Food allergy is an important public health problem that affects children and adults and may be increasing in prevalence. Despite the risk of severe allergic reactions and even death, there is no current treatment for food allergy: the disease can only be managed by allergen avoidance or treatment of symptoms. The diagnosis and management of food allergy also may vary from one clinical practice setting to another. Finally, because patients frequently confuse nonallergic food reactions, such as food intolerance, with food allergies, there is an unfounded belief among the public that food allergy prevalence is higher than it truly is. In response to these concerns, the National Institute of Allergy and Infectious Diseases, working with 34 professional organizations, federal agencies, and patient advocacy groups, led the development of clinical guidelines for the diagnosis and management of food allergy. These Guidelines are intended for use by a wide variety of health care professionals, including family practice physicians, clinical specialists, and nurse practitioners. The Guidelines include a consensus definition for food allergy, discuss comorbid conditions often associated with food allergy, and focus on both IgE-mediated and non-IgE-mediated reactions to food. Topics addressed include the epidemiology, natural history, diagnosis, and management of food allergy, as well as the management of severe symptoms and anaphylaxis. These Guidelines provide 43 concise clinical recommendations and additional guidance on points of current controversy in patient management. They also identify gaps in the current scientific knowledge to be addressed through future research.

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Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAID-Sponsored Expert Panel Report

This parameter was developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American College of Allergy, Asthma & Immunology (ACAAI); and the Joint Council of Allergy, Asthma & Immunology (JCAAI). The AAAAI and the ACAAI have jointly accepted responsibility for establishing "Food Allergy: A practice parameter update—2014." This is a complete and comprehensive document at the current time. The medical environment is a changing one, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, ACAAI, and JCAAI. These parameters are not designed for use by pharmaceutical companies in drug promotion.

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Food allergy: a practice parameter update-2014.

http://www.similacalimentumhesaplama.com/assets/files/Fiocchi_A_WAO_DRACMA_guidelines_2010_ISPA_c_sayfa_9_57_58.pdf

World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow's Milk Allergy (DRACMA) Guidelines

Food protein-induced enterocolitis (FPIES) is a non-IgE cell- mediated food allergy that can be severe and lead to shock. Despite the potential seriousness of reactions, awareness of FPIES is low; high-quality studies providing insight into the pathophysiology, diagnosis, and management are lacking; and clinical outcomes are poorly established. This consensus document is the result of work done by an international workgroup convened through the Adverse Reactions to Foods Committee of the American Academy of Allergy, Asthma & Immunology and the International FPIES Association advocacy group. These are the first international evidence-based guidelines to improve the diagnosis and management of patients with FPIES. Research on prevalence, pathophysiology, diagnostic markers, and future treatments is necessary to improve the care of patients with FPIES. These guidelines will be updated periodically as more evidence becomes available.

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International consensus guidelines for the diagnosis and management of food protein–induced enterocolitis syndrome: Executive summary—Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology

Since the description of atypical teratoid/rhabdoid tumors of the central nervous system and renal/extrarenal malignant rhabdoid tumors in children, the clinicopathologic spectrum of neoplasms having in common a highly variable rhabdoid cell component (0% to 100%) and consistent loss of nuclear SMARCB1 (INI1) expression has been steadily expanding to include cribriform neuroepithelial tumor of the ventricle, renal medullary carcinoma and a subset of collecting duct carcinoma, epithelioid sarcoma, subsets of miscellaneous benign and malignant soft tissue tumors, and rare rhabdoid carcinoma variants of gastroenteropancreatic, sinonasal, and genitourinary tract origin. Although a majority of SMARCB1-deficient neoplasms arise de novo, the origin of SMARCB1-deficient neoplasia in the background of a phenotypically or genetically definable differentiated SMARCB1-intact "parent neoplasm" has been convincingly demonstrated, highlighting the rare occurrence of rhabdoid tumors as "double-hit neoplasia." As a group, SMARCB1-deficient neoplasms occur over a wide age range (0 to 80 y), may be devoid of rhabdoid cells or display uniform rhabdoid morphology, and follow a clinical course that varies from benign to highly aggressive causing death within a few months irrespective of aggressive multimodality therapy. Generally applicable criteria that would permit easy recognition of these uncommon neoplasms do not exist. Diagnosis is based on site-specific and entity-specific sets of clinicopathologic, immunophenotypic, and/or molecular criteria. SMARCB1 immunohistochemistry has emerged as a valuable tool in confirming or screening for SMARCB1-deficient neoplasms. This review summarizes the different phenotypic and topographic subgroups of SMARCB1-deficient neoplasms including sporadic and familial, benign and malignant, and rhabdoid and nonrhabdoid variants, highlighting their phenotypic heterogeneity and molecular complexity.

The expanding family of SMARCB1(INI1)-deficient neoplasia: implications of phenotypic, biological, and molecular heterogeneity.

This study was performed to identify clinical factors that facilitate the diagnosis of typical cow's milk protein-induced enterocolitis (CMPIE). Data from 142 consecutive patients (aged 15 to 45 days, cow's milk formula- or cow's milk and breast milk mixed-fed) admitted due to vomiting and/or diarrhea were retrospectively analyzed. These 142 subjects were divided into three groups: the CMPIE, infection, and non-infection group. Each group was composed of 16 (11.3%), 102 (71.8%), and 24 (16.9%) patients, respectively. On admission, poor weight gain (p=0.003), hypoalbuminemia (p=0.035), peripheral leukocytosis (p=0.012), and metabolic acidosis (p=0.015) were found to be more significant in the CMPIE group than those in other two groups. In CMPIE, serum albumin levels decreased from 3.3+/-0.9 g/dL on admission to 2.6+/-0.3 g/dL during admission (p<0.05), and methemoglobinemia was observed in 3 patients (18.8%) (p=0.012). Multiple logistic regression analysis showed that the independent predictors of CMPIE versus the infection group were failure to gain weight (OR, 10.75 [95% CI, 1.53-66.12]) (p= 0.014) and hypoalbuminemia (OR, 9.53 [95% CI, 1.62-49.01]) (p=0.010). The early recognition of indexes of suspicion for CMPIE may be of help in the diagnosis and treatment of this disorder.

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Indexes of suspicion of typical cow's milk protein-induced enterocolitis.

This study was performed to investigate the significance of gastric juice analysis (GJA) as a diagnostic criterion of a positive challenge in a standard oral cow's milk challenge (OCC) to confirm typical cow's milk protein-induced enterocolitis (CMPIE). Data from 16 CMPIE patients (aged 14 to 44 days) were analyzed. A standard OCC was openly executed using 0.15 g/kg of protein. Three symptoms (vomiting, lethargy, and bloody or pus-like stool), and four laboratory findings (GJA [3 hr], changes in peripheral blood absolute neutrophil count [ANC] [6 hr], C-reactive protein [6 hr], and stool smear test for occult blood or leukocytes) were observed after OCC. Before OCC, baseline studies were conducted; a stool smear test, blood sampling, and GJA. Positive OCC results were; vomiting (87.5%) (observed 1-3 hr after OCC), lethargy (62.5%) (1-3 hr), bloody or pus-like stool (43.8%) (6-10 hr), abnormal GJA (93.8%), an ANC rise >3,500 cells/µL (93.8%), and an abnormal stool smear test (75.0%). A single GJA test after a standard OCC is a sensitive diagnostic criterion of a positive challenge, and may provide an early confirmatory diagnosis of CMPIE. An investigation of positive OCC outcomes helps to find out a diagnostic algorithm of criteria of a positive challenge in CMPIE.

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The Significance of Gastric Juice Analysis for a Positive Challenge by a Standard Oral Challenge Test in Typical Cow's Milk Protein-Induced Enterocolitis

The clinicopathological findings in previous studies concerning food protein-induced proctocolitis (FPIPC) are quite diverse in terms of results and conclusions. The aim of this study was to suggest advanced clinicopathological diagnostic criteria that facilitate the early confirmation of FPIPC. Data of 38 FPIPC patients, who had re- ceived sigmoidoscopy and biopsy, was analyzed. Microscopic findings were com- pared with observations of previous studies. Feeding at onset of bleeding was exclu- sively breast-fed (94.7%) and formula-fed or mixed-fed (5.3%). Endoscopic abnor- malities were observed in all patients; nodular hyperplasias with circumscribed and/or central pit-like erosions in 94.7% and erythema in 5.3%. Histopathological findings were; lymphoid aggregates in 94.7%, eosinophils in lamina propria of ≥60 cells/10 HPF in 97.4% and of >20 cells/HPF in 63.2%, epithelial or muscularis mucosa eo- sinophil infiltration in 97.4%, and crypt abscess in 2.6%. The majority of FPIPC patients are exclusively breast-fed and nodular hyperplasias with erosions may be a disease specific endoscopic finding. Histologic diagnosis of FPIPC is compatible with eosino- phils in the lamina propria of ≥60 cells/10 high power fields; however, >20 cells/ HPF is not an appropriate diagnostic criterion.

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Advanced criteria for clinicopathological diagnosis of food protein-induced proctocolitis.

Cribriform neuroepithelial tumor (CRINET) is a very rare and recently described entity of INI1-deficient intraventricular neuroepithelial tumor of primitive non-rhabdoid cells with distinct cribriform formation and has a relatively favorable prognosis. A 14-month-old boy had presented with gait imbalance and was crawling for the last 2 weeks. MRI revealed a large, complex solid and cystic mass with dimensions of 55 × 55 × 50 mm in the vicinity of the third ventricle. Histopathologically, the tumor was composed of relatively small undifferentiated neuroepithelial cells arranged in a cribriform pattern and intervening solid sheets with true rosettes. Immunohistochemically, the tumor cells showed complete loss of nuclear INI1 expression and distinct expression of epithelial membrane antigen (EMA) along the luminal borders of the tubules or glands. The typical rhabdoid feature of tumor cells was absent. Ultrastructurally, the tumor cells were neuroepithelial cells that contained short linear rough endoplasmic reticula and distinct intercellular junctions. Here, we describe a new case of CRINET and also discuss its clinicopathological, immunohistochemical, and ultrastructural features.

Cribriform neuroepithelial tumor in the third ventricle: a case report and literature review.

We examined the ultrastructural features of the lung parenchyma and the expression of apoptosis of the respiratory cells by TUNEL technique. Male Sprague-Dawley rats (n=30) were intra-tracheally injected with cadmium (2.5 mg/kg) into both lungs. The light and electron microscopic features of the lung tissues were examined on Days 1, 3, 7 and 10 after the injection of cadmium. Specimen preparations for the light and electron microscopic TUNEL stains were performed. Ultrastructurally, on Days 1 and 3, the alveolar spaces were filled with edematous fluid, and desquamated type I epithelial cells. On Days 7 and 10, the alveolar spaces and interstitium were patchy infiltrated with young fibroblasts and some collagen deposition. The light microscopic TUNEL stain showed that apoptosis of the alveolar cells was most prominent on Day 1, and then the number of apoptosis was markedly decreased on Days 3, 7 and 10. The electron microscopic TUNEL stain showed the electron dense homogenous nuclear expression, and the formation of intra-nuclear blebs which protrude to the outside of nuclei. On Days 7 and 10, there are frequent apoptotic nuclear bodies in the alveolar macrophages. We could examine the identification of the equivocal apoptotic cells and various morphologic expression of apoptotic nuclei on the electron microscopic TUNEL stain.

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Sang Pyo Kim

Papers

Indexes of suspicion of typical cow's milk protein-induced enterocolitis.

The Significance of Gastric Juice Analysis for a Positive Challenge by a Standard Oral Challenge Test in Typical Cow's Milk Protein-Induced Enterocolitis

Advanced criteria for clinicopathological diagnosis of food protein-induced proctocolitis.

Cribriform neuroepithelial tumor in the third ventricle: a case report and literature review.

Cadmium Induced Acute Lung Injury and TUNEL Expression of Apoptosis in Respiratory Cells