ABSTRACT
A rare presentation of acute pancreatitis is with electrocardiographic (ECG) changes that mimic myocardial ischemia. We present a report of a patient that presented with hemodynamic instability and new ECG changes of ST segment elevations in contiguous leads II, III, and aVF mimicking an inferior wall myocardial infarction. Emergent coronary angiography showed no significant coronary obstruction, but it was followed by a left-sided hemiplegia with radiographic evidence of diffuse embolic stroke. The patient was later found to have an underlying diagnosis of pancreatitis. Additional history that later became available indicated a history of severe acute pancreatitis treated elsewhere a few months prior to the current admission. We present the first comprehensive review of the literature comprising 36 total cases with pancreatitis masquerading as acute myocardial infarction, with inferior wall STEMI pattern being the most frequent. We present this case to highlight the diagnostic dilemma posed by this masquerade of a high acuity myocardial infarction and to highlight alternative diagnoses to be considered in such clinical circumstances.
ABSTRACT
PURPOSE OF REVIEW: Cyclic vomiting syndrome (CVS) is a chronic functional gastrointestinal disorder characterized by episodic nausea and vomiting and is diagnosed using Rome IV criteria. CVS is being recognized more frequently in adults with a prevalence of 2%. It is associated with several functional disorders like autonomic dysfunction, anxiety, and depression, but the strongest association is with migraine. We will elucidate the close relationship between migraine and CVS and briefly discuss its association with other gastrointestinal disorders. RECENT FINDINGS: We highlight similarities in pathophysiology, clinical presentation, and response to medications between CVS and migraine (tricyclic antidepressants, triptans, antiepileptics). We also discuss novel therapies like CGRP inhibitors which are effective in migraine and have potential for adaptation in patients with CVS. Using migraine as a template should enable investigators to elucidate the mechanisms underlying this disorder, develop novel therapies, and direct future research in CVS.
ABSTRACT
Immunoglobulin gene somatic hypermutation (SHM) and class switch DNA recombination (CSR) play important roles in the generation of autoantibodies in systemic lupus erythematosus. Systemic lupus is characterized by the production of an array of pathogenic high-affinity mutated and class-switched, mainly IgG, antibodies to a variety of self-antigens, including nuclear components, such as dsDNA, histones, and chromatin. We previously found that MRL/Fas(lpr/lpr) mice, which develop a systemic autoimmune syndrome sharing many features with human lupus, display greatly upregulated CSR, particularly to IgG2a, in B cells of the spleen, lymph nodes, and Peyer's patches. In MRL/Fas(lpr/lpr) mice, the significant upregulation of CSR is associated with increased expression of activation-induced cytidine deaminase (AID), which is critical for CSR and SHM. We also found that HoxC4 directly activates the promoter of the AID gene to induce AID expression, CSR and SHM. Here, we show that in both lupus patients and lupus-prone MRL/Fas(lpr/lpr) mice, the expression of HoxC4 and AID is significantly upregulated. To further analyze the role of HoxC4 in lupus, we generated HoxC4(-/-) MRL/Fas(lpr/lpr) mice. In these mice, HoxC4-deficiency resulted in reduced AID expression, impaired CSR, and decreased serum anti-dsDNA IgG, particularly IgG2a, autoantibodies, which were associated with a reduction in IgG deposition in kidney glomeruli. In addition, consistent with our previous findings in MRL/Fas(lpr/lpr) mice that upregulated AID expression is associated with extensive DNA lesions, comprising deletions and insertions in the IgH locus, we found that c-Myc to IgH (c-Myc/IgH) translocations occur frequently in B cells of MRL/Fas(lpr/lpr) mice. The frequency of such translocations was significantly reduced in HoxC4(-/-) MRL/Fas(lpr/lpr) mice. These findings suggest that in lupus B cells, upregulation of HoxC4 plays a major role in dysregulation of AID expression, thereby increasing CSR and autoantibody production and promoting c-Myc/IgH translocations.