Food-specific antibodies and urologic chronic pelvic pain syndrome.

（请保持文字，不要PDF） 在此输入文本，它是应用程序的新摘要信息。此部分不得超过30行文本。 间质性膀胱炎/膀胱疼痛综合征（IC/BPS）和慢性前列腺炎/慢性骨盆疼痛综合征（CP/ CPPS）是常见的、昂贵的且使人衰弱的综合征，其特征是持续性膀胱和/或骨盆疼痛以及泌尿系统症状，例如尿急和尿频。这些疾病的原因，统称为泌尿系慢性盆腔疼痛综合征（UCPPS），是未知的，其病理生理学知之甚少，使治疗具有挑战性。虽然已经提出了几种治疗UCPPS的方法，但尚未发现 在所有患者中一致地工作，并且每一种都是侵入性的或容易产生显著的副作用。因此，显然需要新的治疗方法。其中一个有希望但研究不足的方法是饮食排斥。这种方法得到了一项小型单臂试验（n=10）、两份病例报告、我们最近的慢性盆腔疼痛研究多学科方法1（MAPP-1）研究网络病例交叉研究以及几项患者调查结果的支持，这些调查结果表明，很大一部分患者认为饮食触发了他们的耀斑。然而，由于患者报告的触发因素众多且范围广泛（多达144个候选者），因此确定适合所有患者的常见饮食已被证明具有挑战性。消除饮食也难以实施和测试，因为在“消除”阶段需要消除大量可能的食物触发物，在“重新引入”阶段需要重新引入大量食物触发物，以及盲法消除饮食的挑战。因此，迫切需要个性化这些饮食的工具。在偏头痛、克罗恩病、肠易激综合征和哮喘患者的初步试验中，研究人员 观察到显着的症状减少后，排除饮食通知食物特异性IgG抗体浓度。这种方法很有前途，因为它减少了时间，复杂性和饮食排除的负担，同时增加了成功的机会和严格的盲法评估的潜力。食物特异性IgG抗体也是告知UCPPS治疗的合理候选物，因为它们通过与UCPPS病理学有关的生物机制（例如肥大细胞脱粒和组胺释放）起作用，并且在与患者报告的食物触发经历一致的“延迟”时间范围（数小时至数天）内起作用。然而，在我们可以启动一项随机对照试验（RCT）的食物特异性IgG抗体知情的排除饮食UCPPS，额外的经验证据是必要的，以支持这种方法。对于生物标志物排除饮食已经显示出初步疗效的许多情况，研究人员首先证明了患者比对照组具有食物特异性IgG抗体的可能性更大。我们还在10名UCPPS患者（100%有食物特异性IgG抗体）的小样本中获得了有希望的初步数据 与历史对照的15-33%相比）。在R 01中，我们计划通过正式测试UCPPS患者是否比对照组具有更大的食物敏感性来建立这些有希望的发现，使用来自MAPP-1研究的100例病例和100例对照的现有血浆样本和临床表型数据。

(PLEASE KEEP IN WORD, DO NOT PDF) Enter the text here that is the new abstract information for your application. This section must be no longer than 30 lines of text. Interstitial cystitis/bladder pain syndrome (IC/BPS) and chronic prostatitis/chronic pelvic pain syndrome (CP/ CPPS), are common, costly, and debilitating syndromes characterized by persistent bladder and/or pelvic pain, and urinary symptoms, such as urgency and frequency. The cause of these conditions, together referred to as urologic chronic pelvic pain syndrome (UCPPS), is unknown and their pathophysiology is poorly understood,making treatment challenging. Although several therapies have been proposed for UCPPS, none has been found to work consistently in all patients and each is either invasive or prone to significant side effects. Therefore, new therapeutic approaches are clearly needed. One such promising, but understudied, approach is dietary exclusion. This approach is supported by findings from one small single-arm trial (n=10), two case reports, our recent Multidisciplinary Approach to the Study of Chronic Pelvic Pain 1 (MAPP-1) Research Network case-crossover study, and several patient surveys indicating that a large proportion of patients believe that diet triggers their flares. However, as patient-reported triggers are numerous and wide-ranging (up to 144 candidates), identification of one common diet suitable for all patients has proven challenging. Elimination diets are also difficult to implement and test because of the large number of possible food triggers that need to be eliminated in the “elimination” phase, the large number that need to be re-introduced in the “re-introduction” phase, and the challenges of blinding elimination diets. Therefore, tools to personalize these diets are urgently needed. In pilot trials of patients with migraines, Crohn’s disease, irritable bowel syndrome, and asthma, researchers have observed significant symptom reductions following exclusion diets informed by food-specific IgG antibody concentrations. This approach is promising because it reduces the time, complexity, and burden of dietary exclusion, while simultaneously increasing its chance of success and potential for rigorous blinded evaluation. Food-specific IgG antibodies are also plausible candidates to inform UCPPS therapy because they act by biologic mechanisms implicated in UCPPS pathology (e.g. mast cell degranulation and histamine release) and in a “delayed” time frame (hours to days) consistent with patient-reported food trigger experiences. However, before we can initiate a randomized controlled trial (RCT) of food-specific IgG antibody-informed exclusion diets for UCPPS, additional empirical evidence is necessary to support this approach. For many conditions for which biomarker-informed exclusion diets have shown preliminary efficacy, researchers first demonstrated a greater likelihood of having food-specific IgG antibodies in patients than controls. We have also generated promising pilot data in a small sample of 10 UCPPS patients (100% had food-specific IgG antibodies compared to 15-33% of historical controls). In this R01, we plan to build on these promising findings by formally testing whether UCPPS patients have greater food sensitivity than controls, using existing plasma samples and clinical phenotyping data from 100 cases and 100 controls from the MAPP-1 study.