Sylvia Costa Lima Farhat

Air pollution in autoimmune rheumatic diseases: a review.

Air pollution consists of a heterogeneous mixture of gasses and particles that include carbon monoxide, nitrates, sulfur dioxide, ozone, lead, toxic by-product of tobacco smoke and particulate matter. Oxidative stress and inflammation induced by inhaled pollutants may result in acute and chronic disorders in the respiratory system, as well as contribute to a state of systemic inflammation and autoimmunity. This paper reviews the mechanisms of air contaminants influencing the immune response and autoimmunity, and it focuses on studies of inhaled pollutants triggering and/or exacerbating rheumatic diseases in cities around the world. Remarkably, environmental factors contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica in rheumatoid arthritis and systemic lupus erythematosus. Other diseases such as scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica. Likewise, primary vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA) may be triggered by silica exposure. Only few studies showed that air pollutants could trigger or exacerbate juvenile idiopathic arthritis and systemic lupus erythematosus. In contrast, no studies of tropospheric pollution triggering inflammatory myopathies and spondyloarthropathies were carried out. In conclusion, air pollution is one of the environmental factors involved in systemic inflammation and autoimmunity. Further studies are needed in order to evaluate air pollutants and their potentially serious effects on autoimmune rheumatic diseases and the mechanisms involved in the onset and the exacerbation of these diseases.

Ozone Is Associated With an Increased Risk of Respiratory Exacerbations in Patients With Cystic Fibrosis

Background Tropospheric oxidant pollutants may injure the respiratory tract. Cystic fibrosis (CF) respiratory disease involves significant inflammation and excessive oxidative stress, and exposure to air pollutants can magnify the lung damage. The objective of this study was to investigate the association between the short-term variation in the concentration of air pollutants in metropolitan São Paulo, Brazil, and the occurrence of respiratory exacerbations in children and adolescents with CF. Methods A longitudinal panel of repeated measurements was obtained from 103 patients attending the outpatient center of our institution from September 6, 2006 through September 4, 2007. Daily concentrations of inhaled particulate matter, sulfur dioxide, nitrogen dioxide, ozone (O3), carbon monoxide, and meteorologic variables, such as the minimum temperature and relative humidity, were evaluated. The generalized estimation equation model for binomial distribution was used to assess the impact of these measurements on the occurrence of acute respiratory exacerbations. Results In total, 103 patients with CF (median age, 8.9 years) made 408 visits, with a mean ± SD of 4 ± 1.74 visits per patient (range, 2-9). A respiratory disease exacerbation was diagnosed on 142 visits (38.4%). An interquartile range increase in the O3 concentration (45.62 μg/m3) had a positive, delayed (2 days after exposure) effect on the risk of a respiratory exacerbation (relative risk = 1.86; 95% CI, 1.14-3.02). Conclusions This study demonstrates that exposure to short-term air pollution in a large urban center increases the risk of a pulmonary exacerbation in patients with CF.

Atmospheric pollution: influence on hospital admissions in paediatric rheumatic diseases

Objective: To investigate the lag structure effects from exposure to atmospheric pollution in acute outbursts in hospital admissions of paediatric rheumatic diseases (PRDs). Methods: Morbidity data were obtained from the Brazilian Hospital Information System in seven consecutive years, including admissions due to seven PRDs (juvenile idiopathic arthritis, systemic lupus erythematosus, dermatomyositis, Henoch–Schönlein purpura, polyarteritis nodosa, systemic sclerosis and ankylosing spondylitis). Cases with secondary diagnosis of respiratory diseases were excluded. Daily concentrations of inhaled particulate matter (PM10), sulphur dioxide (SO2) nitrogen dioxide (NO2), ozone (O3) and carbon monoxide (CO) were evaluated. Generalized linear Poisson regression models controlling for short-term trend, seasonality, holidays, temperature and humidity were used. Lag structures and magnitude of air pollutants’ effects were adopted to estimate restricted polynomial distributed lag models. Results: The total number of admissions due to acute outbursts PRD was 1,821. The SO2 interquartile range (7.79 µg/m3) was associated with an increase of 1.98% (confidence interval 0.25–3.69) in the number of hospital admissions due to outcome studied after 14 days of exposure. This effect was maintained until day 17. Of note, the other pollutants, with the exception of O3, showed an increase in the number of hospital admissions from the second week. Conclusion: This study is the first to demonstrate a delayed association between SO2 and PRD outburst, suggesting that oxidative stress reaction could trigger the inflammation of these diseases.

Elevated C-reactive protein and spontaneous bacterial peritonitis in children with chronic liver disease and ascites.

Objectives: The aims of this study were to compare laboratory indices of spontaneous bacterial peritonitis (SBP) and noninfected ascites in children with chronic liver disease and to determine the infectious agents involved in SBP. Methods: The medical records of 90 children with chronic liver disease and ascites studied between January 2005 and August 2011 were reviewed for laboratory data of diagnostic significance in SBP. Standard laboratory tests included blood cell count, coagulation indices, liver and renal function tests, C-reactive protein (CRP), serum sodium concentration, serum albumin, and serum cultures. Ascitic fluid obtained from 152 paracentesis procedures was assayed for cytology, Gram stains, neutrophil counts, and bacteriological cultures. Results: The SBP group manifested significantly lower albumin levels and elevated CRP levels, prothrombin times, international normalized ratios, and leukocyte number (P < 0.05 in each case). CRP was shown to be an independent variable in the prediction of SBP. Values of serum creatinine, sodium concentration, urea, total bilirubin and differential leukocyte shift were comparable in SBP and noninfected ascites. Streptococcus pneumoniae was the most prevalent infectious agent in the ascitic fluid (44%). Conclusions: CRP may be useful in early detection and monitoring of SBP in children with liver disease.

Risk Factors for Juvenile Dermatomyositis: Exposure to Tobacco and Air Pollutants During Pregnancy

To evaluate the influence of exposure to inhaled environmental factors during pregnancy on the diagnosis of juvenile dermatomyositis (DM).

Alternative management of diabetic ketoacidosis in a Brazilian pediatric emergency department

DKA is a severe metabolic derangement characterized by dehydration, loss of electrolytes, hyperglycemia, hyperketonemia, acidosis and progressive loss of consciousness that results from severe insulin deficiency combined with the effects of increased levels of counterregulatory hormones (catecholamines, glucagon, cortisol, growth hormone). The biochemical criteria for diagnosis are: blood glucose > 200 mg/dl, venous pH <7.3 or bicarbonate <15 mEq/L, ketonemia >3 mmol/L and presence of ketonuria. A patient with DKA must be managed in an emergency ward by an experienced staff or in an intensive care unit (ICU), in order to provide an intensive monitoring of the vital and neurological signs, and of the patients clinical and biochemical response to treatment. DKA treatment guidelines include: restoration of circulating volume and electrolyte replacement; correction of insulin deficiency aiming at the resolution of metabolic acidosis and ketosis; reduction of risk of cerebral edema; avoidance of other complications of therapy (hypoglycemia, hypokalemia, hyperkalemia, hyperchloremic acidosis); identification and treatment of precipitating events. In Brazil, there are few pediatric ICU beds in public hospitals, so an alternative protocol was designed to abbreviate the time on intravenous infusion lines in order to facilitate DKA management in general emergency wards. The main differences between this protocol and the international guidelines are: intravenous fluid will be stopped when oral fluids are well tolerated and total deficit will be replaced orally; if potassium analysis still indicate need for replacement, it will be given orally; subcutaneous rapid-acting insulin analog is administered at 0.15 U/kg dose every 2-3 hours until resolution of metabolic acidosis; approximately 12 hours after treatment initiation, intermediate-acting (NPH) insulin is initiated at the dose of 0.6-1 U/kg/day, and it will be lowered to 0.4-0.7 U/kg/day at discharge from hospital.

Parental smoking patterns and their association with wheezing in children.

OBJECTIVE: To investigate parental smoking patterns and their association with wheezing in children. METHODS: We performed a case-control study that included 105 children between 6 and 23 months of age who were divided into two groups: cases (children with 3 previous episodes of wheezing) and controls (healthy children without wheezing). The childrens exposure to cigarette smoking was estimated using a questionnaire completed by the mothers and by the childrens urinary cotinine levels. RESULTS: Based on both the questionnaire results and cotinine levels, exposure to cigarette smoking was higher in the households of cases in which the incidence of maternal smoking was significantly higher than that of paternal smoking. Children in this group were more affected by maternal smoking and by the total number of cigarettes smoked inside the house. Additionally, the questionnaire results indicated that the risk of wheezing was dose dependent. The presence of allergic components, such as atopic dermatitis and siblings with allergic rhinitis and asthma, greatly increased the odds ratio when wheezing was associated with cotinine levels. CONCLUSION: Children exposed to tobacco smoke have an increased risk of developing wheezing syndrome. This risk increases in association with the number of cigarettes smoked inside the house and the presence of other allergic components in the family.

Air pollution and children's health: sickle cell disease

O objetivo deste estudo foi avaliar a associacao entre a poluicao do ar e atendimentos de emergencia pediatrica de pacientes portadores de anemia falciforme. Adotamos um estudo de case-crossover. Visitas de criancas e adolescentes portadores de anemia falciforme ao pronto-socorro pediatrico, em Sao Paulo, Brasil, foram avaliadas a partir de setembro de 1999 ate dezembro de 2004, controlando a temperatura, umidade e dia da semana. Variacoes interquartis das medias moveis de quatro dias de PM10, NO2, SO2, CO e O3 foram associadas com aumentos de 18,9% (IC95%: 11,2-26,5), 19% (IC95%: 8,3-29,6), 14,4% (IC95%: 6,5-22,4), 16,5% (IC95%: 8,9-24,0) e 9,8% (IC95%: 1,1-18,6) nos atendimentos totais, respectivamente. Quando as analises foram estratificadas por dor, verificou-se que PM10 apresentou correlacao 40,3% maior do que a observada em pacientes falciformes sem sintomas de dor. A exposicao a poluicao do ar pode afetar a saude cardiovascular de criancas e promover um fardo significativo para a saude em um grupo suscetivel, como o de pacientes com anemia falciforme.

Exposure to air pollutants increased disease activity in childhood‐onset systemic lupus erythematosus patients

To investigate the association between exposure to air pollutants in the Sao Paulo metropolitan area and disease activity in juvenile‐onset systemic lupus erythematosus (SLE) patients.

Exposure to Air Pollutants and Disease Activity in Juvenile-Onset Systemic Lupus Erythematosus Patients.

To investigate the association between exposure to air pollutants in the Sao Paulo metropolitan area and disease activity in juvenile‐onset systemic lupus erythematosus (SLE) patients.