Among patients with chronic urticaria and vitamin B12 deficiency, 68% reported gastrointestinal symptoms.
Recent studies have linked chronic urticaria (CU) to the presentation of gastrointestinal (GI) symptoms as well as to B12(ie, cobalamin) vitamin deficiency. Armin Abadeh, MD, and colleagues conducted the first study of this correlation, published in Allergy, Asthma & Clinical Immunology.
Dr. Abadeh discussed the findings of this work with Physician’s Weekly.
PW: What motivated you to pursue this topic?Â
Dr. Abadeh: Exploring the association of vitamin B12 deficiency, the presence of GI symptoms, and CU can contribute significantly to the understanding of this complex disease and could potentially enhance current treatment strategies. CU, characterized by recurrent, itchy hives and/or angioedema for over 6 weeks without an identifiable trigger, significantly impairs patients’ QOL. Research shows that CU may have underlying causes, and studies have found links between autoimmune GI disorders and CU, further suggesting the gut-skin axis might play a role in its pathogenesis. Vitamin B12, primarily absorbed in the GI tract, is essential for multiple physiologic functions. Deficiency can lead to complications, such as anemia, neurologic disorders, and possibly exacerbate symptoms in diseases like CU. Therefore, investigating this association could potentially reveal novel mechanisms of pathogenesis and indicate that screening for B12 deficiency in CU patients, especially those with GI symptoms, could be beneficial. This exploration could also lead to new therapeutic approaches, such as supplementation with vitamin B12, which, if proven effective, could significantly improve patient outcomes and QOL.
What are the most important findings from the study?Â
Our study aimed to report the prevalence of GI symptoms and cobalamin deficiency in a Canadian patient population diagnosed with CU. We retrospectively reviewed 100 adult patients and found that approximately 70% reported experiencing GI symptoms (Table). The most common symptom identified was gastroesophageal reflux, found in around 42% of these patients. Cobalamin deficiency, defined as serum B12 level of 250 pmol/L or less, was identified in 31.7% of the patients. Among patients with CU and B12 deficiency, 68% reported GI symptoms. To our knowledge, this was the first and largest study to provide data on the high prevalence of GI symptoms and cobalamin deficiency in a Canadian population diagnosed with CU.
How can physicians incorporate these findings into their practice?Â
Despite the availability of effective treatments for CU, many therapeutic outcomes focus primarily on reducing the number of hives, the intensity of itching, and improving the overall QOL. These treatments, however, often overlook extracutaneous manifestations, or symptoms that occur outside the skin, and the potential effects on a patient’s well-being. Tt might be beneficial to incorporate a routine check for GI symptoms as part of the management for individuals diagnosed with CU. In the same vein, evaluating B12 levels could be considered an integral part of managing patients with longstanding CU. If deficiencies are found, it would be sensible to investigate potential underlying causes that could contribute to vitamin B12 deficiency. For instance, chronic infections, the use of certain medications or underlying medical conditions, could all be contributing factors. Furthermore, inadequate B12 supplementation following certain surgeries (such as gastric or small bowel resections, or bariatric surgery), or dietary restrictions, especially in vegan diets, should also be considered. Identifying these contributing factors can help address vitamin B12 deficiency and potentially improve the overall management of CU.
What would you like future research to focus on?
In light of the observed association between B12 deficiency and CU, it becomes increasingly important to conduct systematic future research to elucidate whether there is a causal relationship between these two conditions. Such studies would serve to clarify the sequence of events: whether B12 deficiency precedes the development of CU or vice versa, or if they indeed arise concurrently. Understanding this temporal relationship could be key in determining the true nature of their association, providing crucial insights into the pathogenesis of CU. Future research should aim to assess the clinical efficacy of B12 replacement therapy in treating CU symptoms, possibly by comparing symptom relief in groups of patients receiving standard CU treatment alone versus those receiving B12 supplementation. These studies might consider long-term effects on the severity and frequency of CU episodes, the incidence of extracutaneous manifestations, and the overall QOL of patients.
