RESUMO
BACKGROUND: Cow's milk protein allergy (CMPA) can be responsible of a variety of symptoms and can be caused by IgE or non-IgEmediated reactions. The remaining questions concern the diagnosis (what are the most suggestive clinical manifestations, the laboratory evaluations which play a supporting role, and the management of CMPA in breast fed infants and formula-fed infants. METHODS: Review of the pub med, science direct, Cochrane library, using the key words cow's milk protein allergy, guideline, and child. Evidence was levelled A, B, C. RESULTS: No symptom is pathognomonic. A thorough history and careful clinical examination are necessary to suspect the disease. Skin prick tests, and serum specific IgE are only indicative of sensitivation to CMP. A double-blind placebo-controlled challenge is considered the gold standard in diagnosis, but in practice only an open challenge is performed. The patient with suspected pathology will follow a cow's milk free diet for 2-4 weeks. Formula-fed infants get an extensively hydrolyzed formula .If the allergy is present, clinical manifestations will disappear. If symptoms do not improve, an amino acid based formula should be considered. In severe Cow's milk protein allergy with life-threatening symptoms, an amino-acid formula is recommended. The infant should be maintained on an elimination diet until the infant is between 9-12 months or at least for 6 months. The overall natural evolution of the disease is favorable with most patients achieving tolerance to milk by the age of five years. CONCLUSION: The importance of defined diagnostic criteria needs to be emphasized. It precludes infants from an unnecessary diet and avoids delay in diagnosis, which can lead to malnutrition.
Assuntos
Imunoglobulina E/imunologia , Hipersensibilidade a Leite/imunologia , Proteínas do Leite/imunologia , Humanos , Lactente , Hipersensibilidade a Leite/diagnóstico , Hipersensibilidade a Leite/terapia , Proteínas do Leite/efeitos adversos , Testes Cutâneos/métodosRESUMO
BACKGROUND: Upper gastrointestinal bleeding (UGIB) is a common pediatric emergency. Esophago-gastro-duodenoscopy (EGD) is the first line diagnostic procedure to identify the source of bleeding. However etiology of UGIB remains unknown in 20% of cases. Furthermore, emergency endoscopy is unavailable in many hospitals in our country. AIMS: Identify clinical predictors of positive upper endoscopy outcomes and develop a clinical prediction rule from these parameters. METHODS: Retrospective study of EGDs performed in children with first episode of UGIB, in the endoscopic unit of Children's Hospital of Tunis, during a period of six years. Statistical analysis used SPSS20. Univariate analysis was performed and multivariate logistic regression was then modelled to derive a clinical prediction rule. RESULTS: We collected 655 endoscopies (23.2% normal, 76.8% pathological). We found that time to EGD within 24 hours from the onset of bleeding (p=0.027; Adj OR: 3.30 [1.14 - 9.53]), rebleeding (p=0.009; Adj OR: 6.01 [1.57 - 23.02]), positive gastric lavage outcome (p=0.001; Adj OR: 4.79 [1.95 - 11.79]) and non steroidal anti-inflammatory drugs intake (p=0.035; Adj OR: 5.66 [1.13 - 28.31]) were predictors of positive upper endoscopy outcomes. By assigning each factor, the adjusted odds ratio (Adj OR), we developed a score with four items, ranging from 4 to 20. Using the receiver operating characteristic (ROC) curve the best cut off ≥ 9 was defined (sensitivity 88.2%, specificity 60.6%, positive predictive value 92.7% and negative predictive value 47.6%). The score discriminated well with a ROC curve area of 0.837 (95% confidence interval [0.769 - 0.905]). CONCLUSIONS: This clinical prediction rule is a simple measure that may identify children who needed emergency endoscopy. A prospective study is required to validate our results and evaluate other clinical features that were insufficient for this analysis.
RESUMO
AIM: To report a new case of hypoparathyroidism in a child with ß-thalassemia major CASE: We report a case of a 17-year-old Tunisian girl with transfusion-dependent thalassemia major presented with paresthesia and pubertal delay. Laboratory investigations showed hypocalcaemia and hyperphosphatemia. Parathyroid hormone level was low (2 ng/l, normal range: 12-72 ng/l) than expected for the degree of hypocalcaemia. Serum ferritin concentration was 1770ng/ml. The patient was started on oral daily calcium supplementation, Alfa calciferol and intensive iron chelation therapy. Follow-up after 6 and 12 months revealed normal Calcium and ECG showed QT interval within normal range. CONCLUSION: Investigating calcium homeostasis at regular intervals and early management of any abnormality can preclude the occurrence of complications.