Fumaric acid: a possible new therapy for macular edema?

INTRODUCTION: Causes of macular edema are multifactorial, but inflammation, vascular factors and mechanical traction are of major importance. Therapeutic options of macular edema depend on the underlying cause. Intravitreal administration of inhibitors of vascular endothelial growth factor leads to inhibition of retinal neovascularization and subsequent edema. OBJECTIVE: Fumaric acid esters are successfully used in dermatology for years according to their antiangiogenic and anti-inflammatory effects. RESULT: For the very first time, we describe a successful therapeutic attempt for macular edema, controlled by optical coherence tomography using fumaric acid esters followed up for 60 months.

Allergic Reaction to Polyether Ether Ketone Following Cross-Reactivity to Epoxy Resin.

Polyether ether ketone (PEEK) is a thermoplastic polymer frequently used in engineering but also in medical devices. Only 1 case of allergic reaction to PEEK used as an implanted medical device has been reported so far; however, the route of sensitization remained unclear. Here we report on a 62-year-old male patient with a preknown, severe type IV allergy to epoxy resin. He reported strong pain in his shoulder after implantation of a PEEK-containing device after a rotator cuff injury. For testing, the device was implanted in a small pouch subcutaneously on the abdomen. The patient reported massive pain starting 8 hours after the implantation, strictly limited to the procedural area and showing perifocal erythema. A possible explanation of the sensitization mode is the source material for PEEK and epoxy resin, as both are mainly based on bisphenols. An allergic reaction to PEEK with preknown epoxy resin sensitization has not been reported so far. As epoxy resins are a frequent cause of occupational contact dermatitis and PEEK is widely used for medical and nonmedical devices, we believe that this is of great clinical relevance.

Tryptophan Metabolism in Allergic Disorders.

Allergic diseases such as asthma and rhinitis, as well the early phase of atopic dermatitis, are characterized by a Th2-skewed immune environment. Th2-type cytokines are upregulated in allergic inflammation, whereas there is downregulation of the Th1-type immune response and related cytokines, such as interferon-x03B3; (IFN-x03B3;). The latter is a strong inducer of indoleamine 2,3-dioxygenase-1 (IDO-1), which degrades the essential amino acid tryptophan, as part of an antiproliferative strategy of immunocompetent cells to halt the growth of infected and malignant cells, and also of T cells - an immunoregulatory intervention to avoid overactivation of the immune system. Raised serum tryptophan concentrations have been reported in patients with pollen allergy compared to healthy blood donors. Moreover, higher baseline tryptophan concentrations have been associated with a poor response to specific immunotherapy. It has been shown that the increase in tryptophan concentrations in patients with pollen allergy only exists outside the pollen season, and not during the season. Interestingly, there is only a minor alteration of the kynurenine to tryptophan ratio (Kyn/Trp, an index of tryptophan breakdown). The reason for the higher tryptophan concentrations in patients with pollen allergy outside the season remains a matter of discussion. To this regard, the specific interaction of nitric oxide (NO∙) with the tryptophan-degrading enzyme IDO-1 could be important, because an enhanced formation of NO∙ has been reported in patients with asthma and allergic rhinitis. Importantly, NO∙ suppresses the activity of the heme enzyme IDO-1, which could explain the higher tryptophan levels. Thus, inhibitors of inducible NO∙ synthase should be reconsidered as candidates for antiallergic therapy out of season that may abrogate the arrest of IDO-1 by decreasing the production of NO∙. Considering its association with the pathophysiology of atopic disease, tryptophan metabolism may play a relevant role in the pathophysiology of allergic disorders.

Histamine 50-skin-prick test: a tool to diagnose histamine intolerance.

Background. Histamine intolerance results from an imbalance between histamine intake and degradation. In healthy persons, dietary histamine can be sufficiently metabolized by amine oxidases, whereas persons with low amine oxidase activity are at risk of histamine toxicity. Diamine oxidase (DAO) is the key enzyme in degradation. Histamine elicits a wide range of effects. Histamine intolerance displays symptoms, such as rhinitis, headache, gastrointestinal symptoms, palpitations, urticaria and pruritus. Objective. Diagnosis of histamine intolerance until now is based on case history; neither a validated questionnaire nor a routine test is available. It was the aim of this trial to evaluate the usefullness of a prick-test for the diagnosis of histamine intolerance. Methods. Prick-testing with 1% histamine solution and wheal size-measurement to assess the relation between the wheal in prick-test, read after 20 to 50 minutes, as sign of slowed histamine degradation as well as history and symptoms of histamine intolerance. Results. Besides a pretest with 17 patients with HIT we investigated 156 persons (81 with HIT, 75 controls): 64 out of 81 with histamine intolerance(HIT), but only 14 out of 75 persons from the control-group presented with a histamine wheal ≥3 mm after 50 minutes (P < .0001). Conclusion and Clinical Relevance. Histamine-50 skin-prickt-test offers a simple tool with relevance.