Other Autoimmune Diseases (other + autoimmune_diseases)

Distribution by Scientific Domains
Distribution within Medical Sciences

Selected Abstracts

Autoimmunity as a prognostic factor in melanoma patients treated with adjuvant low-dose interferon alpha

Imke Satzger
Abstract Interferon alpha is used for the adjuvant treatment of malignant melanoma at different dosages (high-, intermediate-, low-dose therapy). Only a minority of patients might benefit from this therapy, and markers to identify such patients are missing. A recent study suggested that melanoma patients developing autoantibodies or clinical manifestations of autoimmunity during adjuvant high-dose interferon alpha treatment had a significant survival benefit. We retrospectively reviewed 134 melanoma patients from our institution treated with adjuvant low-dose interferon alpha therapy and correlated the development of autoimmune diseases with prognosis. Interferon (IFN) therapy was routinely monitored by history, physical examination and laboratory tests before, after the first month and then after every 3 months of therapy. During a median follow up of 46.0 months (8.5,79.0 months) 28 patients (20.9%) suffered from recurrences and melanoma related deaths occurred in 16 patients (11.9%). In 20 patients (14.9%) autoimmune thyroiditis (AIT) was diagnosed during IFN therapy, one of these 20 patients developed rheumatoid arthritis later while continuing IFN therapy. Other autoimmune diseases were not observed. In 2 patients (one with AIT and one with arthritis) the autoimmune disease led to discontinuation of IFN therapy, in the other patients AIT remained subclinical or responded well to treatment while IFN therapy was continued. Kaplan,Meier analyses revealed a significant better recurrence free survival and a trend for a better overall survival for patients with AIT. Thus, autoimmunity triggered by low-dose IFN therapy appears to indicate an improved prognosis and should encourage continuation of IFN therapy. © 2007 Wiley-Liss, Inc. [source]

Recommendation for a definition of acute symptomatic seizure

EPILEPSIA, Issue 4 2010
Ettore Beghi
Summary Purpose:, To consider the definition of acute symptomatic seizures for epidemiological studies, and to refine the criteria used to distinguish these seizures from unprovoked seizures for specific etiologies. Methods:, Systematic review of the literature and of epidemiologic studies. Results:, An acute symptomatic seizure is defined as a clinical seizure occurring at the time of a systemic insult or in close temporal association with a documented brain insult. Suggestions are made to define acute symptomatic seizures as those events occurring within 1 week of stroke, traumatic brain injury, anoxic encephalopathy, or intracranial surgery; at first identification of subdural hematoma; at the presence of an active central nervous system (CNS) infection; or during an active phase of multiple sclerosis or other autoimmune diseases. In addition, a diagnosis of acute symptomatic seizure should be made in the presence of severe metabolic derangements (documented within 24 h by specific biochemical or hematologic abnormalities), drug or alcohol intoxication and withdrawal, or exposure to well-defined epileptogenic drugs. Discussion:, Acute symptomatic seizures must be distinguished from unprovoked seizures and separately categorized for epidemiologic purposes. These recommendations are based upon the best available data at the time of this report. Systematic studies should be undertaken to better define the associations in question, with special reference to metabolic and toxic insults, for which the time window for the occurrence of an acute symptomatic seizure and the absolute values for toxic and metabolic dysfunction still require a clear identification. [source]

Genetic background of primary biliary cirrhosis

Atsushi Tanaka
The clustering of patients in a representative family as well as relatively high concordance rate in monozygotic twins strongly indicate that genetic factors play a crucial role in modulating primary biliary cirrhosis (PBC) by conferring susceptibility to, or providing protection from, the disease. Therefore, much like other autoimmune diseases, intensive investigations have attempted to elucidate which genes are incriminated in the etiology of PBC. So far, a number of genes, including major histocompatibility complex (MHC) class I and II, cytokines and cell surface molecules, have been examined to seek the possibility of whether single nucleotide polymorphisms (SNP) of the gene might be associated with susceptibility to PBC. Nevertheless, it appears that methodologicaldifficulties, mainly the limitation of the number of individuals tested in each study, hamper the detection of a convincing and reproducible link between genetic polymorphisms and the etiology of PBC. Also, the difference in genetic background among several ethnic groups may play a role in concealing the association. In this review, I will highlight the genetic association in PBC, and review the association of genetic polymorphisms with the etiology of PBC, which have been reported in various ethnicities. [source]

Autoimmune disease concomitance among inflammatory bowel disease patients in the United States, 2001-2002

Russell Cohen MD
Abstract Background: Recent studies suggest that inflammatory bowel disease (IBD) may share an underlying pathogenesis with other autoimmune diseases. Methods: Two United States data sets with patient-level medical and drug claims were used to explore the occurrence of autoimmune diseases in patients with IBD, particularly Crohn's disease (CD) and ulcerative colitis (UC), with that in controls. From 2001 to 2002 IBD patients were identified using International Classification of Diseases, 9th revision, diagnosis codes in the IMS Health Integrated Administration Claims Database and the Market Scan Commercial Claims and Encounters Database. Controls were selected by matching on sex, age, Census Bureau region, and length of previous medical insurance coverage. Odds ratios (ORs) evaluated the risk relationship between IBD patients and controls within an estimated Mantel-Haenszel 95% confidence interval. Sensitivity analysis tested the case identification method used to select IBD patients. Results: The risk for ankylosing spondylitis (AS) was substantially increased across both data sets: OR (95% confidence interval [CI]) of 7.8 (5.6,10.8) in IMS Health and 5.8 (3.9,8.6) in MarketScan. The risk for rheumatoid arthritis (RA) was 2.7 (2.4,3.0) and 2.1 (1.8,2.3), respectively; for multiple sclerosis (MS); the ORs were 1.5 (1.2,1.9) and 1.6 (1.2,2.1), respectively. There was no increased risk for type 1 diabetes mellitus, and the results for psoriatic arthritis (PsA) were inconsistent. The sensitivity analysis supported these findings. Conclusions: A much higher risk for RA, AS, PsA, and MS was observed in IBD patients compared with controls. Prospective epidemiologic studies are needed to confirm these findings and explore the pathogenic mechanism of this relationship. (Inflamm Bowel Dis 2008) [source]

Molecular abnormalities of T-cells in systemic lupus erythematosus

Abstract Substantial evidence supports that T-cells play a central role in the pathogenesis of systemic lupus erythematosus (SLE). To explore the molecular basis of the defective function of SLE T-cells, we focused on the signal transduction system via T-cell antigen receptor (TCR) in peripheral blood T-cells from SLE patients. Comprehensive analysis to identify the molecules responsible for the defects showed the expression of the TCR , chain was attenuated, or absent in more than half of SLE patients. Moreover, the aberrant transcripts of the TCR , chain, including spliced variants lacking exon 7 and with a short 3,-UTR, were detected in SLE T-cells. Although attenuated expression of the TCR , chain is also observed in patients with cancers, infections, and other autoimmune diseases, sustained attenuation of TCR , expression and aberrant transcripts are only observed in SLE. In this review we discuss the unique features of the TCR , defects in SLE. [source]

Treatment of autoimmune ovarian disease by co-administration with mouse zona pellucida protein 3 and DNA vaccine through induction of adaptive regulatory T cells

Jinyao Li
Abstract Background Autoimmune ovarian disease (AOD) caused by auto-reactive T cells is considered a major reason for human premature ovarian failure, which affects 5% of women worldwide. Methods and Results To develop an effective treatment for AOD, we showed that the co-administration of mouse zona pellucida protein 3 (mZP3) protein and DNA vaccine encoding the mZP3 was able to meliorate AOD in an AOD murine model induced by the mZP3. We observed that established AOD in mice reverted to a normal ovarian morphology without notable T-cell infiltration in the co-administrated group; whereas mice in the control groups developed severe AOD. The amelioration appears to be antigen specific because other co-administration combinations failed to reverse AOD and correlates with significant reductions of pathogenic T-cell responses and productions of tumor necrosis factor-, and interferon-,. Furthermore, the melioration is apparently associated with the induction of mZP3 specific regulatory T cells that exhibit a phenotypic CD4+CD25,FoxP3+IL-10+ in the co-administrated group, which can be transferred to reverse AOD in vivo. Conclusions Thus, co-administration of mZP3 DNA and protein vaccines can be used to treat established AOD, and may provide a novel immunotherapy strategy to treat other autoimmune diseases. Copyright © 2008 John Wiley & Sons, Ltd. [source]

Lower expression levels of the programmed death 1 receptor on CD4+CD25+ T cells and correlation with the PD-1.3A genotype in patients with systemic lupus erythematosus

Helga Kristjansdottir
Objective A genetic polymorphism in the programmed death 1 (PD-1) gene encoding the coinhibitory PD-1 immunoreceptor, PD-1.3A, is associated with systemic lupus erythematosus (SLE). The aim of this study was to assess PD-1 receptor expression in patients with SLE, in comparison with relatives and unrelated healthy controls, and to identify correlations of lower expression levels of PD-1 receptor with the PD-1.3A genotype. Methods Patients with SLE, patients' relatives, and unrelated healthy control subjects from Iceland and Sweden were studied. Peripheral blood mononuclear cells (PBMCs) were stimulated with anti-CD3/anti-CD28, and PD-1 expression was analyzed by flow cytometry. PD-1.3A/G genotyping was performed using polymerase chain reaction,restriction fragment length polymorphism analysis. Results PD-1 expression on PBMCs was induced after antibody stimulation, showing increases of 2.1-fold in SLE patients, 3.1-fold in relatives, and 5.1-fold in healthy controls. The frequency of PD-1+ cells was significantly lower in SLE patients compared with relatives and healthy controls. PD-1 expression on PD-1+ cells and on CD4+CD25+ T cells was significantly lower in SLE patients and relatives compared with healthy controls. PD-1 expression was significantly elevated on CD25high cells. Levels of PD-1 expression on CD25high and CD25intermediate cells were significantly lower in SLE patients compared with healthy controls. PD-1 was expressed on both FoxP3, and FoxP3+ cells. Lower expression of PD-1 was significantly correlated with the PD-1.3A/G genotype. Conclusion The results demonstrate significantly lower PD-1 receptor expression in SLE patients and their relatives and reveal a significant correlation of lower PD-1 expression with the PD-1.3A allele. Thus, PD-1.3A may contribute to abnormalities in PD-1 receptor expression on CD4+CD25+ T cells in patients with SLE, providing support for an important role of the PD-1 pathway in SLE and, possibly, in other autoimmune diseases. [source]

Analysis of maternal,offspring HLA compatibility, parent-of-origin effects, and noninherited maternal antigen effects for HLA,DRB1 in systemic lupus erythematosus

Paola G. Bronson
Objective Genetic susceptibility to systemic lupus erythematosus (SLE) is well established, with the HLA class II DRB1 and DQB1 loci demonstrating the strongest association. However, HLA may also influence SLE through novel biologic mechanisms in addition to genetic transmission of risk alleles. Evidence for increased maternal,offspring HLA class II compatibility in SLE and differences in maternal versus paternal transmission rates (parent-of-origin effects) and nontransmission rates (noninherited maternal antigen [NIMA] effects) in other autoimmune diseases have been reported. Thus, we investigated maternal,offspring HLA compatibility, parent-of-origin effects, and NIMA effects at DRB1 in SLE. Methods The cohort comprised 707 SLE families and 188 independent healthy maternal,offspring pairs (total of 2,497 individuals). Family-based association tests were conducted to compare transmitted versus nontransmitted alleles (transmission disequilibrium test) and both maternally versus paternally transmitted (parent-of-origin) and nontransmitted alleles (using the chi-square test of heterogeneity). Analyses were stratified according to the sex of the offspring. Maternally affected offspring DRB1 compatibility in SLE families was compared with paternally affected offspring compatibility and with independent control maternal,offspring pairs (using Fisher's test) and was restricted to male and nulligravid female offspring with SLE. Results As expected, DRB1 was associated with SLE (P < 1 × 10,4). However, mothers of children with SLE had similar transmission and nontransmission frequencies for DRB1 alleles when compared with fathers, including those for the known SLE risk alleles HLA,DRB1*0301, *1501, and *0801. No association between maternal,offspring compatibility and SLE was observed. Conclusion Maternal,offspring HLA compatibility, parent-of-origin effects, and NIMA effects at DRB1 are unlikely to play a role in SLE. [source]

The FAS ,670A>G polymorphism influences susceptibility to systemic sclerosis phenotypes

J. Broen
Objective To investigate the possible role of the FAS ,670A>G functional polymorphism in the genetic predisposition to systemic sclerosis (SSc) susceptibility or clinical phenotype. Methods A total of 2,900 SSc patients and 3,186 healthy controls were included in this study. We analyzed the genotype and allele frequencies of the FAS ,670A>G polymorphism in 9 distinct ethnic cohorts, including 6 cohorts of European ancestry (a Spanish cohort of 228 SSc patients and 265 controls, a Dutch cohort of 203 SSc patients and 277 controls, a German cohort of 313 SSc patients and 247 controls, an Italian cohort of 323 SSc cases and 89 controls, a British cohort of 269 SSc patients, and a Swedish cohort of 182 patients) and 3 distinct ethnic cohorts from the US (a cohort of 1,047 white patients and 692 controls, a cohort of 159 Hispanic patients and 137 controls, and a cohort of 176 black SSc patients and 194 controls). Genotyping was performed using a TaqMan 5, allelic discrimination assay. Results In the British, Italian, and American white cohorts we observed an association of the FAS ,670G allele with limited cutaneous SSc (lcSSc) (odds ratios [ORs] 1.25, 1.43, and 1.18, respectively). A meta-analysis comprising all 9 cohorts revealed an association of both the FAS ,670G allele (OR 1.10) and the FAS ,670GG genotype (OR 1.13) with the lcSSc phenotype. In a meta-analysis including only white subjects, both the FAS ,670G allele and the FAS ,670GG genotype remained associated with lcSSc (allele OR 1.12; genotype OR 1.16). In addition, a recessive model of the ,670GG genotype exhibited a strong association with SSc, lcSSc, and anticentromere antibody,positive lcSSc (OR 1.23, OR 1.33, and OR 1.45, respectively). Conclusion Our data show that the FAS ,670A>G polymorphism plays a role in lcSSc susceptibility. A similar trend has been observed in other autoimmune diseases. [source]

Variants in TNFAIP3, STAT4, and C12orf30 loci associated with multiple autoimmune diseases are also associated with juvenile idiopathic arthritis

Sampath Prahalad
Objective Subtypes of juvenile idiopathic arthritis (JIA) share phenotypic features with other autoimmune disorders. We investigated several genetic variants associated with rheumatoid arthritis (RA) and other autoimmune disorders for association with JIA to test the hypothesis that clinically distinct phenotypes share common genetic susceptibility factors. Methods Cases were 445 children with JIA, and controls were 643 healthy adults. Using the TaqMan assay, subjects were genotyped for 8 single-nucleotide polymorphisms in 7 loci including rs10499194 and rs6920220 in the TNFAIP3 locus, rs6679677 in the RSBN1 locus, rs17696736 in the C12orf30 locus, rs3761847 in the TRAF1/C5 locus, rs2104286 in the IL2RA locus, rs7574865 in the STAT4 locus, and rs2542151 in the PTPN2 locus. Alleles and genotypes were analyzed for association with JIA and JIA subtypes. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Results The strongest associations with JIA risk or protection were observed for TNFAIP3 variants rs10499194 (OR 0.74 [95% CI 0.61,0.91], P < 0.004) and rs6920220 (OR 1.30 [95% CI 1.05,1.61], P = 0.015). We also observed associations between JIA and both STAT4 (OR 1.24 [95% CI 1.02,1.51], P = 0.029) and C12orf30 (OR 1.20 [95% CI 1.01,1.43], P = 0.041) variants. The PTPN2 variant rs2542151 deviated from Hardy-Weinberg equilibrium and was excluded from analyses. Variants in IL2RA, TRAF1/C5, and RSBN1 were not associated with JIA. After stratification by JIA subtype, the TNFAIP3 and C12orf30 variants were associated with oligoarticular JIA, while the STAT4 variant was associated primarily with polyarticular JIA. Conclusion We have demonstrated associations between JIA and variants in the TNFAIP3, STAT4, and C12orf30 regions that have previously shown associations with other autoimmune diseases, including RA and systemic lupus erythematosus. Our results suggest that clinically distinct autoimmune phenotypes share common genetic susceptibility factors. [source]

Familial associations of rheumatoid arthritis with autoimmune diseases and related conditions

Kari Hemminki
Objective In the era of genome-wide association studies, familial risks are used to estimate disease heritability and the likelihood of candidate-gene identification. This study was undertaken to estimate associations of rheumatoid arthritis (RA) with any of 33 autoimmune diseases and related conditions among parents and offspring, singleton siblings, twins, and spouses. Methods The Multigeneration Register in Sweden was used as a reliable source of information on Swedish families throughout the last century. Data on autoimmune diseases in individual family members were obtained through linkage to the Hospital Discharge Register. The standardized incidence ratio (SIR) was calculated as a measure of the relative risk of RA in family members of patients with RA or any of 33 other autoimmune diseases or related conditions, as compared with the relative risk of RA in those lacking an affected family member. Results Among a total of 447,704 patients, 47,361 were diagnosed as having RA. The SIRs for RA were 3.02 in offspring of affected parents, 4.64 in siblings, 9.31 in multiplex families, 6.48 in twins, and 1.17 in spouses. Significant associations with the familial risk of RA in offspring according to parental proband were observed for ankylosing spondylitis (SIR 2.96), localized scleroderma (SIR 2.40), Sjögren's syndrome (SIR 2.25), systemic lupus erythematosus (SIR 2.13), systemic sclerosis (SIR 1.65), Hashimoto thyroiditis/hypothyroidism (SIR 1.54), pernicious anemia (SIR 1.53), sarcoidosis (SIR 1.40), psoriasis (SIR 1.36), Wegener's granulomatosis (SIR 1.34), and asthma or polymyalgia rheumatica (SIR 1.32). Conclusion This is the first study to compare the familial risks of RA in relation to a large number of autoimmune diseases and related conditions using data from a single population. The high discordant familial risks in this population suggest that there is extensive genetic sharing between RA and the associated diseases. [source]

Early targets of nuclear RNP humoral autoimmunity in human systemic lupus erythematosus

Brian D. Poole
Objective The U1 small nuclear RNPs are common targets of autoantibodies in lupus and other autoimmune diseases. However, the etiology and progression of autoimmune responses directed against these antigens are not well understood. The aim of this study was to use a unique collection of serial samples obtained from patients before and after the development of nuclear RNP (nRNP) antibodies to investigate early humoral events in the development of anti-nRNP autoimmunity. Methods Lupus patients with sera available from both before and after the development of nRNP antibody precipitin were identified from the Oklahoma Clinical Immunology Serum Repository. Antibodies in the serial samples were analyzed by enzyme-linked immunosorbent assay, Western blotting, solid-phase epitope mapping, and competition assays. Results The first-detected nRNP antibodies targeted 6 common initial epitopes in nRNP A, 2 in nRNP C, and 9 in nRNP 70K. The initial epitopes of nRNP A and nRNP C were significantly enriched for proline and shared up to 95% sequence homology. The initial nRNP 70K humoral epitopes differed from those of nRNP A and nRNP C. The initial antibodies to nRNP A and nRNP C were cross-reactive with the SmB,-derived peptide PPPGMRPP. Antibody binding against all 3 nRNP subunits diversified significantly over time. Conclusion Autoantibodies to nRNP A and nRNP C initially targeted restricted, proline-rich motifs. Antibody binding subsequently spread to other epitopes. The similarity and cross-reactivity between the initial targets of nRNP and Sm autoantibodies identifies a likely commonality in cause and a focal point for intermolecular epitope spreading. [source]

The PTPN22 C1858T polymorphism is associated with skewing of cytokine profiles toward high interferon-, activity and low tumor necrosis factor , levels in patients with lupus

Silvia N. Kariuki
Objective The C1858T polymorphism in PTPN22 has been associated with the risk of systemic lupus erythematosus (SLE) as well as multiple other autoimmune diseases. We have previously shown that high serum interferon-, (IFN,) activity is a heritable risk factor for SLE. The aim of this study was to determine whether the PTPN22 risk variant may shift serum cytokine profiles to higher IFN, activity, resulting in risk of disease. Methods IFN, was measured in 143 patients with SLE, using a functional reporter cell assay, and tumor necrosis factor , (TNF,) was measured by enzyme-linked immunosorbent assay. The rs2476601 single-nucleotide polymorphism in PTPN22 (C1858T) was genotyped in the same patients. Patients were grouped, using a clustering algorithm, into 4 cytokine groups (IFN, predominant, IFN, and TNF, correlated, TNF, predominant, and both IFN, and TNF, low). Results SLE patients carrying the risk allele of PTPN22 had higher serum IFN, activity than patients lacking the risk allele (P = 0.027). TNF, levels were lower in carriers of the risk allele (P = 0.030), and the risk allele was more common in patients in the IFN,-predominant and IFN, and TNF,-correlated groups as compared with patients in the TNF,-predominant and both IFN, and TNF,-low groups (P = 0.001). Twenty-five percent of male patients carried the risk allele, compared with 10% of female patients (P = 0.024); however, cytokine skewing was similar in both sexes. Conclusion The autoimmune disease risk allele of PTPN22 is associated with skewing of serum cytokine profiles toward higher IFN, activity and lower TNF, levels in vivo in patients with SLE. This serum cytokine pattern may be relevant in other autoimmune diseases associated with the PTPN22 risk allele. [source]

Assessing vitamin D in the central nervous system

T. Holmøy
Holmøy T, Moen SM. Assessing vitamin D in the central nervous system. Acta Neurol Scand: 2010: 122 (Suppl. 190): 88,92. © 2010 John Wiley & Sons A/S. Epidemiological and experimental evidence suggest that vitamin D deficiency is a risk factor for multiple sclerosis and other autoimmune diseases. The activated form of vitamin D exerts several immunomodulating properties in vitro and in vivo, that could contribute to explain the association with multiple sclerosis. Hypovitaminosis D is also associated with several other neurological diseases that is less likely mediated by dysregulated immune responses, including Parkinson's disease and Alzheimer's disease, schizophrenia and affective disorders, suggesting a more diverse role for vitamin D in the maintenance of brain health. Accordingly, both the vitamin D receptor and the enzymes necessary to synthesize bioactive 1,25-dihydroxyvitamin D are expressed in the brain, and hypovitaminosis D is associated with abnormal development and function of the brain. We here review current knowledge on the intrathecal vitamin D homeostasis in heath and disease, highlighting the need to assess vitamin D in the intrathecal compartment. [source]

Allergy, family history of autoimmune diseases, and the risk of multiple sclerosis

A. Alonso
Objective , Previous reports suggested an association between allergy, autoimmunity, and risk of multiple sclerosis (MS), but results have been inconsistent. The present study assessed the association between history of allergy and autoimmune diseases, and the risk of MS. Methods , We conducted a case,control study nested in the Nurses' Health Study (NHS) and NHS II cohorts. A total of 298 women with MS were matched with 1248 healthy controls and 248 women with history of breast cancer. A mailed questionnaire gathered information about history of allergic conditions and autoimmune disorders. Results , History of allergy was not associated with MS risk [odds ratio (OR) 1.0, 95% confidence interval (CI) 0.8,1.4]. As expected, cases were more likely to have a positive family history of MS than controls (OR 9.7, 95% CI 6.1,15.3). A modest association was found between family history of other autoimmune diseases and MS risk (OR 1.4, 95% CI 1.0,1.8). We obtained similar results when we used women with breast cancer as comparison group. Conclusion , Family history of other autoimmune diseases was associated with a higher MS risk, suggesting a common genetic background or shared environmental triggers. There was no clear association between personal history of allergy and risk of MS. [source]

Extracorporeal photopheresis: what is it and when should it be used?

J. Scarisbrick
Summary Extracorporeal photopheresis (ECP) is a technique that was developed > 20 years ago to treat erythrodermic cutaneous T-cell lymphoma (CTCL). The technique involves removal of peripheral blood, separation of the buffy coat, and photoactivation with a photosensitizer and ultraviolet A irradiation before re-infusion of cells. More than 1000 patients with CTCL have been treated with ECP, with response rates of 31,100%. ECP has been used in a number of other conditions, most widely in the treatment of chronic graft-versus-host disease (cGvHD) with response rates of 29,100%. ECP has also been used in several other autoimmune diseases including acute GVHD, solid organ transplant rejection and Crohn's disease, with some success. ECP is a relatively safe procedure, and side-effects are typically mild and transient. Severe reactions including vasovagal syncope or infections are uncommon. This is very valuable in conditions for which alternative treatments are highly toxic. The mechanism of action of ECP remains elusive. ECP produces a number of immunological changes and in some patients produces immune homeostasis with resultant clinical improvement. ECP is available in seven centres in the UK. Experts from all these centres formed an Expert Photopheresis Group and published the UK consensus statement for ECP in 2008. All centres consider patients with erythrodermic CTCL and steroid-refractory cGvHD for treatment. The National Institute for Health and Clinical Excellence endorsed the use of ECP for CTCL and suggested a need for expansion while recommending its use in specialist centres. ECP is safe, effective, and improves quality of life in erythrodermic CTCL and cGvHD, and should be more widely available for these patients. [source]

Vitiligo associated with other autoimmune diseases: polyglandular autoimmune syndrome types 3B + C and 4

P. Amerio
Summary Vitiligo is a common skin disease characterized by depigmented maculae resulting from a reduction of the number and function of melanocytes. Many studies suggest that vitiligo might be an autoimmune disease. Vitiligo has been frequently described in association with other autoimmune diseases. Among the diseases described in association with vitiligo are the so-called autoimmune polyglandular syndromes (APS). Vitiligo can be present in all types of APS but the most frequent association appears to be in APS-3. APS-3 was defined as the association between autoimmune thyroiditis and another autoimmune disease. Here we report one patient with thyroiditis, vitiligo and autoimmune gastritis (APS-3B +,C), one patient with chronic autoimmune thyroiditis, vitiligo and alopecia (APS-3C), and one case of a young patient with type 1 diabetes mellitus and vitiligo (APS-4), according to the newest classification. We stress the importance of a thorough assessment for autoimmune diseases in selected patients with vitiligo. [source]