H. W. Baenkler

Bio: H. W. Baenkler is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Food allergy & Histamine. The author has an hindex of 5, co-authored 10 publications receiving 143 citations.

The Differential Diagnosis of Food Intolerance

Abstract: SUMMARY Introduction: More than 20% of the population in industrialized countries suffer from food intolerance or food allergy. Methods: Selective literature search for relevant publications in PubMed and the Cochrane Library combined with further data from the interdisciplinary database on chronic inflammatory and allergic diseases of the Erlangen University Hospital. Results: The majority of cases of food intolerance (15% to 20%) are due to non-immunological causes. These causes range from pseudoallergic reactions to enzymopathies, chronic infections, and psychosomatic reactions that are associated with food intolerance. The prevalence of true food allergy, i.e., immunologically mediated intolerance reactions, is only 2% to 5%. Conclusions: The differential diagnosis of food intolerance is broad. Therefore, a structured diagnostic algorithm with input from multiple clinical disciplines should be applied. The treatment consists of eliminating the offending substance from the diet as well as medications and psychosomatic support, when indicated.

The AP-1 Transcription Factor c-Jun Promotes Arthritis by Regulating Cyclooxygenase-2 and Arginase-1 Expression in Macrophages.

Abstract: Activation of proinflammatory macrophages is associated with the inflammatory state of rheumatoid arthritis. Their polarization and activation are controlled by transcription factors such as NF-κB and the AP-1 transcription factor member c-Fos. Surprisingly, little is known about the role of the AP-1 transcription factor c-Jun in macrophage activation. In this study, we show that mRNA and protein levels of c-Jun are increased in macrophages following pro- or anti-inflammatory stimulations. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment cluster analyses of microarray data using wild-type and c-Jun-deleted macrophages highlight the central function of c-Jun in macrophages, in particular for immune responses, IL production, and hypoxia pathways. Mice deficient for c-Jun in macrophages show an amelioration of inflammation and bone destruction in the serum-induced arthritis model. In vivo and in vitro gene profiling, together with chromatin immunoprecipitation analysis of macrophages, revealed direct activation of the proinflammatory factor cyclooxygenase-2 and indirect inhibition of the anti-inflammatory factor arginase-1 by c-Jun. Thus, c-Jun regulates the activation state of macrophages and promotes arthritis via differentially regulating cyclooxygenase-2 and arginase-1 levels.

Kinetics of histamine released from rectal mucosa.

Abstract: This kinetic study was performed to investigate the different tissue-influencing histamine amounts in Crohn's Disease (CD), Ulcerative Colitis (UC), patients with polyps and cancers (PaCGr) and in a Control Group (CG) For this purpose the endoscopically obtained specimens from rectal mucosa were immediately placed into 1000 microliters of Hank's incubation medium in order to determine the spontaneously released histamine amounts at the time points of 5, 10, 15, 20 and 30 minutes Each time a volume of 100 microliters was removed from the incubation medium and the kinetic value (KV) was detected by using the single isotope radioenzymatic method Influencing of natural histamine catabolism and the comparison of the tissue histamine release with or without air oxygen in the incubation medium using four kinetic programmes (KP1-4) provides clearly different KVs, not only between the KPs but also within the same KP The PaCGr shows higher kinetic values (KVs) compared with the CG In KP1-3 the kinetic courses (KCs) of the Inflammatory Bowel Diseases (IBDs), CD and UC-both not yet divided in active (a) or not active (na) disease stages-cross the KCs of the CG several times Only the differentiation of the IBDs in active and not active disease stages in KP4 reveals that CDa and UCa stand out from the CG by higher KVs, and in contrast, CDna and UCna have lower KVs than the CG The released amounts of histamine in CDa and UCa are significantly higher than in CDna and UCna

Excretion of urinary histamine and N-tele methylhistamine in patients with gastrointestinal food allergy compared to non-allergic controls during an unrestricted diet and a hypoallergenic diet.

Abstract: Background: Patients with gastrointestinal food allergy are characterised by increased production of mast cell derived mediators upon allergen contact and present often with unspecific symptoms. The aim of this study was to evaluate urinary histamine and methylhistamine excretion in patients with food allergy and to compare their values with food-tolerant controls. Methods: In a retrospective case control study the urinary excretion parameters were analysed from 56 patients (40.9, 19 – 58 years) in whom later food challenge tests confirmed food allergy. During their diagnostic work-up urine was collected during a 12-h period under an unrestricted diet with staple foods and a hypoallergenic potato-rice-diet (each 2 days). Healthy controls underwent the same diet types to define normal excretion parameters. Urinary histamine and n-methylhistamine were determined by ELISA or tandem mass spectrometry, respectively, and were expressed as median (25 – 75% range, μg/mmol creatinine x m 2 BSA). Results: During unrestricted diet urinary histamine was significantly higher in gastrointestinal food allergy than healthy controls (1.42, 0.9 – 2.7 vs 0.87, 0.4 – 1.3; p < 0.0001), while the difference between both groups became marginal during potato-rice diet (1.30, 0.7 – 2.1 vs 1.05, 0.5 – 1.5; p = 0.02). N-methylhistamine was found to be significantly elevated in gastrointestinal food allergy both during unrestricted diet (7.1, 5.0 – 11.2) and potato-rice diet (5.7, 3.7 – 8.7) compared to controls (p < 0.0001). Interestingly, urinary methylhistamine excretion (p < 0.004) and clinical symptom score (p < 0.02) fell significantly when the diet was switched from unrestricted to hypoallergenic food, but was not correlated with symptom scores. Conclusions: In gastrointestinal food allergy significantly higher levels of urine histamine and methylhistamine excretion were found under unrestricted diet, reflecting an increased secretion of histamine due to offending foods. Measurement of urinary n-methylhistamine levels may help to find out patients with increased histamine production and/or food-allergen induced clinical symptoms, respectively.

Diagnostic use of mucosa oxygenation and histamine release experiments in patients with gastrointestinally mediated allergy (GMA).

Abstract: Gastrointestinal complaints after ingestion of certain foodstuffs often pose diagnostic problems in various clinical situations like food hypersensitivity, irritable bowel syndrome, inflammatory bowel disease etc [1]. A functional histamine release from intact human biopsies of the small intestine has been described in 1989 [2]. This study investigated histamine release from gut mucosal samples in gastrointestinally mediated allergy (GMA) in response to antigens that had been proven by blinded, placebo-controlled oral challenge (BPCFC) as causative allergens or tolerated foodstuffs.

Resolution of chronic inflammatory disease: universal and tissue-specific concepts

Abstract: Inflammation and its resolution is under-studied in medicine despite being essential for understanding the development of chronic inflammatory disease. In this review article, we discuss the resolution of inflammation in both a biological and translational context. We introduce the concept of impaired resolution leading to diseases like rheumatoid arthritis, Crohn's disease, and asthma, as well as the cellular and molecular components that contribute to resolution of joint, gut, and lung inflammation, respectively. Finally, we discuss potential intervention strategies for fostering the resolution process, and their implications for the therapy of inflammatory diseases.

Fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and nonallergic food intolerance: FODMAPs or food chemicals?

Abstract: Food intolerance in irritable bowel syndrome (IBS) is increasingly being recognized, with patients convinced that diet plays a role in symptom induction. Evidence is building to implicate fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) in the onset of abdominal pain, bloating, wind and altered bowel habit through their fermentation and osmotic effects. Hypersensitivity to normal levels of luminal distension is known to occur in patients with IBS, with consideration of food chemical intolerance likely to answer many questions about this physiological process. This paper summarizes the evidence and application of the most common approaches to managing food intolerance in IBS: the low-FODMAP diet, the elimination diet for food chemical sensitivity and others including possible noncoeliac gluten intolerance.