Evaluation of serum interleukin-17 A and interleukin-22 levels in pediatric patients with autism spectrum disorder: a pilot study.

BACKGROUND: Many neurodevelopmental abnormalities are connected to autism spectrum disorder (ASD), which can result in inflammation and elevated cytokine levels due to immune system dysregulation. Interleukin (IL)-17 A and IL-22 have been linked to the regulation of host defense against pathogens at the barrier surface, the regeneration of injured tissue, and the integration of the neurological, endocrine, and immune systems. Several studies have investigated the possible connection between IL-17 A and ASD as well as the severity of behavioral symptoms, but few of them included IL-22. OBJECTIVES: To measure serum levels of interleukin (IL)-17 A and IL-22 in children with ASD and to investigate their association with disease severity. METHODS: This pilot study was performed on 24 children with ASD and 24 matched controls. Childhood Autism Rating Scale (CARS) assessed ASD severity, and serum levels of IL-17 A and IL-22 were assessed by enzyme-linked immunosorbent assay (ELISA). RESULTS: In ASD patients, serum levels of IL-17 A and IL-22 showed a significant increase compared to controls (p-values < 0.001). We compared serum levels of IL-17 A and IL-22 according to the severity categories by CARS and could not find any significant differences (p-values > 0.05). Only IL-22 had a significant positive correlation with ASD severity by CARS scores. CONCLUSIONS: Raised serum levels of IL-17 A and IL-22 are associated with ASD; only IL-22, not IL-17 A, is correlated with ASD severity. This finding proposes IL-22 as a possible future effective target for ASD treatment. To fully comprehend the significance of these cytokines in ASD and their possible effects on ASD diagnosis and treatment, more research on a wider scale is required.

Reduced levels of plasma polyunsaturated fatty acids and serum carnitine in autistic children: relation to gastrointestinal manifestations.

BACKGROUND: Gastrointestinal (GI) manifestations are common in autistic children. Polyunsaturated fatty acids (PUFAs) and carnitine are anti-inflammatory molecules and their deficiency may result in GI inflammation. The relationship between the increased frequency of GI manifestations and reduced levels of PUFAs and carnitine was not previously investigated in autistic patients. This study was the first to investigate plasma levels of PUFAs and serum carnitine in relation to GI manifestations in autistic children. METHODS: Plasma levels of PUFAs (including linoleic, alphalinolenic, arachidonic "AA" and docosahexaenoic "DHA" acids) and serum carnitine were measured in 100 autistic children and 100 healthy-matched children. RESULTS: Reduced levels of serum carnitine and plasma DHA, AA, linolenic and linoleic acids were found in 66%, 62%, 60%, 43% and 38%, respectively of autistic children. On the other hand, 54% of autistic patients had elevated ω6/ω3 ratio. Autistic patients with GI manifestations (48%) had significantly decreased levels of serum carnitine and plasma DHA than patients without such manifestations. In addition, autistic patients with GI manifestations had significantly increased percentage of reduced serum carnitine (91.7%) and plasma DHA levels (87.5%) than patients without such manifestations (42.3% and 38.5%, respectively), (P < 0.001 and P < 0.001%, respectively). CONCLUSIONS: Reduced levels of plasma DHA and serum carnitine levels may be associated with the GI problems in some autistic patients. However, this is an initial report, studies are recommended to invesigate whether reduced levels of carnitine and DHA are a mere association or have a pathogenic role in GI problems in autistic patients.

Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity.

BACKGROUND: Aside from the skeletal health affection, vitamin D deficiency has been implicated as a potential environmental factor triggering for some autoimmune disorders. Vitamin D might play a role in the regulation of the production of auto-antibodies. Immunomodulatory effects of vitamin D may act not only through modulation of T-helper cell function, but also through induction of CD4(+)CD25(high) regulatory T-cells. We are the first to investigate the relationship between serum levels of 25-hydroxy vitamin D and anti-myelin-associated glycoprotein (anti-MAG) auto-antibodies in autistic children. METHODS: Serum levels of 25-hydroxy vitamin D and anti-MAG auto-antibodies were measured in 50 autistic children, aged between 5 and 12 years, and 30 healthy-matched children. Serum 25-hydroxy vitamin D levels 10-30 ng/mL and < 10 ng/mL were defined as vitamin D insufficiency and deficiency, respectively. RESULTS: Autistic children had significantly lower serum levels of 25-hydroxy vitamin D than healthy children (P < 0.001) with 40% and 48% being vitamin D deficient and insufficient, respectively. Serum 25-hydroxy vitamin D had significant negative correlations with Childhood Autism Rating Scale (P < 0.001). Increased levels of serum anti-MAG auto-antibodies were found in 70% of autistic patients. Serum 25-hydroxy vitamin D levels had significant negative correlations with serum levels of anti-MAG auto-antibodies (P < 0.001). CONCLUSIONS: Vitamin D deficiency was found in some autistic children and this deficiency may contribute to the induction of the production of serum anti-MAG auto-antibodies in these children. However, future studies looking at a potential role of vitamin D in the pathophysiology and treatment of autism are warranted.

The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism.

BACKGROUND: Neurogenic inflammation is orchestrated by a large number of neuropeptides. Tachykinins (substance P, neurokinin A and neurokinin B) are pro-inflammatory neuropeptides that may play an important role in some autoimmune neuroinflammatory diseases. Autoimmunity may have a role in the pathogenesis of autism in some patients. We are the first to measure serum neurokinin A levels in autistic children. The relationship between serum levels of neurokinin A and anti-ribosomal P protein antibodies was also studied. METHODS: Serum neurokinin A and anti-ribosomal P protein antibodies were measured in 70 autistic children in comparison to 48 healthy-matched children. RESULTS: Autistic children had significantly higher serum neurokinin A levels than healthy controls (P < 0.001). Children with severe autism had significantly higher serum neurokinin A levels than patients with mild to moderate autism (P < 0.001). Increased serum levels of neurokinin A and anti-ribosomal P protein antibodies were found in 57.1% and 44.3%, respectively of autistic children. There was significant positive correlations between serum levels of neurokinin A and anti-ribosomal P protein antibodies (P = 0.004). CONCLUSIONS: Serum neurokinin A levels were elevated in some autistic children and they were significantly correlated to the severity of autism and to serum levels of anti-ribosomal P protein antibodies. However, this is an initial report that warrants further research to determine the pathogenic role of neurokinin A and its possible link to autoimmunity in autism. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, should also be studied in autism.

Increased serum levels of anti-ganglioside M1 auto-antibodies in autistic children: relation to the disease severity.

BACKGROUND: Autoimmunity to the central nervous system (CNS) may play a pathogenic role in a subgroup of patients with autism. This study aimed to investigate the frequency of serum anti-ganglioside M1 auto-antibodies, as indicators of the presence of autoimmunity to CNS, in a group of autistic children. We are the first to measure the relationship between these antibodies and the degree of the severity of autism. METHODS: Serum anti-ganglioside M1 antibodies were measured, by ELISA, in 54 autistic children, aged between 4 and 12 years, in comparison to 54 healthy-matched children. Autistic severity was assessed by using the Childhood Autism Rating Scale (CARS). RESULTS: Autistic children had significantly higher serum levels of anti-ganglioside M1 antibodies than healthy children (P < 0.001). The seropositivity of anti-ganglioside M1 antibodies was found in 74% (40/54) of autistic children. Serum levels of anti-ganglioside M1 antibodies were significantly higher in autistic children with severe autism (63%) than those with mild to moderate autism (37%), P = 0.001. Moreover, serum anti-ganglioside M1 antibodies had significant positive correlations with CARS (P < 0.001). CONCLUSIONS: Serum levels of anti-ganglioside M1 antibodies were increased in many autistic children. Also, their levels had significant positive correlations with the degree of the severity of autism. Thus, autism may be, in part, one of the pediatric autoimmune neuropsychiatric disorders. Further wide-scale studies are warranted to shed light on the possible etiopathogenic role of anti-ganglioside M1 auto-antibodies in autism. The role of immunotherapy in autistic patients who have increased serum levels of anti-ganglioside M1 antibodies should also be studied.

Low plasma progranulin levels in children with autism.

BACKGROUND: Autoimmunity to brain may play a pathogenic role in autism. In autoimmune disorders, the formation of antigen-antibody complexes triggers an inflammatory response by inducing the infiltration of neutrophils. Local administration of recombinant progranulin, which is an anti-inflammatory neurotrophic factor, potently inhibit neutrophilic inflammation in vivo, demonstrating that progranulin represents a crucial inflammation-suppressing mediator. We are the first to measure plasma progranulin levels in autism. METHODS: Plasma levels of progranulin were measured, by ELISA, in 40 autistic patients, aged between 3 and 12 years, and 40 healthy-matched children. RESULTS: Autistic children had significantly lower plasma progranulin levels, P = 0.001. Reduced plasma progranulin levels were found in 65% (26/40) of autistic children.On the other hand, there was a non significant difference between plasma progranulin levels of children with mild to moderate autism and patients with severe autism, P = 0.11. CONCLUSIONS: Plasma progranulin levels were reduced in a subgroup of patients with autism. Progranulin insufficiency in some patients with autism may result in many years of reduced neutrotrophic support together with cumulative damage in association with dysregulated inflammation that may have a role in autism. However, these data should be treated with caution until further investigations are performed, with a larger subject population, to determine whether the decrease of plasma progranulin levels is a mere consequence of autism or has a pathogenic role in the disease. The role of progranulin therapy should also be studied in autism.

Increased serum osteopontin levels in autistic children: relation to the disease severity.

Autoimmunity to brain may play an etiopathogenic role in autism. Osteopontin is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. Osteopontin induces IL-17 production by T-helper 17 lymphocytes, the key players in the pathogenesis of autoimmune disorders. Anti-osteopontin treatment reduces the clinical severity of some autoimmune neuroinflammatory diseases by reducing IL-17 production. We are the first to measure serum osteopontin levels, by ELISA, in 42 autistic children in comparison to 42 healthy-matched children. The relationship between serum osteopontin levels and the severity of autism, which was assessed by using the Childhood Autism Rating Scale (CARS), was also studied. Autistic children had significantly higher serum osteopontin levels than healthy controls (P<0.001). Increased serum osteopontin levels were found in 80.95% (34/42) of autistic children. Children with severe autism had significantly higher serum osteopontin levels than patients with mild to moderate autism (P=0.02). Moreover, serum osteopontin levels of autistic patients had significant positive correlations with CARS (P=0.007). In conclusions, serum osteopontin levels were increased in many autistic children and they were significantly correlated to the severity of autism. Further wide-scale studies are warranted to shed light on the etiopathogenic role of osteopontin in autism and to investigate its relation to IL-17 and brain-specific auto-antibodies, which are indicators of autoimmunity, in these patients. The therapeutic role of anti-osteopontin antibodies in amelioration of autistic manifestations should also be studied.

Cardiovascular autonomic function assessed by autonomic function tests and serum autonomic neuropeptides in Egyptian children and adolescents with rheumatic diseases.

OBJECTIVE: Cardiovascular autonomic neuropathy (CAN) in patients with rheumatic diseases may result in sudden death, possibly from arrhythmia and myocardial infarction due to its frequent association with microvascular disease. Autonomic dysfunction may contribute to initiation and perpetuation of rheumatic diseases. Thus, we aimed to assess cardiovascular autonomic function in lupus and juvenile idiopathic arthritis (JIA) patients. METHODS: Assessment of cardiovascular autonomic function was done in 20 lupus and 20 JIA patients, aged 8-16 years, by five non-invasive autonomic function tests (AFTs) and serum levels of neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP), as indicators of sympathetic and parasympathetic functions, respectively, in comparison with 40 matched healthy control subjects. RESULTS: Clinical evidence of CAN was found in 65 and 40% of lupus and JIA patients, respectively, and in none of healthy controls. Lupus and JIA patients had significantly lower serum NPY and VIP than controls (P < 0.001). The five AFTs score had significant negative correlations to NPY and VIP (P < 0.001). Patients with CAN had significantly lower serum NPY and VIP than patients without (P < 0.001). Clinical evidence of CAN was found in 41.7 and 14.3% of asymptomatic lupus and JIA patients, respectively. There was significant positive association between CAN and important disease manifestations, including activity, in these patients. CONCLUSIONS: CAN is common in lupus and JIA patients, even in absence of relevant symptoms. Thus, assessments of cardiac autonomic function, by AFTs and serum autonomic neuropeptides (NPY and VIP), and the therapeutic effects of NPY and VIP are recommended in these patients.

Antineuronal antibodies and electroneurophysiological studies in pediatric patients with neuropsychiatric systemic lupus erythematosus.

Neuropsychiatric systemic lupus erythematosus (NPSLE) is one of the most difficult manifestations of lupus to diagnose. Measurement of serum brain autoantibodies and assessment of cognitive function by electroneurophysiological studies (electroencephalogram (EEG) and P300) have contributed to an earlier and a more specific diagnosis of NPSLE. Thus, we were stimulated to assess the value of serum antineuronal antibodies and electroneurophysiological studies in diagnosis and early prediction of NPSLE. To investigate this, assessment of serum antineuronal antibodies and cognitive function (clinically and by electroneurophysiological studies) was done in 30 lupus patients [14 (46.7%) with and 16 (53.3%) without clinical evidence of NPSLE] in comparison with 30 healthy matched subjects. Patients without clinical evidence of NPSLE were followed-up clinically by monthly neuropsychiatric evaluation for 18 months. Seropositivity for antineuronal antibodies and abnormalities of EEG and P300 (prolonged latency and/or low amplitude) were found in 60%, 50% and 70%, respectively of lupus patients. During follow-up, 8 out of the 16 patients without clinical evidence of NPSLE developed such evidence [six (75%) had antineuronal seropositivity, five (62.5%) had abnormal EEG, six (75%) had P300 abnormalities and all had at least one abnormal result of these parameters at the time of initial evaluation before clinical presentation of NPSLE]. In conclusion, serum antineuronal antibodies and electroneurophysiological studies may be reliable parameters for diagnosis and early prediction of NPSLE, especially when combined together, before clinical manifestations ensue. Further studies on a large scale are warranted to evaluate the predictive value of these parameters in NPSLE.

Serum anti-nuclear antibodies as a marker of autoimmunity in Egyptian autistic children.

Autism may involve an autoimmune pathogenesis in a subgroup of patients. The frequency of anti-nuclear antibodies in 80 autistic children and their relationship to a family history of autoimmunity were studied, compared with 80 healthy, matched children. Children with autism had a significantly higher percent seropositivity of anti-nuclear antibodies (20%) than healthy children (2.5%; P < 0.01). Fifty percent of anti-nuclear antibody-seropositive autistic children had an anti-nuclear antibody titer of > or =1:640 (very high positive); 25%, > or =1:160 (high positive); and the remaining 25%, 1:80. All anti-nuclear antibody-seropositive healthy children had anti-nuclear antibody titers of 1:80. A family history of autoimmunity was significantly higher in autistic children (47.5%) than healthy controls (8.8%; P < 0.001). Anti-nuclear antibody seropositivity was significantly higher in autistic children with a family history of autoimmunity than those without such history (36.8% and 5%, respectively; P < 0.001). Anti-nuclear antibody seropositivity had significant positive associations with disease severity, mental retardation and electroencephalogram abnormalities. Autoimmunity may play a role in a subgroup of children with autism. Further studies are warranted to assess anti-nuclear antibody seropositivity, other markers of autoimmunity (e.g., brain-specific autoantibodies), and the role of immunotherapy in children with autism.

Autoantibody to heterogeneous nuclear ribonucleoprotein-A2 (RA33) in juvenile idiopathic arthritis: clinical significance.

BACKGROUND: Objective biomarkers are needed for early diagnosis of juvenile idiopathic arthritis (JIA). Anti-A33 antibodies are considered good markers for adult rheumatoid arthritis (RA), but little information is available on their occurrence in JIA. The aim of the present study was therefore to investigate the value of anti-RA33 for diagnosis of JIA (both early and established disease), and its relation to markers of disease activity, and bone resorption. SUBJECTS: This case-control study was conducted on 34 children with JIA. Ten patients with arthritis of short duration (<6 weeks) were included, as undifferentiated arthritis. Forty-four age- and sex- matched healthy children served as controls. Beside evaluation and assessment of disease activity, urinary calcium, serum parathyroid hormone and serum anti-RA33 were measured in included subjects. Joints were examined radiologically and modified Larsen index (LI) was estimated. RESULTS: During follow up, eight of the patients with undifferentiated arthritis were diagnosed as having early JIA. Patients with JIA (early and established cases) had higher anti-RA33 levels than the control group (z = 6.04, 3.95, respectively). A total of 66.7% of the patients were positive for anti-RA33, results were comparable in early and established cases. Anti-RA33 values were correlated to disease activity (clinical and laboratory), to laboratory markers (urinary calcium, parathyroid hormone levels) and radiological evidence (LI) of bone resorption (r = 0.95, 0.63, 0.94, respectively). CONCLUSION: Anti-RA33 is detected in two-thirds of JIA patients and occurs with comparable frequency early in the disease. Its levels are correlated to disease activity and markers of bone resorption and it seems to convey diagnostic and prognostic insights for appropriate management.

A possible association between elevated serum levels of brain-specific auto-antibodies and reduced plasma levels of docosahexaenoic acid in autistic children.

Polyunsaturated fatty acids (PUFAs) are not only essential for energy production, but they also exhibit a range of immunomodulatory properties that progress through T cell mediated events. Autoimmunity may have a pathogenic role in a subgroup of autistic children. This study is the first to investigate the relationship between serum levels of anti-myelin basic protein (anti-MBP) brain-specific auto-antibodies and reduced plasma levels of PUFAs in autistic children. Plasma levels of PUFAs (including linoleic, alphalinolenic, arachidonic "AA" and docosahexaenoic "DHA" acids) and serum anti-MBP were measured in 80 autistic children, aged between 4 and 12 years, and 80 healthy-matched children. Autistic patients had significantly lower plasma levels of PUFAs than healthy children. On the other hand, ω6/ω3 ratio (AA/DHA) was significantly higher in autistic patients than healthy children. Low plasma DHA, AA, linolenic and linoleic acids were found in 67.5%, 50%, 40% and 35%, respectively of autistic children. On the other hand, 70% of autistic patients had elevated ω6/ω3 ratio. Autistic patients with increased serum levels of anti-MBP auto-antibodies (75%) had significantly lower plasma DHA (P<0.5) and significantly higher ω6/ω3 ratio (P<0.5) than patients who were seronegative for these antibodies. In conclusions, some autistic children have a significant positive association between reduced levels of plasma DHA and increased serum levels of anti-MBP brain-specific auto-antibodies. However, replication studies of larger samples are recommended to validate whether reduced levels of plasma PUFAs are a mere association or have a role in the induction of the production of anti-MBP in some autistic children.

Systemic auto-antibodies in children with autism.

Autoimmunity to central nervous system may have a role in the pathogenesis of autism. A subset of anti-ds-DNA antibodies has been recently proved to be pathogenic to the brain as well as to the kidney. Due to the paucity of studies investigating the frequency of systemic auto-antibodies in autism, we are the first to investigate the frequency of anti-ds-DNA antibodies in a group of autistic children. The seropositivity of anti-nuclear antibodies (ANA) was also investigated. Serum anti-ds-DNA antibodies and ANA were measured in 100 autistic children, aged between 4 and 11 years, in comparison to 100 healthy-matched children. The seropositivity of anti-ds-DNA antibodies and ANA in autistic children was 34% and 25%, respectively. In addition, 42% of autistic children were seropositive for anti-ds-DNA antibodies and/or ANA. The frequencies of anti-ds-DNA antibodies and ANA in autistic children were significantly higher than that in healthy children (4% and 2%, respectively), (P<0.001 and P<0.001, respectively). Autistic children with a family history of autoimmunity (45%) had significantly higher frequency of serum anti-ds-DNA antibodies (48.9%) than patients without such a history (21.8%), P=0.008. There was a significant positive association between the seropositivity of anti-ds-DNA antibodies and ANA (P<0.001). In conclusion, anti-ds-DNA antibodies and ANA were found in the sera of a subgroup of autistic children. However, replication studies of larger samples are warranted to validate whether these antibodies are a mere association or have a pathogenic role in some autistic children.

The link between some alleles on human leukocyte antigen system and autism in children.

The reason behind the initiation of autoimmunity to brain in some patients with autism is not well understood. There is an association between some autoimmune disorders and specific alleles of human leukocyte antigen (HLA) system. Thus, we examined the frequency of some HLA-DRB1 alleles in 100 autistic children and 100 healthy matched-children by differential hybridization with sequence-specific oligonucleotide probes. The risk of association between acquisition or absence of these alleles and autism and also a history of autoimmune diseases in autistic relatives was studied. Autistic children had significantly higher frequency of HLA-DRB1*11 allele than controls (P<0.001). In contrast, autistic children had significantly lower frequency of HLA-DRB1*03 allele than controls (P<0.001). Acquisition of HLA-DRB1*011 and absence of HLA-DRB1*3 had significant risk for association with autism (odds ratio: 3.21 and 0.17, respectively; 95% CI: 1.65-6.31 and 0.06-0.45, respectively). HLA-DRB1*11 had a significant risk for association with a family history of autoimmunity in autistic children (odds ratio: 5.67; 95% CI: 2.07-16.3). In conclusions, the link of some HLA alleles to autism and to family history of autoimmunity indicates the possible contributing role of these alleles to autoimmunity in some autistic children. Despite a relatively small sample size, we are the first to report a probable protective association of HLA-DRB1*03 allele with autism. It warrants a replication study of a larger sample to validate the HLA-DRB1 genetic association with autism. This is important to determine whether therapeutic modulations of the immune function are legitimate avenues for novel therapy in selected cases of autism.

The link of C4B null allele to autism and to a family history of autoimmunity in Egyptian autistic children.

UNLABELLED: The reason behind the initiation of autoimmunity, which may have a role in autism, is not well understood. There is an association between some autoimmune disorders and complement (C) 4B null allele. We aimed to study the association between C4B null allele and autism. In addition, we are the first to investigate the association between this allele and a family history of autoimmune diseases in autistic children. Therefore, we examined the frequency of C4B null allele, by quantitative real-time PCR, in 80 autistic patients and 80 healthy matched-children. The frequency of C4B null allele was significantly higher in autistic patients (37.5%) than healthy controls (8.75%), P<0.001. The frequency of autoimmune diseases in families of autistic children (40%) was significantly higher than healthy children (10%), P<0.001. In addition, a family history of autoimmunity had a significant risk for association with autism (odds ratio=6, 95%, CI=2.5-14.1). C4B null allele had a significant risk for association with autism (odds ratio=6.26, 95% CI=2.55-15.36) and with a family history of autoimmunity (odds ratio=21, 95% CI=6.5-67.8). CONCLUSIONS: the link of C4B null allele to autism and to a family history of autoimmunity may indicate its possible contributing role to autoimmunity in autism.

Frequency of CD4+CD25high regulatory T cells in the peripheral blood of Egyptian children with autism.

Autoimmunity may have a role in autism, although the origins of autoimmunity in autism are unknown. CD4( +)CD25(high) regulatory T cells play an important role in the establishment of immunological self-tolerance, thereby preventing autoimmunity. The authors are the first to study the frequency of CD4(+)CD25( high) regulatory T cells in the blood of 30 autistic and 30 age- and sex-matched healthy children. Patients with autism had significantly lower frequency of CD4(+)CD25(high) regulatory T cells than healthy children (P < .001). These cells were deficient in 73.3% of children with autism. Autistic patients with allergic manifestations (40%) and those with a family history of autoimmunity (53.3%) had a significantly lower frequency of CD4(+)CD25(high) regulatory T cells than those without (P < .01 and P < .001, respectively). In conclusion, CD4(+)CD25( high) regulatory T cells are deficient in many children with autism. Deficiency of these cells may contribute to autoimmunity in a subgroup of children with autism. Consequently, CD4(+)CD25(high) regulatory T cells could be new potential therapeutic targets in these patients.

The role of measurement of serum autoantibodies in prediction of pediatric neuropsychiatric systemic lupus erythematosus.

UNLABELLED: Neuropsychiatric systemic lupus erythematosus (NPSLE) is one of the most difficult manifestations of lupus to diagnose. Measurement of serum brain antibodies has contributed to early diagnosis and management of NPSLE before development of a debilitating disease. We aimed to assess the value of serum anti-ganglioside M1 antibodies in prediction of NPSLE, in comparison to other antibodies used in routine laboratory diagnosis of NPSLE. In addition, we are the first to study the relationship between these antibodies and cognitive function in lupus patients. Serum anti-ganglioside M1, anti-ribosomal P protein and anti-cardiolipin antibodies were measured in 30 lupus patients without clinical evidence of NPSLE, aged 8-16 years, and 30 healthy matched-subjects. Patients were followed-up clinically by monthly neuropsychiatric evaluation and assessment of cognitive function for 12 months. Twelve patients developed neuropsychiatric manifestations during follow-up. Of those patients, 83.3%, 50% and 16.7% were seropositive for anti-ganglioside M1, anti-ribosomal P and anti-cardiolipin antibodies, respectively at the time of initial evaluation before clinical presentation of NPSLE. There was a significant positive association between anti-ganglioside seropositivity and cognitive dysfunction (P<0.001). In addition, anti-ganglioside seropositivity had a significant risk for association with cognitive dysfunction (odds ratio: 36; 95% CI: 4.3-302.8). CONCLUSIONS: Serum anti-ganglioside M1 antibodies had a higher predictive value for NPSLE than other antibodies used in routine laboratory diagnosis of this disease. Thus, they may be reliable parameters for early diagnosis and management of NPSLE before clinical manifestations ensue. In addition, anti-ganglioside M1 antibodies may play a role in cognitive dysfunction found in some lupus patients.

Oxidative stress in Egyptian children with autism: relation to autoimmunity.

UNLABELLED: We are the first to study the relationship between oxidative stress (by measuring plasma F2-isoprostane, as a marker of lipid peroxidation, and glutathione peroxidase, as an antioxidant enzyme) and autoimmunity (as indicated by serum antineuronal antibodies) in a group of 44 Egyptian autistic children and 44 healthy matched-children. Our results showed that oxidative stress was found in 88.64% of autistic children. Oxidative stress, resulting from elevated plasma F2-isoprostane and/or reduced glutathione peroxidase, had significant risk for antineuronal positivity, which was found in 54.5% of autistic children, (odds ratio: 12.38 and 6.43, respectively, confidence interval: 1.37-112.10 and 1.21-34.19, respectively). CONCLUSIONS: the strong association between oxidative stress and autoimmunity in autistic children may indicate the possible role of oxidative stress, through induction of autoimmunity, in some autistic patients. Therefore, studies considering the role of antioxidants and immunotherapy in amelioration of autistic manifestations are recommended.