e23010 Background: Gender inequalities in medicine are ongoing challenges facing health care providers in different fields. Gender bias in medicine is gaining more attention, raising the awareness of this important topic. Per ASCO 2022 snapshot, females represent 35.8% of total oncologists in the United States. This study aims to spot the light on female representation in ASCO abstracts authors and presidents, adding to the continuous efforts aiming to achieve gender equity in the oncology practice. Methods: Data from the ASCO database and conference materials was gathered for analysis in the different categories. These categories included presidents of ASCO since it was founded in 1964 through 2022, and first authors in abstracts accepted over the past 5 years (2018-2022). Statistical analyses on first authors data were conducted, and a P-value of < 0.001 was deemed to be statistically significant. Results: In the 58-year period (1964-2022), ASCO had 49 men (85%) and 9 women (15%) serve as presidents. 7 out of 9 total female presidents were elected in the last 20 years. In the 5 year period (2018-2022), there was a significant increase in the percentage of abstracts accepted for a female author. 37.1% of the presenters in 2018 were females, compared to 41.4% in 2022, with statistically significant results (P value < 0.001), detailed percentages are shown in tables. Conclusions: Gender gap in the field of oncology goes beyond pay differences to include leadership positions and research authorship. But as shown by our analysis, there has been an increase in representation of females in ASCO abstracts authorship and leadership over the past years. Nonetheless, further work is needed to identify factors contributing to lower representation of women in oncology, and suggested solutions. [Table: see text][Table: see text]
Table 1. (continued) Factor Missed (N 5 3768) Completed (N 5 43262) P-value Adjusted Odds Ratio for Missed Visits (95% CI) P-value Third 664 (17.6%) 11182 (25.8%) 0.64 (0.58 -0.72) , 0.001 Highest 707 (18.8%) 11059 (25.6%) 0.71 (0.63 -0.71) , 0.001 Employment Status , 0.001 Employed 1234 (23.8%) 16868 (39%) Reference Unemployed 1959 (52%) 16783 (38.8%) 1.45 (1.33 -1.58) , 0.001 Retired 488 (13%) 8709 (20.2%) 0.99 (0.88 -1.13) 0.99 Unknown 84 (2.2%) 852 (2%) 0.98 (0.73 -1.30) 0.88 Marital Status , 0.001 Married 1565 (41.5%) 21463 (49.6%) Reference Single 2153 (57.1%) 21206 (49%) 1.09 (1.10 -1.17) 0.023 Others 50 (1.3%) 593 (1.4%) 0.94 (0.68 -1.29) 0.71 H/o Tobacco Use 756 (20.4%) 5903 (13.8%) , 0.001 1.23 (1.12 -1.35) , 0.001 H/o Alcohol Use 1555 (43.2%) 18694 (45%) 0.074 H/o Illicit Drug Use 352 (9.7%) 2657 (6.4%) , 0.001 1.14 (1.01 -1.29) 0.03 Primary Language , 0.001 English 3639 (96.6%) 42355 (97.9%) Reference Spanish 64 (1.7%) 413 (1%) 1.20 (0.89 -1.63) 0.21 Other 64 (1.7%) 495 (1.1%) 1.
lymphangiogram showed abdominal collateral lymphatics and iliac lymphangiectasia. Overall, these findings were consistent with PLE. A high protein diet and medium-chain triglyceride supplementation were initiated, and she had normalization of serum albumin levels. Genetic analysis showed a SHOC2 gene mutation. Discussion: PLE consists of loss of serum proteins through the digestive tract, which may initially present as hypoalbuminemia in the absence of liver disease. This disorder is important to recognize due to the association between low albumin and increased mortality risk. Lymphatic disease presenting with lymphedema, chylothorax, and lymphangiectasia is well known in NS and may play a role in PLE development. PLE has been tied to the mutation of protein tyrosine phosphatase non-receptor type 11, but to our knowledge, has not been reported with SHOC2 mutation. Because little is understood about PLE in NS, there is no standard treatment. However, supplementation with medium-chain triglycerides and periodic albumin infusions has proven effective. The association between PLE and NS may be more common than acknowledged. This case identifies SHOC2 mutation with PLE and encourages consideration of PLE in NS in hopes of decreasing mortality and increasing quality of life.
Introduction: Drug induced liver injury can be a result of many medications and remains as one of the most challenging disorders faced by GI specialists. The most common causes in the Western world include antimicrobials, antiepileptics, anticancer medications, herbal and dietary supplements. It is important to make the distinction between intrinsic and idiosyncratic types of DILI. Intrinsic DILI is capable of causing injury in a predictable pattern in humans when given in high doses. Idiosyncratic DILI only affects susceptible individuals and has less of an association to dosing. The latter being the more difficult type to diagnose and treat. An important value, the R-factor, is used to define hepatotoxicity injury patters. An R-factor , 2 suggests a cholestatic pattern, R-factor . 5 suggests a hepatocellular pattern, and in between a mixed pattern of injury. Early withdrawal of the offending agent is the treatment of choice for any cause of DILI as this prevents progression of acute liver failure. Case Description/Methods: We present a case of a 61 year old male (S, J) with acute elevations in his liver enzymes and alkaline phosphatase. Patient was admitted for alcohol withdrawal. The following day, patient was intubated secondary to hypercapnic respiratory failure and days later developed ventilator associated pneumonia for which he was started on antimicrobial therapy, cefepime and vancomycin. After 9 days of receiving cefepime, patient's alkaline phosphatase and liver transaminases acutely increased. Patient's baseline levels were normal on arrival to the hospital. His lab values were the following: ALT 263, AST 507, and alkaline phosphatase 279 with an R factor of 2.8 showing a mixed injury pattern. A right upper quadrant ultrasound showed hepatomegaly and an acute hepatitis panel was ordered which resulted negative. No episodes of significant hypotension were reported. The antibiotic was immediately discontinued with resolution of patient's levels back to normal. Discussion: Though not as commonly reported, increased ALT, AST or alkaline phosphatase can be a result of cefepime use. Our patient on admission did not have abnormal liver chemistry tests despite his history of alcohol use. R-factor for our patient showed a mixed pattern of liver injury. First line tests when suspecting DILI such as acute viral hepatitis serologies and imaging studies were ordered. Our patient was not re-started on cefepime and his liver enzymes returned to baseline.
comprehensive metabolic panel being normal. Contrasted CT scan of the abdomen and pelvis revealed no abnormalities. A right upper quadrant ultrasound was notable for left sided intrahepatic biliary dilatation. Over the next day, his mentation worsened, with repeat labs notable for bicarbonate 13, creatinine 3.08, AST 12050, ALT 3950, total bilirubin 2.4 with direct bilirubin 1.5, INR 3.11 and ammonia 164. A broad infectious workup was unremarkable including negative viral hepatitis serologies. Smooth muscle antibody was weakly positive at a low titer of 1:20. Anti-nuclear and anti-mitochondrial antibodies were negative. Serum IgG level was normal. Endoscopic retrograde cholangiopancreatography revealed a severe left intrahepatic biliary stricture with resulting stent placement into the left hepatic duct. Bile duct brushing was negative for atypical cells. Liver biopsy demonstrated centrilobular necrosis and parenchymal collapse with focal bridging necrosis and mixed inflammatory infiltrate. A diagnosis of AIH secondary to DILI leading to acute liver failure was made, with either Naproxen or Cephalexin being the inciting drugs. Discussion: He was started on a prednisone taper and showed improvements in mental status and kidney and liver function on lab-work prior to discharge. Labs obtained on clinic follow-up one month after discharge revealed complete resolution of his kidney and liver injury. This case illustrates a rare clinical entity as neither Naproxen nor Cephalexin are classically associated with causing AIH or acute liver failure.
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