QTc and QRS Abnormalities are Associated with Outcome in Pediatric Heart Failure.

Adult studies have shown that depolarization and repolarization abnormalities are associated with worsening heart failure; however, this relationship is not well understood in pediatric congenital heart disease. We evaluated the association between QTc and QRS duration to systolic function and outcome in children with heart failure and reduced ejection fraction (HFrEF). We performed a retrospective, single-center, 14-year cohort study of HFrEF children. Clinical records, echocardiograms, and electrocardiograms were reviewed for every clinical encounter. Diagnosis, interventions, outcomes, QRS and QTc duration, and systolic function were collected. Repeated-measure ANOVA evaluated the association between depolarization and repolarization to cardiac function. Cox regression analysis examined the effects of age, time since diagnosis, and measured and change in QTc and QRS duration on time to transplant/death. We enrolled 136 cardiomyopathy (CM) and 47 structural heart disease (SHD) patients. Prolonged QRS (p = 0.0001) and QTc (p = 0.02) were associated with systolic dysfunction. This association was significant in SHD group (QRS p < 0.0001, QTc p = 0.048), but not CM group (QRS p = 0.5, QTc p = 0.3). Progressive lengthening of QTc was significantly associated with transplant or death in the overall cohort (HR 1.02, CI 1.011-1.028), SHD, (HR 1.020, CI 1.001-1.039), and CM (HR 1.017, CI 1.007-1.027). QTc and QRS prolongation are each associated with ventricular dysfunction in pediatric SHD with heart failure. QTc prolongation is an indication for poor outcomes in SHD and CM groups, leading to a higher risk of death or transplantation. Progressive lengthening of QTc over time in children with HFrEF may indicate increased risk in this population.

Exogenous estrogen therapy, testicular cancer, and the male to female transgender population: a case report.

BACKGROUND: Over the last 40 years, there has been a significant increase in the incidence of testicular cancer. The epidemiologic evidence to understand this phenomenon is unclear, however exogenous estrogen exposure is thought to be a driver in the development of testicular cancer. This is of particular importance in the transgender population because utilization of exogenous estrogen therapy is an essential aspect of the transition process. CASE: We present the case of a 38-year-old Caucasian male to female transgender patient who presented with metastatic testicular cancer 15 months after initiating estrogen therapy. She presented to our emergency department with worsening back pain and fatigue. A clinical examination revealed a right-sided testicular mass. A computed tomography scan of her abdomen/pelvis identified a right groin lesion measuring 6.4 cm, a retroperitoneal mass causing right-sided hydronephrosis, an extensive deep vein thrombosis, and pathologic abdominal lymphadenopathy. Germ cell tumor markers revealed an alpha-fetoprotein of < 2.5 µg/L and a beta-human chorionic gonadotrophin of 2526 IU/L. Her lactate dehydrogenase was 5294 U/L. Medical oncology advised the discontinuation of hormonal therapy at this time. On the basis of elevation in germ cell tumor markers and the burden of disease, she was treated with four cycles of bleomycin, etoposide, and cisplatin chemotherapy. A decision to defer upfront radical inguinal orchiectomy was made due to not wanting to have an early interruption in anticoagulation. Following the completion of the chemotherapy, a 6 cm retroperitoneal mass persisted. Due to the location of the mass and surgical morbidity associated with excision, she was followed with positron emission tomography-computed tomography by Uro-oncology, with no evidence of recurrent disease 2 years since the time of diagnosis. CONCLUSIONS: While there are recognized risks associated with estrogen therapy less is known about the extent to which exogenous estrogen can serve as a driver of malignancy. With recent experimental evidence revealing a pro-growth impact of estrogen on human testicular cells, continued reporting of similar cases in the literature is imperative to see if a link between exogenous estrogen exposure and testicular cancer exists.

Patterns of Referral for Adjuvant Chemotherapy for Stage II and III Colon Cancer: A Population-Based Study.

PURPOSE: Reasons for variable utilization of adjuvant chemotherapy (ACT) for colon cancer have not been well described. We report medical oncology (MO) referral patterns and subsequent use of ACT. METHODS: Treatment records were linked to the population-based Ontario Cancer Registry to describe MO referral and ACT use among 5289 patients with stage II-III colon cancer treated in 2002-2008. Modified Poisson regression was used to analyze factors associated with MO referral and ACT use. Multilevel modeling was used to explore the proportion of variation in practice attributable to providers. RESULTS: There was wide geographic variation in MO referral rates for stage II (range 37-80 %, p < 0.001) and stage III disease (range 77-98 %, p < 0.001). Use of ACT among referred patients varied across regions for stage II (range 12-49 %, p < 0.001) but not stage III (range 67-79 %, p = 0.353). For both stages, younger patients (p < 0.001) with less comorbidity (p < 0.010) were more likely to be referred to MO and treated with ACT. Applying the fitted regression model to nonreferred stage III patients suggests that 38 % had >50 % probability of having ACT if they had seen a MO. Among stage III patients, 15 % percent of the variance in MO referral rate and 6 % of the variance in ACT utilization rate is attributable to the surgeon and MO respectively. CONCLUSIONS: A substantial proportion of non-referred patients with stage III colon cancer may have been offered ACT if they had seen MO. A small proportion of variance in referral rate and ACT treatment is attributable to providers.