Racial disparities in patient survival after liver transplantation in the United States

Background. Racial disparities in healthcare span such areas as access, outcomes after procedures, and patient satisfaction. Previous work suggested that minorities experience less healthcare and worse survival rates. In adult orthotopic liver transplantation (OLT) mixed results have been reported, with some showing African-American recipients having poor survival compared to Caucasians, and others finding no such discrepancy. ^ Purpose. This study’s purpose was to analyze the most recent United Network for Organ Sharing (UNOS) data, both before and after the implementation of the Model for End-Stage Liver Disease (MELD)/Pediatric End-Stage Liver Disease (PELD) scoring system, to determine if minority racial groups still experience poor outcomes after OLT. ^ Methods. The UNOS dataset for 1992-2001 (Era I) and 2002-2007 (Era II) was used. Patient survival rates for each Era and for adult and pediatric recipients were analyzed with adjustment. A separate multivariate analysis was performed on African-American adult patients in Era II in order to identify unique predictors for poor patient survival. ^ Results. The overall study included 66,118 OLT recipients. The majority were Caucasian (78%), followed by Hispanics (13%) and African-Americans (9%). Hispanic and African-American adults were more likely to be female, have Hepatitis C, to be in the intensive care unit (ICU) or ventilated at time of OLT, to have a MELD score ≥23, to have a lower education level, and to have public insurance when compared to Caucasian adults (all p-values < 0.05). Hispanic and African-American pediatric recipients were more likely have public insurance and less likely to receive a living donor OLT than were Caucasian pediatric OLT recipients (p <0.05). There was no difference in the likelihood of having a PELD score ≥21 among racial groups (p >0.40). African-American adults in Era I and Era II had worse patient survival rates than both Caucasians and Hispanic (pair-wise p-values <0.05). This same disparity was seen for pediatric recipients in Era I, but not in Era II. Multivariate analysis of African-American recipients revealed no unique predictors of patient death. ^ Conclusions. African-American race is still a predictor of poor outcome after adult OLT, even after adjustment for multiple clinical, demographic, and liver disease severity variables. Although African-American and Hispanic subgroups share many characteristics previously thought to increase risk of post-OLT death, only African-American patients have poor survival rates when compared to Caucasians. ^

A case comparison study of dietary factors and risk of colorectal polyps

Little is known about the etiology of colorectal adenomatous polyps, although they are generally considered to be precursor lesions to colorectal carcinoma. To investigate the associations of colorectal adenomatous polyps with dietary intake of calcium, total fat and fiber, a case comparison study was conducted among 98 persons who had first occurrences of adenomatous polyps and 408 persons who did not have colorectal polyps.^ The study population comprised Black, White and Hispanic males and females ages 35 to 80 inclusive, who underwent a sigmoidoscopy or total colonoscopy at collaborating clinics in the Texas Medical Center at Houston between September 1991 and November 1992, and met the eligibility criteria. Case participants were those who had a first-time diagnosis of adenomatous polyps. Comparison participants were individuals who underwent the same diagnostic procedure as the cases and met the same eligibility criteria but had no colorectal polyps. A food frequency questionnaire was administered by interview to obtain information about diet during the 28 days preceding the interview.^ Dietary intake of total fiber was inversely associated with risk of adenomatous polyps. An increment of 15 gm/day in energy-adjusted intake of fiber was associated with a relative odds of 0.39 with a 95% confidence interval of 0.20 to 0.79, after adjustment for age, sex, ethnicity, body mass index, cigarette smoking, family history of colorectal cancer and intake of nonsteroidal anti-inflammatory drugs. No association between dietary intake of total fat and risk of adenomatous polyps was observed. When total fat was analyzed as percent of energy, an increment of 15.3% in intake was associated with a relative odds of 0.98 with a 95% confidence interval of 0.53 to 1.80. However, few persons in the study group had intakes below 25% of energy from total fat. An inverse association was observed between energy-adjusted intake of dietary calcium and risk of adenomatous polyps, but this was not statistically significant; an increment of 638 mg/day was associated with a relative odds of 0.77 with a 95% confidence interval of 0.41 to 1.38. Intake of calcium did not appear to strongly modify the association between intake of fat and risk of adenomatous polyps, perhaps because the study group included few people with calcium intake below 400 mg/day.^ These results support the idea that dietary fiber decreases risk of adenomatous polyps. Further studies are needed on the association of dietary calcium and fat with risk of colorectal adenomatous polyps in populations where individuals vary widely in intake of these nutrients. ^

TRPV1 Channels Contribute to Behavioral Hypersensitivity and Spontaneous Activity in Nociceptors After Spinal Cord Injury

A majority of persons who have sustained spinal cord injury (SCI) develop chronic pain. While most investigators have assumed that the critical mechanisms underlying neuropathic pain after SCI are restricted to the central nervous system (CNS), recent studies showed that contusive SCI results in a large increase in spontaneous activity in primary nociceptors, which is correlated significantly with mechanical allodynia and thermal hyperalgesia. Upregulation of ion channel transient receptor vanilloid 1 (TRPV1) has been observed in the dorsal horn of the spinal cord after SCI, and reduction of SCI-induced hyperalgesia by a TRPV1 antagonist has been claimed. However, the possibility that SCI enhances TRPV1 expression and function in nociceptors has not been tested. I produced contusive SCI at thoracic level T10 in adult, male rats and harvested lumbar (L4/L5) dorsal root ganglia (DRG) from sham-treated and SCI rats 3 days and 1 month after injury, as well as from age-matched naive control rats. Whole-cell patch clamp recordings were made from small (soma diameter <30 >μm) DRG neurons 18 hours after dissociation. Capsaicin-induced currents were significantly increased 1 month, but not 3 days, after SCI compared to neurons from control animals. In addition, Ca2+ transients imaged during capsaicin application were significantly greater 1 month after SCI. Western blot experiments indicated that expression of TRPV1 protein in DRG is also increased 1 month after SCI. A major role for TRPV1 channels in pain-related behavior was indicated by the ability of a specific TRPV1 antagonist, AMG9810, to reverse SCI-induced hypersensitivity of hindlimb withdrawal responses to heat and mechanical stimuli. Similar reversal of behavioral hypersensitivity was induced by intrathecal delivery of oligodeoxynucleotides antisense to TRPV1, which knocked down TRPV1 protein and reduced capsaicin-evoked currents. TRPV1 knockdown also decreased the incidence of spontaneous activity in dissociated nociceptors after SCI. Limited activation of TRPV1 was found to induce prolonged repetitive firing without accommodation or desensitization, and this effect was enhanced by SCI. These data suggest that SCI enhances TRPV1 expression and function in primary nociceptors, increasing the excitability and spontaneous activity of these neurons, thus contributing to chronic pain after SCI.