The use of neoadjuvant lobar radioembolization prior to major hepatic resection for malignancy results in a low rate of post hepatectomy liver failure

BackgroundNeoadjuvant yttrium-90 transarterial radioembolization (TARE) is increasingly being used as a strategy to facilitate resection of otherwise unresectable tumors due to its ability to generate both tumor response and remnant liver hypertrophy. Perioperative outcomes after the use of neoadjuvant lobar TARE remain underinvestigated.MethodsA single center retrospective review of patients who underwent lobar TARE prior to major hepatectomy for primary or metastatic liver cancer between 2007 and 2018 was conducted. Baseline demographics, radioembolization parameters, pre- and post-radioembolization volumetrics, intra-operative surgical data, adverse events, and post-operative outcomes were analyzed.ResultsTwenty-six patients underwent major hepatectomy after neoadjuvant lobar TARE. The mean age was 58.3 years (17–88 years). 62% of patients (n=16) had primary liver malignancies while the remainder had metastatic disease. Liver resection included right hepatectomy or trisegmentectomy, left or extended left hepatectomy, and sectorectomy/segmentectomy in 77% (n=20), 8% (n=2), and 15% (n=4) of patients, respectively. The mean length of stay was 8.3 days (range, 3–33 days) and there were no grade IV morbidities or 90-day mortalities. The incidence of post hepatectomy liver failure (PHLF) was 3.8% (n=1). The median time to progression after resection was 4.5 months (range, 3.3–10 months). Twenty-three percent (n=6) of patients had no recurrence. The median survival was 28.9 months (range, 16.9–46.8 months) from major hepatectomy and 37.6 months (range, 25.2–53.1 months) from TARE.ConclusionsMajor hepatectomy after neoadjuvant lobar radioembolization is safe with a low incidence of PHLF.     

Detection of numerical chromosomal abnormalities in neoplastic hematopoietic cells by in situ hybridization with a chromosome-specific probe.

The feasibility of using molecular hybridization techniques for the detection of malignant clones that contain numerical chromosomal abnormalities was tested in clinical specimens from patients who had hematologic malignancies. A biotinylated DNA probe specific for chromosome 9 was used for in situ hybridization to interphase and terminally differentiated cells, and fluoresceinated avidin or avidin followed by biotinylated alkaline phosphatase was used for probe detection. In a blinded analysis of ten clinical samples from patients with hematologic malignancies and cytogenetically documented monosomy 9 or trisomy 9, the abnormality was identified correctly in each of five cases of monosomy 9 and five cases of trisomy 9. In two cases of trisomy 9, the detection of this numerical chromosomal abnormality in nuclei of segmented neutrophils permitted the deduction that some granulocytic cells were derived from the abnormal clone, but were still capable of terminal differentiation. Analysis of the position of the probe signal in such nuclei did not disclose any ordered localization of the chromosome 9 homologues with respect to segmentation. These results demonstrate that interphase cytogenetic analysis is feasible in peripheral blood and bone marrow specimens, and that this technique may be a useful adjunct to conventional cytogenetic analysis for the clinical management of patients with hematopoietic malignancies.     

Deletions of interferon genes in acute lymphoblastic leukemia

Structural rearrangements involving the short arm of chromosome 9, including bands 9p21 and 22, are found in the leukemia cells of 7 to 13 percent of patients with acute lymphoblastic leukemia. The interferon-alpha gene cluster and the interferon-beta 1 gene have been localized to this chromosomal region. We have previously demonstrated deletions of these genes in several cell lines established in vitro from patients with lymphoblastic leukemia. We report here homozygous or hemizygous deletions of the interferon-alpha and interferon-beta 1 genes in samples of leukemia cells from patients with lymphoblastic leukemia. Of 62 patients examined, 18 (29 percent) had such deletions. Four patients (7 percent) had homozygous deletions of the interferon-alpha gene cluster; of these, one also had a homozygous deletion and three had hemizygous deletions of the interferon-beta 1 gene. Fourteen patients (23 percent) had hemizygous deletions of both the interferon-alpha gene cluster and the interferon-beta 1 gene. In 8 of the 18 patients with deletions, the deletions of interferon genes were submicroscopic; in the 11 other patients, chromosomal rearrangements of 9p, including translocations or deletions, were visible on light microscopy. These chromosomal and molecular deletions are likely to be related to the loss of a tumor-suppressor gene (or genes) located on 9p, which may be an interferon gene or an unrelated but closely linked gene.     

Estimate of Burden and Direct Healthcare Cost of Infectious Waterborne Disease in the United States

Provision of safe drinking water in the United States is a great public health achievement. However, new waterborne disease challenges have emerged (e.g., aging infrastructure, chlorine-tolerant and biofilm-related pathogens, increased recreational water use). Comprehensive estimates of the health burden for all water exposure routes (ingestion, contact, inhalation) and sources (drinking, recreational, environmental) are needed. We estimated total illnesses, emergency department (ED) visits, hospitalizations, deaths, and direct healthcare costs for 17 waterborne infectious diseases. About 7.15 million waterborne illnesses occur annually (95% credible interval [CrI] 3.88 million–12.0 million), results in 601,000 ED visits (95% CrI 364,000–866,000), 118,000 hospitalizations (95% CrI 86,800–150,000), and 6,630 deaths (95% CrI 4,520–8,870) and incurring US $3.33 billion (95% CrI 1.37 billion–8.77 billion) in direct healthcare costs. Otitis externa and norovirus infection were the most common illnesses. Most hospitalizations and deaths were caused by biofilm-associated pathogens (nontuberculous mycobacteria, Pseudomonas, Legionella), costing US $2.39 billion annually.     

Predictors of chronic pain after laparoscopic inguinal hernia repair

BackgroundMultiple studies have analyzed predictors for chronic pain after open hernia repair. The purpose of this study is to determine which factors predict the development of chronic pain after a laparoscopic inguinal hernia repair.MethodsWe identified patients who underwent laparoscopic inguinal hernia repair between 2008 and 2020 at a single institution. Quality of life was measured using the Surgical Outcomes Measurement System and Carolinas Comfort Scale. We categorized patients with chronic pain if their score on Carolinas Comfort Scale was greater than or equal to 3. Multivariable logistic regression analysis was used to identify predictors of chronic pain.ResultsA total of 960 patients met inclusion criteria. Mean age was 59 (± 14, standard deviation) years, 89 (9.3%) of whom were female. Six percent of patients met criteria for chronic pain (Carolinas Comfort Scale ≥3). On multivariable analysis, predictors for chronic pain were age 45 (P < .001), female sex (P = .006), preoperative pain visual analog scale ≥1 (P = .025), prior inguinal hernia repair (P = .045), higher American Society of Anesthesiologists class (P = .041), use of multifilament polyester mesh (P = .0448), and intraoperative placement of a urinary catheter (P = .009).ConclusionLaparoscopic inguinal hernia repair results in 6.0% of patients experiencing chronic pain. We identified multiple predictors for chronic pain.     

Cholesterol-lowering effect of continuous enteral nutrition in man

We have studied the effect of polymeric cholesterol-free enteral nutrition (EN) on serum lipid and apolipoprotein levels in 30 consecutive non-diabetic, non-hyperlipaemic gastrointestinal patients. EN-40 +/- (SEM) 2 kcal/kg/day including 35% vegetable lipids (50% highly polyunsaturated fat, 50% medium chain triglycerides)-was delivered continuously (24h) via the gastric route for at least 2 weeks (mean duration: 35 +/- 4 days). In the entire group, serum total cholesterol decreased by 10.5% (p < 0.01) on day 7 and 17.5% (p < 0.01) on day 28 (n = 12); this was accompanied by 21% and 20% decreases in LDL-cholesterol and apolipoprotein B (p < 0.05) levels respectively, on day 28. In the 19 patients who were normocholesterolaemic on day 0, serum total cholesterol decreased by 15% (p < 0.01) on day 7 and by 28% (p < 0.05) on day 28 (n = 7). Conversely, in the other 11 patients with a low (<3.7 mmol/L) pre-EN serum total cholesterol level, no significant changes were observed during EN. We conclude that continuous, cholesterol-free EN has, in normocholesterolaemic patients, a marked cholesterol-lowering effect; the respective role of the composition of the diet and the continuous delivery of nutrient within the gut have yet to be investigated.     

Histoenzymatic and permeability changes in human brain adjacent to meningioma.

Cerebral specimens were removed from ten patients with meningioma. Vascular permeability was tested with sodium fluorescein and a correlative study of the oxidative and hydrolytic enzyme activity was performed. Vascular permeability change was observed in half of the specimens of cortex taken from the region of the tumor. Labeled tracer diffusion was found to be either perivascular or involved microscopic ischemic areas. Fluorescein diffusion of the edematous white matter was observed in only two specimens. Enzyme activity in walls of the blood vessels was modified in the fluorescent specimens. Alkaline phosphatase and oxidoreductase activities were decreased. Experimental results have shown a relationship between increased vascular permeability and metabolic disorder of both vascular walls and cerebral cortex. Our findings agree with Zülch's hypothesis regarding a "hemodynamic" mechanism in the formation of edema by extraneural compression.