cultural competences of diabetes services were assessed using CCAT; 56% of practices were found to be highly culturally competent and 26% were found to be moderately culturally competent. (5) Ten practices (29%) reported higher proportionate attendance at diabetes annual checks in the majority white British population compared with minority ethnic groups. (6) Cultural diversity in relation to language and strong cultural traditions around food were most commonly reported as barriers to culturally competent service delivery. CONCLUSIONS: Seven of the eight cultural barriers identified in the global evidence were present in the city. Use of the CCAT to assess existing service provision and the good baseline recording of ethnicity provide a sound basis for commissioning culturally competent interventions in the future.

The impact of culturally competent diabetes care interventions for improving diabetes-related outcomes in ethnic minority groups: a systematic review.

AIM: To examine the evidence on culturally competent interventions tailored to the needs of people with diabetes from ethnic minority groups. METHODS: MEDLINE (NHS Evidence), CINAHL and reference lists of retrieved papers were searched from inception to September 2011; two National Health Service specialist libraries were also searched. Google, Cochrane and DARE databases were interrogated and experts consulted. Studies were included if they reported primary research on the impact of culturally competent interventions on outcome measures of any ethnic minority group with diabetes. Paper selection and appraisal were conducted independently by two reviewers. The heterogeneity of the studies required narrative analysis. A novel culturally competent assessment tool was used to systematically assess the cultural competency of each intervention. RESULTS: Three hundred and twenty papers were retrieved and 11 included. Study designs varied with a diverse range of service providers. Of the interventions, 64% were found to be highly culturally competent (scoring 90-100%) and 36% moderately culturally competent (70-89%). Data were collected from 2616 participants on 22 patient-reported outcome measures. A consistent finding from 10 of the studies was that any structured intervention, tailored to ethnic minority groups by integrating elements of culture, language, religion and health literacy skills, produced a positive impact on a range of patient-important outcomes. CONCLUSIONS: Benefits in using culturally competent interventions with ethnic minority groups with diabetes were identified. The majority of interventions described as culturally competent were confirmed as so, when assessed using the culturally competent assessment tool. Further good quality research is required to determine effectiveness and cost-effectiveness of culturally competent interventions to influence diabetes service commissioners.

Epitopes, avidity and IgG subclasses of tyrosine hydroxylase autoantibodies in vitiligo and alopecia areata patients.

BACKGROUND: We previously detected antibodies against tyrosine hydroxylase (TH) in 23% of patients with nonsegmental vitiligo and in 19% of patients with alopecia areata (AA). OBJECTIVES: To identify TH epitopes recognized by TH antibodies in patients with vitiligo and AA. METHODS: Recombinant plasmids containing defined fragments of TH cDNA were constructed. The cloned TH cDNA fragments were subsequently translated in vitro to produce a series of [(35) S]-labelled TH protein fragments which were then used in radioimmunoassays to analyse the immunoreactivity of sera from 18 TH antibody-positive patients with vitiligo and so initially define TH epitope domains. Further localization of TH epitopes was investigated by antibody absorption experiments using synthetic TH peptides and nonradiolabelled, in vitro-expressed TH protein fragments. Antibody binding to identified epitopes was confirmed in TH peptide enzyme-linked immunosorbent assays. RESULTS: Analysis of the results obtained indicated the presence of two major antibody-binding sites on TH between amino acids 1 and 14 (epitope 1-14) and between amino acids 61 and 80 (epitope 61-80). Of 18 patients with vitiligo and six with AA, 17 (94%) and five (83%), respectively, had antibodies against epitope 1-14. In addition, 11/18 (61%) vitiligo and 2/6 (33%) AA patient sera displayed immunoreactivity against epitope 61-80. CONCLUSIONS: Two major binding sites for human TH antibodies are located at the N-terminus of the protein. The humoral immune response to TH in vitiligo and AA is heterogeneous in nature in that patients may have antibodies to more than one TH epitope. TH antibodies from patients with vitiligo or AA can recognize identical epitopes.

Demonstration of autoantibodies against tyrosine hydroxylase in patients with alopecia areata.

BACKGROUND: There is strong evidence to suggest that alopecia areata (AA) is a tissue-specific, T cell-mediated autoimmune disease, which is usually characterized by patchy areas of hair loss on the scalp. Tyrosine hydroxylase (TH) is a known B-cell autoantigen in patients with autoimmune polyendocrine syndrome type 1 (APS1) associated with the presence of AA. In addition, melanocyte-specific proteins, gp100 and MelanA, are putative T-cell autoantigens in AA and so may also represent targets of the humoral immune response. OBJECTIVE: To analyse the sera of patients with AA for the presence of antibodies against TH and the melanocyte-specific proteins tyrosinase, tyrosinase-related protein (TRP)-1, TRP-2, gp100 and MelanA. METHODS: Radioimmunoassays were used to detect the relevant antibodies in sera from patients with AA (n = 32) and in sera from healthy individuals (n = 28). RESULTS: Of 32 patients with AA, six (19%) were positive for TH antibodies. A significant increase in the frequency of TH antibodies in the AA patient group was evident when compared with controls (P = 0·03). Only three of 32 (9%) patients exhibited antibody responses to tyrosinase, TRP-1, TRP-2 and gp100. No immunoreactivity against MelanA was detected in any patient with AA. CONCLUSION: Antibodies against TH can be present in patients with AA unrelated to APS1. Humoral immune responses against tyrosinase, TRP-1, TRP-2, gp100 and MelanA are not prevalent in patients with AA. Overall, a dominant melanocyte-specific B-cell autoantigen in AA has yet to be identified.

Population-based association analyses of the HOPA12bp polymorphism for schizophrenia and hypothyroidism.

HOPA is an Xq13 chromosome gene that codes for a RXR nuclear receptor co-activator. In a prior study of the genetic basis of schizophrenia, we showed that exonic polymorphisms in HOPA were associated with increased risk of schizophrenia and hypothyroidism in a large cohort of probands from New York. In an attempt to replicate these findings, we examined this relationship in a cohort of 173 schizophrenic probands (128 males and 45 females providing 218 alleles) from Iowa. Consistent with the prior findings, we found an increased rate of the HOPA12bP exonic polymorphism in schizophrenic probands compared with random newborn controls (9 of 218 alleles vs. 33 of 2,049 alleles, P < 0.02). Furthermore, retrospective review of the medical records showed that two of the nine probands possessing the HOPA12bp allele in whom thyroid function was assessed were hypothyroid compared with 6 of 164 probands possessing the normal HOPAwild allele(s) (P < 0.06). We conclude that the HOPA12bp polymorphism shows a nominally significant association with schizophrenia and a nominal trend for association with hypothyroidism in our study and that further studies are required to define the features of this syndrome and the molecular mechanisms of disease pathogenesis.

Investigation of a candidate gene for schizophrenia on Xq13 previously associated with mental retardation and hypothyroidism.

Weak support for linkage of schizophrenia to proximal Xq has previously been reported. In addition, an increased prevalence of thyroid disorder has been noted in families of individuals with schizophrenia. Recently, a gene mapped to Xq13 termed HOPA has been found to be associated with mental retardation, hypothyroidism, and depression and to function as a coactivator for the thyroid receptor. We therefore examined the HOPA gene in a group of 111 probands from a larger cohort of multiplex families with schizophrenia, several of whom (n = 53) also had a family history of hypothyroidism. Four males and two females were found with an alteration in exon 42 of the HOPA gene compared with 8/492 males and 18/471 females (942 X chromosomes) compared with consecutively screened newborns (chi(2) = 3.92, P < 0.05). However, when available family members of each of the probands with an exon 42 variation were subsequently screened, the mutation did not segregate with schizophrenia in three of five families, although all 6 probands with an exon 42 variation did have hypothyroidism in either themselves (n = 3) or their mothers (n = 3) (P < 0.008). These findings replicate prior findings demonstrating an association between HOPA polymorphisms and hypothyroidism. In addition, the increased frequency of HOPA variants in this population may also provide a genetic basis for the familial association of thyroid disease and schizophrenia.

The structure and expression of the human neuroligin-3 gene.

The neuroligins are a family of proteins that are thought to mediate cell to cell interactions between neurons. During the sequencing at an Xq13 locus associated with a mental retardation syndrome in some studies, we discovered a portion of the human orthologue of the rat neuroligin-3 gene. We now report the structure and the expression of that gene. The gene spans approximately 30kb and contains eight exons. Unlike the rat gene, it codes for at least two mRNAs and at least one of which is expressed outside the CNS. Interestingly, the putative promoter for the gene overlaps the last exon of the neighboring HOPA gene and is located less than 1kb from an OPA element in which a polymorphism associated with mental retardation is found. These findings suggest a possible role for the neuroligin gene in mental retardation and that the role of the gene in humans may differ from its role in rats.