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Allergologie Select 2023Not available.
Guideline for allergological diagnosis of drug hypersensitivity reactions: S2k Guideline of the German Society for Allergology and Clinical Immunology (DGAKI) in cooperation with the German Dermatological Society (DDG), the Association of German Allergologists (ÄDA), the German Society for...
Not available.
PubMed: 37705676
DOI: 10.5414/ALX02422E -
American Journal of Physiology. Heart... Aug 2023Heart failure (HF) is a leading cause of morbidity and mortality particularly in older adults and patients with multiple metabolic comorbidities. Heart failure with...
Heart failure (HF) is a leading cause of morbidity and mortality particularly in older adults and patients with multiple metabolic comorbidities. Heart failure with preserved ejection fraction (HFpEF) is a clinical syndrome with multisystem organ dysfunction in which patients develop symptoms of HF as a result of high left ventricular (LV) diastolic pressure in the context of normal or near normal LV ejection fraction (LVEF; ≥50%). Challenges to create and reproduce a robust rodent phenotype that recapitulates the multiple comorbidities that exist in this syndrome explain the presence of various animal models that fail to satisfy all the criteria of HFpEF. Using a continuous infusion of angiotensin II and phenylephrine (ANG II/PE), we demonstrate a strong HFpEF phenotype satisfying major clinically relevant manifestations and criteria of this pathology, including exercise intolerance, pulmonary edema, concentric myocardial hypertrophy, diastolic dysfunction, histological signs of microvascular impairment, and fibrosis. Conventional echocardiographic analysis of diastolic dysfunction identified early stages of HFpEF development and speckle tracking echocardiography analysis including the left atrium (LA) identified strain abnormalities indicative of contraction-relaxation cycle impairment. Diastolic dysfunction was validated by retrograde cardiac catheterization and analysis of LV end-diastolic pressure (LVEDP). Among mice that developed HFpEF, two major subgroups were identified with predominantly perivascular fibrosis and interstitial myocardial fibrosis. In addition to major phenotypic criteria of HFpEF that were evident at early stages of this model (3 and 10 days), accompanying RNAseq data demonstrate activation of pathways associated with myocardial metabolic changes, inflammation, activation of extracellular matrix (ECM) deposition, microvascular rarefaction, and pressure- and volume-related myocardial stress. Heart failure with preserved ejection fraction (HFpEF) is an emerging epidemic affecting up to half of patients with heart failure. Here we used a chronic angiotensin II/phenylephrine (ANG II/PE) infusion model and instituted an updated algorithm for HFpEF assessment. Given the simplicity in generating this model, it may become a useful tool for investigating pathogenic mechanisms, identification of diagnostic markers, and for drug discovery aimed at both prevention and treatment of HFpEF.
Topics: Animals; Mice; Heart Failure; Stroke Volume; Angiotensin II; Ventricular Function, Left; Cardiomyopathies; Disease Models, Animal; Fibrosis; Phenylephrine
PubMed: 37204871
DOI: 10.1152/ajpheart.00038.2023 -
Revista Alergia Mexico (Tecamachalco,... Dec 2023The term food intolerance has been used non-specifically to define a wide range of disorders related to food intake. Recently, the use of the term "non-immunological...
The term food intolerance has been used non-specifically to define a wide range of disorders related to food intake. Recently, the use of the term "non-immunological adverse reactions to foods" (RANIAs) was recommended as a more correct clinical definition. The pathophysiological mechanisms can be diverse, sometimes unknown, and there are no validated diagnostic tests, making it difficult to obtain accurate data. The clinical manifestations of non-immunological adverse reactions to foods affect more than one organ or system; and gastrointestinal symptoms (pain, abdominal distension, flatulence, and diarrhea) are the most common. Non-immunological adverse reactions to foods are divided into independent and dependent on host factors. Foods may contain chemicals with pharmacological activity and be present naturally, such as vasoactive amines (histamine) and salicylates, or added for preservation, to improve appearance or flavor (monosodium glutamate, tartrazine, sulfites, and benzoates). In some cases, these types of reactions may be like to hypersensitivity reactions. Concomitant alcohol consumption may worsen symptoms by inhibiting histamine breakdown and increasing intestinal permeability. In patients diagnosed with non-immunological adverse reactions to foods, it is important to rule out some psychological problems: aversions or eating disorders.
Topics: Humans; Food Intolerance; Histamine; Amines; Benzoates; Diarrhea
PubMed: 38506870
DOI: 10.29262/ram.v70i4.1337 -
Nutrients Apr 2024Histamine intolerance is a condition characterized by the accumulation of histamine to a point that exceeds the body's capacity to eliminate it. Researchers have... (Review)
Review
Histamine intolerance is a condition characterized by the accumulation of histamine to a point that exceeds the body's capacity to eliminate it. Researchers have attributed several reasons to this condition, such as genetic factors, alcohol, and dietary deficiencies, among other elements. Symptoms of histamine intolerance have been found to extend beyond the gastrointestinal tract and to the whole body, with these symptoms being sporadic and non-specific. This review will explore various aspects related to histamine intolerance, such as its causes, symptoms, diagnosis, and information related to management.
Topics: Humans; Histamine; Food Intolerance; Food Hypersensitivity
PubMed: 38674909
DOI: 10.3390/nu16081219 -
Cell Feb 2024Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although...
Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.
Topics: Animals; Mice; Anti-Bacterial Agents; Butyrates; Carbohydrate Metabolism, Inborn Errors; Clostridium; Escherichia coli; Gastrointestinal Microbiome; Sorbitol
PubMed: 38366592
DOI: 10.1016/j.cell.2024.01.029 -
Otolaryngology--head and Neck Surgery :... Jul 2023Previous studies have suggested that patients with aspirin-exacerbated respiratory disease (AERD) have a high likelihood of alcohol intolerance. The purpose of this... (Review)
Review
OBJECTIVE
Previous studies have suggested that patients with aspirin-exacerbated respiratory disease (AERD) have a high likelihood of alcohol intolerance. The purpose of this systematic review is to identify if there is sufficient evidence to confirm this correlation and the impact of medical therapy on subsequent alcohol tolerance.
DATA SOURCES
PubMed, EMBASE, SCOPUS, EBSCO, Google Scholar, Cochrane Library, and Grey literature. We also performed snowballing on the identified observational studies (OS) for additional data.
REVIEW METHODS
A systematic review was conducted from 1968 to 2022 to identify those studies describing AERD symptomatology triggered by alcohol intake. The primary outcome was to analyze the current literature for the association between alcohol intolerance and AERD symptoms. The secondary outcome looked for improvement in alcohol tolerance after aspirin desensitization or biological therapy.
RESULTS
A total of 775 studies were identified and 40 abstracts were evaluated. From these, 5 studies met the inclusion criteria. Of the 5 manuscripts, there was 1 case-control, 2 cohort, and 2 cross-sectional studies. A total of 522 participants with AERD and a history of alcohol consumption were included, with 52.8% reporting at least 1 sinopulmonary exacerbation after alcohol intake. One of 3 studies noted improvement in alcohol tolerance after medical therapy with aspirin desensitization.
CONCLUSION
The current literature suggests that patients with AERD have a high risk of alcohol intolerance. Additionally, aspirin desensitization may improve alcohol tolerance in this patient population.
Topics: Humans; Aspirin; Cross-Sectional Studies; Asthma, Aspirin-Induced; Sinusitis; Desensitization, Immunologic; Nasal Polyps
PubMed: 36939486
DOI: 10.1002/ohn.248 -
Nature Reviews. Gastroenterology &... May 2024
Topics: Humans; Sorbitol; Food Intolerance
PubMed: 38528200
DOI: 10.1038/s41575-024-00921-4 -
Diabetes Sep 2023In obesity, CD11c+ innate immune cells are recruited to adipose tissue and create an inflammatory state that causes both insulin and catecholamine resistance. We found...
UNLABELLED
In obesity, CD11c+ innate immune cells are recruited to adipose tissue and create an inflammatory state that causes both insulin and catecholamine resistance. We found that ablation of Gnas, the gene that encodes Gαs, in CD11c expressing cells protects mice from obesity, glucose intolerance, and insulin resistance. Transplantation studies showed that the lean phenotype was conferred by bone marrow-derived cells and did not require adaptive immunity. Loss of cAMP signaling was associated with increased adipose tissue norepinephrine and cAMP signaling, and prevention of catecholamine resistance. The adipose tissue had reduced expression of catecholamine transport and degradation enzymes, suggesting that the elevated norepinephrine resulted from decreased catabolism. Collectively, our results identified an important role for cAMP signaling in CD11c+ innate immune cells in whole-body metabolism by controlling norepinephrine levels in white adipose tissue, modulating catecholamine-induced lipolysis and increasing thermogenesis, which, together, created a lean phenotype.
ARTICLE HIGHLIGHTS
We undertook this study to understand how immune cells communicate with adipocytes, specifically, whether cAMP signaling in the immune cell and the adipocyte are connected. We identified a reciprocal interaction between CD11c+ innate immune cells and adipocytes in which high cAMP signaling in the immune cell compartment induces low cAMP signaling in adipocytes and vice versa. This interaction regulates lipolysis in adipocytes and inflammation in immune cells, resulting in either a lean, obesity-resistant, and insulin-sensitive phenotype, or an obese, insulin-resistant phenotype.
Topics: Animals; Mice; Adipose Tissue, White; Catecholamines; Diet, High-Fat; Insulin; Insulin Resistance; Mice, Inbred C57BL; Norepinephrine; Obesity
PubMed: 37257047
DOI: 10.2337/db22-1035