Background: Total parenteral nutrition (TPN) provides all nutritional needs intravenously. Although lifesaving, enthusiasm is significantly tempered due to side effects of liver and gut injury, as well as lack of mechanistic understanding into drivers of TPN injury. We hypothesized that the state of luminal nutritional deprivation with TPN drives alterations in gut–systemic signaling, contributing to injury, and tested this hypothesis using our ambulatory TPN model. Methods: A total of 16 one-week-old piglets were allocated randomly to TPN (n = 8) or enteral nutrition (EN, n = 8) for 3 weeks. Liver, gut, and serum were analyzed. All tests were two-sided, with a significance level of 0.05. Results: TPN resulted in significant hyperbilirubinemia and cholestatic liver injury, p = 0.034. Hepatic inflammation (cluster of differentiation 3 (CD3) immunohistochemistry) was higher with TPN (p = 0.021). No significant differences in alanine aminotransferase (ALT) or bile ductular proliferation were noted. TPN resulted in reduction of muscularis mucosa thickness and marked gut atrophy. Median and interquartile range for gut mass was 0.46 (0.30–0.58) g/cm in EN, and 0.19 (0.11–0.29) g/cm in TPN (p = 0.024). Key gut–systemic signaling regulators, liver farnesoid X receptor (FXR; p = 0.021), liver constitutive androstane receptor (CAR; p = 0.014), gut FXR (p = 0.028), G-coupled bile acid receptor (TGR5) (p = 0.003), epidermal growth factor (EGF; p = 0.016), organic anion transporter (OAT; p = 0.028), Mitogen-activated protein kinases-1 (MAPK1) (p = 0.037), and sodium uptake transporter sodium glucose-linked transporter (SGLT-1; p = 0.010) were significantly downregulated in TPN animals, whereas liver cholesterol 7 alpha-hydroxylase (CyP7A1) was substantially higher with TPN (p = 0.011). Conclusion: We report significant alterations in key hepatobiliary receptors driving gut–systemic signaling in a TPN piglet model. This presents a major advancement to our understanding of TPN-associated injury and suggests opportunities for strategic targeting of the gut–systemic axis, specifically, FXR, TGR5, and EGF in developing ameliorative strategies.

Cervical cancer is the fourth most common cancer in women worldwide, with a large majority of prevalence (85%) in developing countries. As of 2012, it accounts for 7.5% of all female cancer deaths. Despite its high prevalence, skeletal muscle metastasis from cervical cancer is extremely uncommon. In our extensive literature search, we were able to find only 8 cases where skeletal muscle metastasis was the only site of recurrence. We report a case of a 52-year-old African-American woman with a past medical history of cervical cancer (stage IIIB) who presented with pain and swelling in her left upper arm over the preceding 2 months. MRI of the left upper arm showed a solid well-circumscribed mass measuring 7.0 × 2.8 × 2.5 cm, deep to the biceps. Biopsy of the mass revealed a metastatic squamous cell carcinoma that was p16-positive. PET scan showed that the lesion was the sole site of metastasis. She received local radiation with concurrent chemotherapy. Follow-up MRI 6 months after the completion of therapy showed resolution of the mass. She has remained disease-free for the last 24 months as evidenced by a PET/CT scan in May 2016. In this case report, we discuss the role of imaging and pathology in the diagnosis of a solitary metastatic lesion. This case also emphasizes the importance of a close follow-up which aids in early intervention, increasing overall survival.

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