Persistent opioid use after curative-intent hepatectomy for neoplastic disease.

BACKGROUND AND OBJECTIVES: This study analyzed persistent opioid use in opioid-naïve and nonopioid-naïve patients undergoing hepatectomy for neoplastic disease. METHODS: A retrospective review was performed of a prospective database using inclusion criteria of hepatectomy for neoplastic disease from October 2013 to December 2017. Prescription data were collected from the North Carolina Controlled Substance Reporting System. Persistent opioid use was defined as patients who continued filling opioid prescriptions 90 days to 1 year after surgery. Patients who did not receive opioid prescriptions between 12 months and 31 days before surgery were defined as naïve. RESULTS: The analysis included 75 surgeries on naïve and 58 surgeries on nonnaïve patients. 56% of naïve patients and 79% of nonnaïve patients developed persistent opioid use, respectively (p = .0056). Naïve patients received 2.24 ± 4.30 MMEs/day, while nonnaïve patients received 5.50 ± 5.98 MMEs/day during Postoperative days 90-360 (95% CI, 1.41-5.10; p < .001). Naïve patients with a lower Preoperative ECOG score were more likely to develop persistent opioid use (OR, 0.45; 95% CI, 0.21-0.99; p = .048). CONCLUSION: More than half of naïve patients undergoing hepatectomy developed persistent opioid use within the first year, though significantly less than nonnaïve patients. Improved performance status was associated with an increased risk of persistent opioid use in naïve patients.

Intravascular B-cell lymphoma: case report of a rare cause of pulmonary arterial hypertension.

BACKGROUND: Intravascular large B-cell lymphoma (IVLBCL) is a rare disease characterized by proliferation of malignant lymphoid cells within the small vessels of various organs resulting in diffuse thrombosis. It most commonly affects the central nervous system and the skin, but if it involves the pulmonary arteries it can cause acute severe pulmonary hypertension (PH) and right heart failure. Early diagnosis is essential as the clinical course is extremely aggressive. In this report, we present a case of rapidly progressive PH and subsequent right ventricular (RV) failure secondary to IVLBCL. We review the important differential diagnoses and diagnostic evaluation needed to make a correct and early diagnosis. CASE SUMMARY: A 53-year-old, previously healthy man developed 2 months of progressive shortness of breath. After being treated for presumptive pneumonia, he was admitted with hypoxic respiratory failure, altered mental status, and severe PH. He developed RV failure and subsequent liver failure. He was ruled out for pulmonary embolism. Despite aggressive management with inhaled nitric oxide and epoprostenol, inotropes, and continuous renal replacement therapy, the patient passed away. Post-mortem examination revealed the presence of IVLBCL with extensive involvement notable of the brain, heart, lungs, and pulmonary arteries. DISCUSSION: The acute development of severe PH and RV failure in the absence of pulmonary emboli is uncommon and represents a challenging diagnostic and management clinical scenario. When accompanied by altered mental status, constitutional symptoms and an elevated lactate dehydrogenase, clinicians should have a high index of suspicion for intravascular lymphoma, as early diagnosis is critical to maintain a reasonable chance of survival.

Pleiotrophin produced by multiple myeloma induces transdifferentiation of monocytes into vascular endothelial cells: a novel mechanism of tumor-induced vasculogenesis.

Enhanced angiogenesis is a hallmark of cancer. Pleiotrophin (PTN) is an angiogenic factor that is produced by many different human cancers and stimulates tumor blood vessel formation when it is expressed in malignant cancer cells. Recent studies show that monocytes may give rise to vascular endothelium. In these studies, we show that PTN combined with macrophage colony-stimulating factor (M-CSF) induces expression of vascular endothelial cell (VEC) genes and proteins in human monocyte cell lines and monocytes from human peripheral blood (PB). Monocytes induce VEC gene expression and develop tube-like structures when they are exposed to serum or cultured with bone marrow (BM) from patients with multiple myeloma (MM) that express PTN, effects specifically blocked with antiPTN antibodies. When coinjected with human MM cells into severe combined immunodeficient (SCID) mice, green fluorescent protein (GFP)-marked human monocytes were found incorporated into tumor blood vessels and expressed human VEC protein markers and genes that were blocked by anti-PTN antibody. Our results suggest that vasculogenesis in human MM may develop from tumoral production of PTN, which orchestrates the transdifferentiation of monocytes into VECs.