Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gastrointestinal tract constitutes one of the largest sites of exposure to the outside environment. The function of the gastrointestinal tract in monitoring and sealing the host interior from intruders is called the gut barrier. A variety of specific and nonspecific mechanisms are in operation to establish the host barrier; these include luminal mechanisms and digestive enzymes, the epithelial cells together with tight junctions in between them, and the gut immune system. Disruptions in the gut barrier follow injury from various causes including nonsteroidal anti-inflammatory drugs and oxidant stress, and involve mechanisms such as adenosine triphosphate depletion and damage to epithelial cell cytoskeletons that regulate tight junctions. Ample evidence links gut barrier dysfunction to multiorgan system failure in sepsis and immune dysregulation. Additionally, contribution of gut barrier dysfunction to gastrointestinal disease is an evolving concept and is the focus of this review. An overview of the evidence for the role of gut barrier dysfunction in disorders such as Crohn's disease, celiac disease, food allergy, acute pancreatitis, non-alcoholic fatty liver disease, and alcoholic liver disease is provided, together with critical insight into the implications of this evidence as a primary disease mechanism.
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PMID:Intestinal permeation and gastrointestinal disease. 1190 49

The necessity to optimise the management of atopic dermatitis of infants needs knowledge of three components: increase of prevalence, extreme frequency of food allergy and increase in the frequency of the syndrome of multiple allergies, that frequently develops into asthmatic disease. Management of DA in infancy (first year of life) is based on the global strategy of understanding the physiological Th2 polarisation at birth, that does not allow a re-equilibration of the Th1-Th2 balance that progresses in the first six months of life (in normal infants) making in this period a window of opportunity for sensitizations. Prevention in high-risk children (familial history of atopy) covers the non-exposure to in door pollutants (tobacco and volatile organic compounds), breast-feeding or a hypoallergenic formula for a hydrolysate of pork and soya proteins or better an extensive hydrolysate of casein. Four situations require moving to an amino acid substitute: failure to thrive, severe atopic dermatitis, a syndrome of multiple food allergies, allergy to hydrolysates. Reintroduction of foods should be considered with the least delay so as to induce digestive tolerance. It should take into account the clinical development, the intensity of the sensitisation and eventually depend on a realistic test of introduction. Management of DA searches for recovery of generalized eczema, failure to immediate improvement of quality of life prevention of immediate complications (local sepsis) acceleration of return to food tolerance. Prevention of ulterior development of asthma by immediately introducing measures to diminish respiratory exposure to allergens and tobacco is hoped for.
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PMID:Optimal management of atopic dermatitis in infancy. 1251 91

Food protein-induced enterocolitis syndrome (FPIES) is a non-immunoglobulin E (IgE)-mediated gastrointestinal food hypersensitivity, mostly in infants. Patients usually present very ill and often misdiagnosed as acute gastroenteritis, sepsis, ileus, metabolic disorders, necrotizing enterocolitis, or severe gastroesophageal reflux disease. We present a case of an infant who had three acute FPIES episodes: the first was at 5 months of age after chewing on a cellophane wrapper, the second was due to sweet potato, and the third was due to rice cereal. It was realized that in the first episode, the wrapper was covering a rice cake. Evaluation at 7 months of age, while asymptomatic, showed normal complete blood count, low serum immunoglobulin E level, and negative allergy skin prick tests, indicating non-IgE sensitivity. Conclusion This case of FPIES has peculiar features in that it occurred in an exclusively breastfed infant and by non-ingestant oral contact with a trivial quantity of rice allergen.
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PMID:Food protein-induced enterocolitis syndrome to trivial oral mucosal contact. 2371 55

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated gastrointestinal food hypersensitivity that manifests as profuse, repetitive vomiting, often with diarrhea, leading to acute dehydration and lethargy or weight loss and failure to thrive if chronic. FPIES is elicited most commonly by milk and soy proteins; however, rice, oat, and other solid foods may also elicit FPIES. Certain FPIES features overlap with food protein-induced enteropathy and proctocolitis, whereas others overlap with anaphylaxis. FPIES is not well recognized among pediatricians and emergency department physicians; the affected children are often mismanaged as having acute viral gastrointestinal illness, sepsis, or surgical disease, delaying diagnosis of FPIES for many months. The aim of this review is to provide case-driven presentation of the features of FPIES. Although randomized clinical trials on management options are missing, the relevant current literature and authors' experience are reviewed in detail.
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PMID:Food protein-induced enterocolitis syndrome (FPIES): current management strategies and review of the literature. 2456 36

Food protein-induced enterocolitis syndrome (FPIES) is an under-recognized non-IgE-mediated gastrointestinal food allergy. The diagnosis of FPIES is based on clinical history, sequential symptoms and the timing, after excluding other possible causes. It is definitively diagnosed by an oral food challenge test. Unfortunately, the diagnosis of FPIES is frequently delayed because of non-specific symptoms and insufficient definitive diagnostic biomarkers. FPIES is not well recognized by clinicians; the affected infants are often mismanaged as having viral gastroenteritis, food poisoning, sepsis, or a surgical disease. Familiarity with the clinical features of FPIES and awareness of the indexes of suspicion for FPIES are important to diagnose FPIES. Understanding the recently defined clinical terms and types of FPIES is mandatory to suspect and correctly diagnose FPIES. The aim of this review is to provide a case-driven presentation as a guide of how to recognize the clinical features of FPIES to improve diagnosis and management of patients with FPIES.
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PMID:Is This Symptom Even a Food Allergy?: Clinical Types of Food Protein-induced Enterocolitis Syndrome. 2506 81

Non-IgE-mediated food allergic disorders account for up to 40% of milk protein allergy in infants and young children. We aim to review the recent literature and to provide an update on diagnosis and management of food protein-induced enterocolitis syndrome (FPIES) and food protein-induced allergic proctocolitis (FPIAP). The peer-reviewed articles indexed in PubMed have been reviewed. FPIES manifests in infants as profuse, repetitive vomiting and lethargy, often with diarrhea, leading to acute dehydration, or weight loss and failure to thrive, in chronic form. FPIES is caused most commonly by cow's milk (CM) and soy proteins; rice, oat, and other solid foods may also trigger FPIES. FPIES rarely occurs in the exclusively breastfed infants. FPIES is underrecognized; children are often mismanaged as having acute viral gastrointestinal illness, sepsis, or surgical disease, delaying diagnosis of FPIES for many months. Approximately 25% of children with FPIES develop food-specific IgE antibodies and some transition to immediate food allergy; IgE positivity is associated with a more protracted course. FPIES is a self-limiting condition, with most cases resolving by age three to five years. Ondansetron may be helpful in managing acute FPIES. FPIAP is a benign condition of bloody stools in a well-appearing infant, with usual onset between one and four weeks of age. Up to 60% of cases occur in exclusively breastfed infants and resolve with maternal elimination of CM and soy proteins. The majority of cases resolve by age 12 months. FPIES may transition to IgE-mediated food allergy in some patients; IgE positivity to the FPIES food is a marker of a more persistent disease. FPIAP is benign and resolves by age 12 months in most patients.
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PMID:Food protein-induced enterocolitis syndrome and allergic proctocolitis. 2597 34

Using a variety of approaches, researchers have studied the health effects of solar ultraviolet (UV) radiation exposure and vitamin D. This review compares the contributions from geographical ecological studies with those of observational studies and clinical trials. Health outcomes discussed were based on the author's knowledge and include anaphylaxis/food allergy, atopic dermatitis and eczema, attention deficit hyperactivity disorder, autism, back pain, cancer, dental caries, diabetes mellitus type 1, hypertension, inflammatory bowel disease, lupus, mononucleosis, multiple sclerosis, Parkinson disease, pneumonia, rheumatoid arthritis, and sepsis. Important interactions have taken place between study types; sometimes ecological studies were the first to report an inverse correlation between solar UVB doses and health outcomes such as for cancer, leading to both observational studies and clinical trials. In other cases, ecological studies added to the knowledge base. Many ecological studies include other important risk-modifying factors, thereby minimizing the chance of reporting the wrong link. Laboratory studies of mechanisms generally support the role of vitamin D in the outcomes discussed. Indications exist that for some outcomes, UVB effects may be independent of vitamin D. This paper discusses the concept of the ecological fallacy, noting that it applies to all epidemiological studies.
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PMID:The role of geographical ecological studies in identifying diseases linked to UVB exposure and/or vitamin D. 2719 55

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated gastrointestinal food hypersensitivity triggered by food proteins. It may present acutely, with repetitive vomiting, diarrhoea and lethargy leading to dehydration and eventually shock or insidiously with intermittent emesis, chronic diarrhoea or failure to thrive. We describe a paediatric male patient with recurrent sepsis-like episodes of fever, lethargy, ashen-grey skin colouration and vomiting followed by diarrhoea. These episodes were triggered by cow's milk formula and grains. Laboratory tests revealed leucocytosis, thrombocytosis, metabolic acidosis and elevated C reactive protein. After exclusion of other differential diagnoses, the diagnosis of FPIES was established on clinical improvement with withdrawal of the offending food and positive oral food challenge. FPIES diagnosis requires a high index of suspicion and is frequently delayed, which contributes to an increased morbidity. This is due to the wide spectrum of clinical presentations and due to the absence of specific diagnostic tests.
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PMID:Food protein-induced enterocolitis syndrome: a challenging diagnosis. 2943 5

Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated gastrointestinal food hypersensitivity disorder, typically provoked by cow's milk or soy in formula-fed infants. This case shows that diagnosis of FPIES should be suspected in exclusively breast-fed infants and pediatricians should be suspicious of this in infants with shock and sepsis.
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PMID:Acute-on-chronic food protein-induced enterocolitis syndrome in an exclusively breast-fed infant. 3065 11

Food protein-induced enterocolitis syndrome (FPIES) is a poorly understood non-IgE gastrointestinal-mediated food allergy that predominantly affects infants and young children. Cells of the innate immune system appear to be activated during an FPIES reaction. Acute FPIES typically presents between one and 4 hours after ingestion of the trigger food, with the principal symptom being profuse vomiting, and is often accompanied by pallor and lethargy. Additional features can include hypotension, hypothermia, diarrhoea, neutrophilia and thrombocytosis. In Australia, the most commonly reported foods responsible for FPIES are (in descending order) rice, cow's milk, egg, oats and chicken. Most children with FPIES react to only one food trigger, and thus, avoidance of multiple foods is often not indicated. FPIES is often misdiagnosed as sepsis or gastroenteritis. However, a diagnosis of FPIES is favoured if there is rapid resolution of symptoms within hours of presentation, an absence of fever, and a lack of a significant rise in C-reactive protein at presentation. Diagnosis is often hampered by the lack of awareness of FPIES, absence of reliable biomarkers, the non-specific nature of the presenting symptoms, and the delay between allergen exposure and symptoms. Although some national peak allergy bodies have attempted to improve the diagnosis and management of FPIES, up until 2017 there were no internationally agreed guidelines for its diagnosis and management.
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PMID:Food protein-induced enterocolitis syndrome: guidelines summary and practice recommendations. 3065 96


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