Correction to: IgG4 sclerosing disease of the esophagus: a case­based review.

In the original article published, the name of the second author is incorrect.

IgG4 sclerosing disease of the esophagus: a case-based review.

IgG4-related disease (IgG4-RD) is an inflammatory and fibrosing disease which causes tumor-like swelling of organs and commonly mimics symptoms of malignancy. It has been increasing in prevalence in the last decade, but esophageal involvement remains rare. IgG4-RD was first known to involve certain organs, such as the pancreas. It has, since, been described as a systemic disease process. IgG4-RD should be considered in patients presenting with dysphagia. Initiation of appropriate treatment with corticosteroids can avoid unnecessary procedures and improve outcomes. The aim of this review is to discuss 17 cases of IgG4-RD of the esophagus. Literature review was conducted using NCBI database (PMC and PubMed filters) using the keywords "IgG4 disease," "sclerosing," "esophagus" and "gastrointestinal." The search was narrowed to include cases describing IgG4 disease of the esophagus using the same filters. Literature review identified 16 documented cases of IgG4-RD involving the esophagus. Upon literature review, it remains clear that it is extremely rare for IgG4-RD to affect the esophagus. Sixteen cases have been reported. We present a 17th case and discuss the implications of IgG4-RD. It is important to keep a broad differential diagnosis that includes IgG4-RD for patients presenting with dysphagia, especially when symptoms are refractory.

Gout and Metabolic Syndrome: a Tangled Web.

PURPOSE OF REVIEW: The complexity of gout continues to unravel with each new investigation. Gout sits at the intersection of multiple intrinsically complex processes, and its prevalence, impact on healthcare costs, and association with important co-morbidities make it increasingly relevant. The association between gout and type 2 diabetes, hypertension, hyperlipidemia, cardiovascular disease, renal disease, and obesity suggest that either gout, or its necessary precursor hyperuricemia, may play an important role in the manifestations of the metabolic syndrome. In this review, we analyze the complex interconnections between gout and metabolic syndrome, by reviewing gout's physiologic and epidemiologic relationships with its major co-morbidities. RECENT FINDINGS: Increasing evidence supports gout's association with metabolic syndrome. More specifically, both human studies and animal models suggest that hyperuricemia may play a role in promoting inflammation, hypertension and cardiovascular disease, adipogenesis and lipogenesis, insulin and glucose dysregulation, and liver disease. Fructose ingestion is associated with increased rates of hypertension, weight gain, impaired glucose tolerance, and dyslipidemia and is a key driver of urate biosynthesis. AMP kinase (AMPK) is a central regulator of processes that tend to mitigate against the metabolic syndrome. Within hepatocytes, leukocytes, and other cells, a fructose/urate metabolic loop drives key inhibitors of AMPK, including AMP deaminase and fructokinase, that may tilt the balance toward metabolic syndrome progression. Preliminary evidence suggests that agents that block the intracellular synthesis of urate may restore AMPK activity and help maintain metabolic homeostasis. Gout is both an inflammatory and a metabolic disease. With further investigation of urate's role, the possibility of proper gout management additionally mitigating metabolic syndrome is an evolving and important question.