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The article presents a case study of a 31-year-old female patient that presented postpartum abdominal pain with fever and was diagnosed with hepatic adenoma. Topics discussed include brief details about the medical history and pregnancy of the patient prior to hospital admission, the results of the physical and laboratory examinations performed such as blood tests and urinalysis, and the patient outcomes recorded following treatment.

Objective  Breast cancer is one of the most frequently diagnosed cancers in pregnancy and is commonly treated with chemotherapy. To date, studies examining effects of chemotherapy during pregnancy on fetal growth have yielded conflicting results, and most are limited by small sample sizes or are nonspecific with respect to cytotoxic regimen or type of cancer treated. We sought to evaluate the effect of chemotherapy for breast cancer in pregnancy on birthweight and small for gestational age infants. Study Design  This is a retrospective cohort study of 74 women diagnosed with pathologically confirmed breast cancer during pregnancy between 1997 and 2018 at one of three academic medical centers, who had a singleton birth with known birthweight. Forty-nine received chemotherapy and 25 did not receive chemotherapy. Linear regression modeling was used to compare birthweight (by gestational age and sex-specific z -score) by chemotherapy exposure. Subanalyses of specific chemotherapy regimen and duration of chemotherapy exposure were also performed. Placental, neonatal, and maternal outcomes were also analyzed by chemotherapy exposure. Results  In the adjusted model, chemotherapy exposure was associated with lower birthweight (Δ z -score = −0.49, p  = 0.03), but similar rates of small for gestational age (defined as birthweight <10th percentile for gestational age) infants (8.2 vs. 8.0%, p  = 1.0; Fisher's exact test). Each additional week of chemotherapy (Δ z -score = −0.05, p  = 0.03) was associated with decreased birthweight, although no association was found with specific chemotherapy regimen. Chemotherapy exposure was associated with lower median placental weight percentile by gestational age (9th vs. 75th, p  < 0.05). Secondary maternal outcomes were similar between the group that did and did not receive chemotherapy. Conclusion  Chemotherapy for breast cancer in pregnancy in this cohort is associated with lower birthweight but no difference in the rate of small for gestational age infants. Key Points Chemotherapy for breast cancer in pregnancy is associated with decreased birthweight but similar rates of small for gestational age infants. Birthweight did not differ according to chemotherapy regimen. There is no difference in the rate of small for gestational age infants. [ABSTRACT FROM AUTHOR]

Objective  This study was aimed to assess whether the "39-week" rule is being extended to high-risk pregnancies and if so whether this has led to changes in neonatal morbidity or stillbirth. Study Design  Birth certificate data between 2010 and 2014 from 23 states (55% of births in the United States) were used. Pregnancies were classified as high risk if they had any one of the following: maternal age greater than or equal to 40 years, prepregnancy body mass index (BMI) greater than or equal to 40 kg/m 2 , chronic (prepregnancy) hypertension, or diabetes (pregestational or gestational). Delivery timing changes for all pregnancies at term (37 weeks or greater) were compared with changes in the high-risk population. Neonatal morbidities (neonatal intensive care unit [NICU] admission, need for assisted ventilation, 5-minute Apgar score, and macrosomia), maternal morbidities (intensive care unit [ICU] admission, cesarean delivery, operative vaginal delivery, chorioamnionitis, and severe perineal laceration), and stillbirth rates were compared across time periods. Multivariate logistic regression was used to analyze whether gestational age–specific morbidity changes were due to shifts in delivery timing. Results  For the overall population, there was a shift in delivery timing between 2010 and 2014, a 2.5% decrease in 38-week deliveries, and a 2.3% increase in 39-week deliveries (p  < 0.01). This gestational age shift was identical in the high-risk population (2.7% decrease in 38-week deliveries and 2.9% increase in 39-week deliveries). For the high-risk population, NICU admission increased from 5.4 to 6.3% in 2014 (p  < 0.01) and assisted ventilation rates declined from 3.8 to 2.9% (p  < 0.01). These changes, however, were independent of changes in delivery timing. There was no increase in the rate of stillbirth (0.23% in 2010 and 0.23% in 2014; p  = 0.50). Conclusion  There was a significant shift in delivery timing for high-risk pregnancies in the United States between 2010 and 2014. This shift, however, did not result in statistically significant changes in either neonatal morbidity or stillbirth. Key Points From 2010 to 2014, term deliveries for high-risk pregnancies shifted towards 39 weeks. The shift towards 39 weeks in high-risk pregnancies was not accompanied by any improvement in neonatal morbidity. The shift towards 39 weeks in high-risk pregnancies did not result in an increase in the stillbirth rate. [ABSTRACT FROM AUTHOR]

Objective  Potentially avoidable maternity complications (PAMCs) have been validated as an indicator of access to quality prenatal care. African-American mothers have exhibited a higher incidence of PAMCs, which has been attributed to unequal health coverage. The objective of this study was to assess if racial disparities in the incidence of PAMCs exist in a universally insured population. Study Design  PAMCs in each racial group were compared relative to White mothers using multivariate logistic regression. Stratified subanalyses assessed for adjusted differences in the odds of PAMCs for each racial group within direct versus purchased care. Results  A total of 675,553 deliveries were included. Among them, 428,320 (63%) mothers were White, 112,170 (17%) African-American, 37,151 (6%) Asian/Pacific Islanders, and 97,912 (15%) others. African-American women (adjusted odds ratio [aOR]: 1.05, 95% CI: 1.02–1.08) were more likely to have PAMCs compared with White women, and Asian women (aOR: 0.92, 95% CI: 0.89–0.95) were significantly less likely to have PAMCs compared with White women. On stratified analysis according to the system of care, equal odds of PAMCs among African-American women compared with White women were realized within direct care (aOR: 1.03, 95% CI: 1.00–1.07), whereas slightly higher odds among African-American persisted in purchased (aOR: 1.05, 95% CI: 1.01–1.10). Conclusion  Higher occurrence of PAMCs among minority women sponsored by a universal health coverage was mitigated compared with White women. Protocol-based care as in the direct care system may help overcome health disparities. [ABSTRACT FROM AUTHOR]

Abstract Short-term consumption of a high-fat diet impairs exercise capacity in both rats and humans, and increases expression of the mitochondrial uncoupling protein, UCP3, in rodent cardiac and skeletal muscle via activation of the transcription factor, peroxisome proliferator-activated receptor α (PPARα). Unlike long-chain fatty acids however, medium-chain fatty acids do not activate PPARα and do not increase muscle UCP3 expression. We therefore investigated exercise performance and cardiac mitochondrial function in rats fed a chow diet (7.5% kcal from fat), a long-chain triglyceride (LCT) rich diet (46% kcal from LCTs) or a medium-chain triglyceride (MCT) rich diet (46% kcal from MCTs). Rats fed the LCT-rich diet for 15 days ran 55% less far than they did at baseline, whereas rats fed the chow or MCT-rich diets neither improved nor worsened in their exercise capacities. Moreover, consumption of an LCT-rich diet increased cardiac UCP3 expression by 35% and decreased oxidative phosphorylation efficiency, whereas consumption of the MCT-rich diet altered neither UCP3 expression nor oxidative phosphorylation efficiency. Our results suggest that the negative effects of short-term high-fat feeding on exercise performance are predominantly mediated by long-chain rather than medium-chain fatty acids, possibly via PPARα-dependent upregulation of UCP3.