Introduction: Metabolic syndrome represents a cluster of related metabolic abnormalities, including central obesity, hypertension, dyslipidemia, hyperglycemia, and insulin resistance, with central obesity and insulin resistance in particular recognized as causative factors. These metabolic derangements present significant risk factors for cardiovascular disease, which is commonly recognized as the primary clinical outcome, although other outcomes are possible. Metabolic syndrome is a progressive condition that encompasses a wide array of disorders with specific metabolic abnormalities presenting at different times. These abnormalities can be detected and monitored via serum biomarkers. This review will compile a list of promising biomarkers that are associated with metabolic syndrome and this panel can aid in early detection and management of metabolic syndrome in high risk populations, such as in West Virginia.Methods: A literature review was conducted using PubMed, Science Direct, and Google Scholar to search for markers related to metabolic syndrome. Biomarkers searched included adipokines (leptin, adiponectin), neuropeptides (ghrelin), pro-inflammatory cytokines (IL-6, TNF-α), anti-inflammatory cytokines (IL-10), markers of antioxidant status (OxLDL, PON-1, uric acid), and prothrombic factors (PAI-1).Results: According to the literature, the concentrations of pro-inflammatory cytokines (IL-6, TNF-α), markers of pro-oxidant status (OxLDL, uric acid), and prothrombic factors (PAI-1) were elevated in metabolic syndrome. Additionally, leptin concentrations were found to be elevated in metabolic syndrome as well, likely due to leptin resistance. In contrast, concentrations of anti-inflammatory cytokines (IL-10), ghrelin, adiponectin, and antioxidant factors (PON-1) were decreased in metabolic syndrome, and these decreases also correlated with specific disorders within the cluster.Conclusion: Based on the evidence presented within the literature, the aforementioned biomarkers correlate significantly with metabolic syndrome and could provide a minimally-invasive means for early detection and specific treatment of these disorders. Further research is encouraged to determine the efficacy of applying these biomarkers to diagnosis and treatment in a clinical setting.

Cardiotoxicity is an important issue for breast cancer patients receiving anthracycline-trastuzumab therapy in the adjuvant setting. Studies show that 3–36% of patients receiving anthracyclines and/or trastuzumab experience chemotherapy related cardiac dysfunction (CRCD) and approximately 17% of patients must stop chemotherapy due to the consequences of CRCD. There is currently no standardized, clinically verified way to detect CRCD early, but common practices include serial echocardiography and troponin measurements, which can be timely, costly, and not always available in areas where health care resources are scarce. Furthermore, detection of CRCD, before there is any echocardiographic evidence of dysfunction or clinical symptoms present, would allow maximal benefit of chemotherapy and minimize cardiac complications. Creating a panel of serum biomarkers would allow for more specificity and sensitivity in the early detection of CRCD, which would be easy to implement and cost effective in places with limited health care. Based on a review of the literature, we propose creating a biomarker panel consisting of topoisomerase 2β, serum troponin T/I, myeloperoxidase, NT-proBNP, miR-208b, miR-34a, and miR-150 in breast cancer patients receiving anthracyclines and/or trastuzumab to detect CRCD before any signs of overt cardiotoxicity are apparent.

BackgroundNeutropenic enterocolitis is a life-threatening inflammation of the colon with a mortality rate above 50% primarily seen in neutropenic patients on cytotoxic chemotherapy. The following cases illustrate three patients with this condition following midostaurin administration after standard induction chemotherapy with daunorubicin/idrarubicin and cytarabine for acute myeloid leukemia (AML). Midostaurin is a multitargeted FMS-Like Tyrosine kinase 3 (FLT3) receptor inhibitor used in AML treatment after induction chemotherapy.MethodsReview of records of three patients seen by the infectious disease service.ResultsIn these cases, patients were diagnosed with AML with FLT3 mutation. All three were admitted and started on standard induction chemotherapy. Midostaurin was started on chemotherapy day 8 at which time all patients were neutropenic. The patients developed fevers, abdominal pain, and diarrhea within 36 hours of starting midostaurin and had abdominal CT findings consistent with neutropenic enterocolitis. For two patients, midostaurin was discontinued and symptoms improved upon discontinuation. One patient completed the course of midostaurin with symptom resolution after its completion. Of note, all were started on appropriate prophylactic antibiotics at chemotherapy initiation and were started on broad-spectrum antibiotics at onset of fevers and abdominal symptoms. Appropriate evaluation was also done for each patient to rule out other causes of abdominal symptoms, including testing for Clostridium difficile colitis.ConclusionThese cases are significant because they illustrate individuals treated with standard induction chemotherapy for AML and started on midostaurin while neutropenic who began reporting symptoms of neutropenic enterocolitis within 36 hours of receiving midostaurin. This shows a possible increased toxicity when midostaurin is given after induction chemotherapy in the setting of neutropenia. Stone et al. showed increased intestinal symptoms with midostaurin, but no cases of neutropenic enterocolitis have been reported. With increased midostaurin use in the past year, further studies are warranted to establish and raise awareness of a possible direct association between midostaurin and gastrointestinal toxicity.Disclosures All authors: No reported disclosures.

Background Syphilis is an ulcerative sexually transmitted genital infection caused by Treponema pallidum, which is a member of the order Spirochaetales, family Spirochaetaceae, and genus Treponema. The incidence rate of Syphilis has been steadily rising since 2000; from 2.1 cases per 100,000 population to up to 7.5 cases per 100,000 population in 2014–2015 (the highest rate since 1994). In the state of West Virginia, we have witnessed an increase in the number of cases from 0.5 cases per 100,000 population in 2011, to 5.9 cases per 100,000 population in 2015. Systemic symptoms can include cardiovascular and neurological manifestations. We report to your attention four cases of syphilis mainly with neurological and ocular manifestations.Methods We report a series of four cases of neurosyphilis we encountered between 2013 and 2016. Main presentation of all four cases was ocular; primarily redness and photophobia. Diagnosis was confirmed by standard ophthalmological examination with positive initial rapid plasma regain titers (RPR) and fluorescent treponemal antibody absorption testing (FTA-ABS). The cerebrospinal fluid venereal disease research laboratory test (CSF-VDRL) was positive in two of the four cases (in which lumbar puncture was performed). Two of the four cases suffered from an overt immunodeficiency (HIV and laryngeal cancer on chemotherapy) and subjects of all four cases confessed to high-risk sexual behaviors. All four cases were managed with continuous infusions of Penicillin G potassium 24 million International Units for 14 days with variable response.ResultsResponse to treatment was variable in that initial complete resolution was achieved in one patient (Case #3), another (Case #1) was retreated in 6 months due to rising RPR titers on follow-up with subsequent improvement. Two patients were lost to follow-up (Cases #2 and #4).Conclusion Sir William Osler reportedly said: “He who knows syphilis knows medicine”. The steady rise in the incidence of Syphilis warrants that health care providers consider such a diagnosis in the evaluation of suggestive neurological and ocular manifestations in predisposed patients. We also stress on the importance of follow-up to detect failure of initial treatment.Disclosures All authors: No reported disclosures.