An Unexpected Lymphoma: A Rare Case of Primary Gastric Burkitt's Lymphoma.

Primary gastric Burkitt's lymphoma is an aggressive non-Hodgkin's lymphoma that has been rarely reported in the literature. The majority of primary gastric lymphomas are diffuse large B-cell lymphomas and mucosa-associated lymphoid tissue (MALT) lymphomas. Patients with primary gastric Burkitt's lymphoma can present with abdominal pain, hematemesis, melena, perforation, and obstruction. Diagnosis is made with a combination of clinical, radiological, and pathological findings. Treatment data are limited due to the limited cases reported. We present a case of a 47-year-old female who presented with diffuse abdominal pain, melena, and coffee-ground emesis that was diagnosed with primary gastric Burkitt's lymphoma following biopsies taken from a gastric ulcerated mass found on upper endoscopy.

Sex, age, and regional differences in L-type calcium current are important determinants of arrhythmia phenotype in rabbit hearts with drug-induced long QT type 2.

In congenital and acquired long QT type 2, women are more vulnerable than men to torsade de pointes. In prepubertal rabbits (and children), the arrhythmia phenotype is reversed; however, females still have longer action potential durations than males. Thus, sex differences in K(+) channels and action potential durations alone cannot account for sex-dependent arrhythmia phenotypes. The L-type calcium current (I(Ca,L)) is another determinant of action potential duration, Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointes. Therefore, sex, age, and regional differences in I(Ca,L) density and in EAD susceptibility were analyzed in epicardial left ventricular myocytes isolated from the apex and base of prepubertal and adult rabbit hearts. In prepubertal rabbits, peak I(Ca,L) at the base was 22% higher in males than females (6.4+/-0.5 versus 5.0+/-0.2 pA/pF; P<0.03) and higher than at the apex (6.4+/-0.5 versus 5.0+/-0.3 pA/pF; P<0.02). Sex differences were reversed in adults: I(Ca,L) at the base was 32% higher in females than males (9.5+/-0.7 versus 6.4+/-0.6 pA/pF; P<0.002) and 28% higher than the apex (9.5+/-0.7 versus 6.9+/-0.5 pA/pF; P<0.01). Apex-base differences in I(Ca,L) were not significant in adult male and prepubertal female hearts. Western blot analysis showed that Ca(v)1.2alpha levels varied with sex, maturity, and apex-base, with differences similar to variations in I(Ca,L); optical mapping revealed that the earliest EADs fired at the base. Single myocyte experiments and Luo-Rudy simulations concur that I(Ca,L) elevation promotes EADs and is an important determinant of long QT type 2 arrhythmia phenotype, most likely by reducing repolarization reserve and by enhancing Ca(2+) overload and the propensity for I(Ca,L) reactivation.

Mutation in glycerol-3-phosphate dehydrogenase 1 like gene (GPD1-L) decreases cardiac Na+ current and causes inherited arrhythmias.

BACKGROUND: Brugada syndrome is a rare, autosomal-dominant, male-predominant form of idiopathic ventricular fibrillation characterized by a right bundle-branch block and ST elevation in the right precordial leads of the surface ECG. Mutations in the cardiac Na+ channel SCN5A on chromosome 3p21 cause approximately 20% of the cases of Brugada syndrome; most mutations decrease inward Na+ current, some by preventing trafficking of the channels to the surface membrane. We previously used positional cloning to identify a new locus on chromosome 3p24 in a large family with Brugada syndrome and excluded SCN5A as a candidate gene. METHODS AND RESULTS: We used direct sequencing to identify a mutation (A280V) in a conserved amino acid of the glycerol-3-phosphate dehydrogenase 1-like (GPD1-L) gene. The mutation was present in all affected individuals and absent in >500 control subjects. GPD1-L RNA and protein are abundant in the heart. Compared with wild-type GPD1-L, coexpression of A280V GPD1-L with SCN5A in HEK cells reduced inward Na+ currents by approximately 50% (P<0.005). Wild-type GPD1-L localized near the cell surface to a greater extent than A280V GPD1-L. Coexpression of A280V GPD1-L with SCN5A reduced SCN5A cell surface expression by 31+/-5% (P=0.01). CONCLUSIONS: GPD1-L is a novel gene that may affect trafficking of the cardiac Na+ channel to the cell surface. A GPD1-L mutation decreases SCN5A surface membrane expression, reduces inward Na+ current, and causes Brugada syndrome.

Genetics of acquired long QT syndrome.

The QT interval is the electrocardiographic manifestation of ventricular repolarization, is variable under physiologic conditions, and is measurably prolonged by many drugs. Rarely, however, individuals with normal base-line intervals may display exaggerated QT interval prolongation, and the potentially fatal polymorphic ventricular tachycardia torsade de pointes, with drugs or other environmental stressors such as heart block or heart failure. This review summarizes the molecular and cellular mechanisms underlying this acquired or drug-induced form of long QT syndrome, describes approaches to the analysis of a role for DNA variants in the mediation of individual susceptibility, and proposes that these concepts may be generalizable to common acquired arrhythmias.

A rare case of primary diffuse large B-cell lymphoma of the colon.

The gastrointestinal tract is the most common site in the United States for extra-nodal lymphoma involvement. Primary colorectal involvement is very rare, only accounting for 0.3% of the large intestine cancers. There has been a small increase in the incidence in these high-risk patient populations which include IBD, Celiac disease, H. pylori and other autoimmune diseases. We report a case of 47 years old male with no risk factors, who presented to the hospital with non-specific signs and symptoms. Imaging revealed cecal mass with distended bowel and colonoscopy revealed large mass obstructing the whole lumen of the cecum. The histopathology showed diffuse large B-cell lymphoma and patient underwent hemicolectomy. Chemotherapy was started and the patient improved.

A common SCN5A polymorphism modulates the biophysical effects of an SCN5A mutation.

Our understanding of the genetic basis of disease has expanded with the identification of rare DNA sequence variations ("mutations") that evoke inherited syndromes such as cystic fibrosis, congenital epilepsy, and cardiac arrhythmias. Common sequence variants ("polymorphisms") have also been implicated as risk factors in multiple diseases. Mutations in SCN5A, the cardiac Na(+) channel gene, that cause a reduction in Na(+) current may evoke severe, life-threatening disturbances in cardiac rhythm (i.e., Brugada syndrome), isolated cardiac conduction disease, or combinations of these disorders. Conduction disease is manifest clinically as heart rate slowing (bradycardia), syncope, or "lightheadedness". Recent electrophysiologic studies reveal that mutations in particular families exhibiting cardiac conduction disease cause marked effects on several competing voltage-dependent gating processes, but nonetheless cause a mild "net" reduction in Na(+) current. Here we show that a common SCN5A polymorphism (H558R) in the Na(+) channel I-II interdomain cytoplasmic linker, present in 20% of the population, can mitigate the in vitro effects of a nearby mutation (T512I) on Na(+) channel function. The mutation and the polymorphism were both found in the same allele of a child with isolated conduction disease, suggesting a direct functional association between a polymorphism and a mutation in the same gene.

A sodium channel pore mutation causing Brugada syndrome.

BACKGROUND: Brugada and long QT type 3 syndromes are linked to sodium channel mutations and clinically cause arrhythmias that lead to sudden death. We have identified a novel threonine-to-isoleucine missense mutation at position 353 (T353I) adjacent to the pore-lining region of domain I of the cardiac sodium channel (SCN5A) in a family with Brugada syndrome. Both male and female carriers are symptomatic at young ages, have typical Brugada-type electrocardiogram changes, and have relatively normal corrected QT intervals. OBJECTIVES: To characterize the properties of the newly identified cardiac sodium channel (SCN5A) mutation at the cellular level. RESULTS: Using whole-cell voltage clamp, we found that heterologous expression of SCN5A containing the T353I mutation resulted in 74% +/- 6% less peak macroscopic sodium current when compared with wild-type channels. A construct of the T353I mutant channel fused with green fluorescent protein failed to traffic properly to the sarcolemma, with a large proportion of channels sequestered intracellularly. Overnight exposure to 0.1 mM mexiletine, a Na(+) channel blocking agent, increased T353I channel trafficking to the membrane to near normal levels, but the mutant channels showed a significant late current that was 1.6% +/- 0.2% of peak sodium current at 200 ms, a finding seen with long QT mutations. CONCLUSIONS: The clinical presentation of patients carrying the T353I mutation is that of Brugada syndrome and could be explained by a cardiac Na(+) channel trafficking defect. However, when the defect was ameliorated, the mutated channels had biophysical properties consistent with long QT syndrome. The lack of phenotypic changes associated with the long QT syndrome could be explained by a T353I-induced trafficking defect reducing the number of mutant channels with persistent currents present at the sarcolemma.

Oxidative mediated lipid peroxidation recapitulates proarrhythmic effects on cardiac sodium channels.

Sudden cardiac death attributable to ventricular tachycardia/fibrillation (VF) remains a catastrophic outcome of myocardial ischemia and infarction. At the same time, conventional antagonist drugs targeting ion channels have yielded poor survival benefits. Although pharmacological and genetic models suggest an association between sodium (Na+) channel loss-of-function and sudden cardiac death, molecular mechanisms have not been identified that convincingly link ischemia to Na+ channel dysfunction and ventricular arrhythmias. Because ischemia can evoke the generation of reactive oxygen species, we explored the effect of oxidative stress on Na+ channel function. We show here that oxidative stress reduces Na+ channel availability. Both the general oxidant tert-butyl-hydroperoxide and a specific, highly reactive product of the isoprostane pathway of lipid peroxidation, E2-isoketal, potentiate inactivation of cardiac Na+ channels in human embryonic kidney (HEK)-293 cells and cultured atrial (HL-1) myocytes. Furthermore, E2-isoketals were generated in the epicardial border zone of the canine healing infarct, an arrhythmogenic focus where Na+ channels exhibit similar inactivation defects. In addition, we show synergistic functional effects of flecainide, a proarrhythmic Na+ channel blocker, and oxidative stress. These data suggest Na+ channel dysfunction evoked by lipid peroxidation is a candidate mechanism for ischemia-related conduction abnormalities and arrhythmias.

Quantitation of protein kinase A-mediated trafficking of cardiac sodium channels in living cells.

OBJECTIVE: Na(+) current derived from expression of the principal cardiac Na(+) channel, Na(v)1.5, is increased by activation of protein kinase A (PKA). This effect is blocked by inhibitors of cell membrane recycling, or removal of a cytoplasmic endoplasmic reticulum (ER) retention motif, suggesting that PKA stimulation increases trafficking of cardiac Na(+) channels to the plasma membrane. METHODS: To test this hypothesis, green fluorescent protein (GFP) was fused to Na(v)1.5 (Na(v)1.5-GFP), and the effects of PKA activation were investigated in intact, living cells that stably expressed the fusion protein. Using confocal microscopy, the spatial relationship of GFP-tagged channels relative to the plasma membrane was quantitated using a measurement that could control for variables present during live-cell imaging, and permit an unbiased analysis for all cells in a given field. RESULTS: In the absence of kinase stimulation, intracellular fluorescence representing Na(v)1.5-GFP channels was greatest in the perinuclear area, with additional concentration of channels beneath the cell surface. Activation of PKA promoted trafficking of Na(+) channels from both regions to the plasma membrane. Experimental results using a chemiluminescence-based assay further confirmed that PKA stimulation increased expression of Na(v)1.5 channels at the cell membrane. CONCLUSIONS: Our results provide direct evidence for PKA-mediated trafficking of cardiac Na(+) channels into the plasma membrane in living, mammalian cells, and they support the existence of multiple intracellular storage pools of channel protein that can be mobilized following a physiologic stimulus.

Usefulness of PA32540 in Protecting the Gastric Layer While Providing Secondary Prevention for Coronary Artery Disease.

Aspirin has been the mainstay for secondary prevention of coronary artery disease to decrease early recurrence and severity of recurrent cardiovascular events. However, an increase in gastrointestinal bleeding due to aspirin is preventing many patients from adhering to this daily regimen. PA32540, a combination pill with aspirin and omeprazole, is a newly emerging intervention that has the potential to reinforce patient compliance with the aspirin regimen due to fewer gastrointestinal adverse effects. This systematic review assessed three recent phase 3 clinical trials investigating the safety and efficacy of PA32540. Clinical trials were chosen based on inclusion criteria such as phase 3, randomized, open-label or blinded studies, utilization of enteric-coated aspirin 325 mg dose, and measured GI adverse effects and major adverse cardiac events (MACE) as primary outcomes. Study A, a 6-month phase-3 study by Whellan et al., used two identically designed, randomized, double-blind trials to compare the GI adverse events and MACE after the use of PA32540 to 325mg of enteric coated Aspirin (EC-ASA) in subjects at risk for aspirin-associated gastric ulcers. Results showed fewer upper GI symptoms, decreased size of ulcers, and improved heartburn symptoms in subjects receiving PA32540 compared to EC-ASA. Study B, a 12-month phase-3 study by Hatoum et al., assessed secondary cardiovascular event prevention in a study population that was treated with PA32540 in comparison to a community setting (CS) group that was started on a standard antiplatelet treatment. Results indicated a 28% reduction of CV events in subjects treated with PA32540 compared to the CS group. Study C, a phase-3 open-label study by Goldstein et al., evaluating secondary prevention of cardiovascular/cerebrovascular events with the use of PA32450 for 12 months found that none of the 12-month completers were reported to have new-onset gastric ulcers. In conclusion, PA32540 could be an effective therapy for secondary prevention of coronary artery disease as studies are showing similar efficacy in preventing MACE with reduced GI side effects.

New mechanism contributing to drug-induced arrhythmia: rescue of a misprocessed LQT3 mutant.

BACKGROUND: The cardiac sodium channel (SCN5A) mutation L1825P has been identified in a patient with drug-induced torsade de pointes precipitated by the IKr blocker cisapride. Although L1825P generates late sodium current typical of SCN5A-linked long-QT syndrome (LQT3) in vitro, the patient reported had a normal QT interval before administration of the drug. To address this discrepancy, we tested the hypothesis that this mutant channel is not processed normally. METHODS AND RESULTS: CHO cells transfected with L1825P displayed significantly reduced peak INa (209+/-36 versus 23+/-3 pA/pF, P<0.05). Confocal imaging and cell-counting studies using epitope-tagged constructs demonstrated that cell surface expression of the mutant was only approximately 9% of wild-type. Incubating transfected cells with cisapride partially rescued misprocessing to 30% of wild-type. As a result, "late" sodium current increased with cisapride from 1.2+/-0.11 to 5.04+/-0.77 pA/pF (P<0.05). CONCLUSIONS: L1825P fails to generate QT prolongation because it does not reach the cell surface. Moreover, the data suggest that cisapride caused torsade de pointes not only by blocking IKr but also by rescuing cell surface expression of the mutant channel, further exaggerating the LQT3 phenotype. This not only represents a new mechanism in the drug-induced long-QT syndrome but also strongly supports the concept that variable cell surface expression contributes to clinical variability in the LQT3 phenotype.

Recreating an artificial biological pacemaker: insights from a theoretical model.

BACKGROUND: Normal cardiac rhythm is critically dependent on the sinoatrial (SA) node, the natural biological pacemaker. Although recent studies have focused on the development of "artificial" biological pacemakers using gene transfer, less is known about the functional consequences of such interventions. OBJECTIVE: The purpose of this study was to investigate the electrophysiological consequences of two approaches used to create a biological pacemaker: overexpression of the hyperpolarization-activated cyclic nucleotide gated channel (HCN "pacemaker" channels) and suppression of the inward-rectifier potassium current, I(K1). METHODS: We used a linear multicellular Luo-Rudy (LRd) AP model consisting of 130 ventricular cells connected by resistive gap junctions. To induce automaticity, I(K1) current was reduced or I(f) (HCN) current was introduced in endocardial and midmyocardial (M) cells. RESULTS: Similar to the previously published results for a single LRd model, myocyte I(K1) suppression induced automaticity in the fiber. While introduction of I(f) also resulted in automaticity, the main differences between I(K1) suppression and I(f) expression were (1) a relatively more gradual phase 4 depolarization with HCN expression, (2) stabilization of cycle lengths during I(K1) suppression, but not during HCN expression, and (3) responsiveness to beta-adrenergic stimulation during HCN expression, but not during I(K1) suppression. Upon further investigation, we found that cycle length instability during HCN expression was primarily due to a gradual reduction of intracellular potassium ([K(+)](i)) from its baseline value of 142 mM to 120 mM in 600 beats and subsequent alteration of potassium-dependent ionic currents. A twofold increase in HCN expression also led to a similar behavior. We attribute this decrease in [K(+)](i) to a large I(K1) during phase 4 depolarization. When intracellular [K(+)](i) loss was minimized, cycle lengths stabilized during HCN expression. CONCLUSIONS: Our results help to further understand the electrophysiologic consequences as well as some of the challenges associated with the creation of biological pacemakers using HCN and I(K1) gene transfer strategies.

Hiatus Hernia: A Rare Cause of Acute Pancreatitis.

Hiatal hernia (HH) is the herniation of elements of the abdominal cavity through the esophageal hiatus of the diaphragm. A giant HH with pancreatic prolapse is very rare and its causing pancreatitis is an even more extraordinary condition. We describe a case of a 65-year-old man diagnosed with acute pancreatitis secondary to pancreatic herniation. In these cases, acute pancreatitis may be caused by the diaphragmatic crura impinging upon the pancreas and leading to repetitive trauma as it crosses the hernia; intermittent folding of the main pancreatic duct; ischemia associated with stretching at its vascular pedicle; or total pancreatic incarceration. Asymptomatic hernia may not require any treatment, while multiple studies have supported the recommendation of early elective repair as a safer route in symptomatic patients. In summary, though rare, pancreatic herniation should be considered as a cause of acute pancreatitis. A high index of suspicion for complications is warranted in cases like these.

Erosive Esophagitis in the Obese: The Effect of Ethnicity and Gender on Its Association.

Background. Data examining the association between obesity and erosive esophagitis (ErE) have been inconsistent, with very little known about interracial variation. Goals. To examine the association between obesity and ErE among patients of different ethnic/racial backgrounds. Methods. The study sample included 2251 patients who underwent esophagogastroduodenoscopy (EGD). The effects of body mass index (BMI) on ErE were assessed by gender and in different ethnic groups. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariate logistic regression analysis. Results. The prevalence of ErE was 29.4% (661/2251). Overweight and obese subjects were significantly more likely to have ErE than individuals with a normal BMI, with the highest risk seen in the morbidly obese (OR 6.26; 95% CI 3.82-10.28; p < 0.0001). Normal weight Black patients were less likely to have ErE as compared to Caucasians (OR 0.46; 95% CI 0.27-0.79; p = 0.005), while the odds ratio comparing normal weight Hispanics to normal weight Whites was not statistically significant. No effect modification was seen between BMI and race/ethnicity or BMI and gender. Significant trends were seen in each gender and ethnicity. Conclusions. The effect of BMI on ErE does not appear to vary by race/ethnicity or gender.

Clinical, genetic, and biophysical characterization of SCN5A mutations associated with atrioventricular conduction block.

BACKGROUND: Three distinct cardiac arrhythmia disorders, the long-QT syndrome, Brugada syndrome, and conduction system disease, have been associated with heterozygous mutations in the cardiac voltage-gated sodium channel alpha-subunit gene (SCN5A). We present clinical, genetic, and biophysical features of 2 new SCN5A mutations that result in atrioventricular (AV) conduction block. Methods and Results- SCN5A was used as a candidate gene in 2 children with AV block. Molecular genetic studies revealed G to A transition mutations that resulted in the substitution of serine for glycine (G298S) in the domain I S5-S6 loop and asparagine for aspartic acid (D1595N) within the S3 segment of domain IV. The functional consequences of G298S and D1595N were assessed by whole-cell patch clamp recording of recombinant mutant channels coexpressed with the beta1 subunit in a cultured cell line (tsA201). Both mutations impair fast inactivation but do not exhibit sustained non-inactivating currents. The mutations also reduce sodium current density and enhance slower inactivation components. Action potential simulations predict that this combination of biophysical abnormalities will significantly slow myocardial conduction velocity. CONCLUSIONS: A distinct pattern of biophysical abnormalities not previously observed for any other SCN5A mutant have been recognized in association with AV block. These data provide insight into the distinct clinical phenotypes resulting from mutation of a single ion channel.

Allelic variants in long-QT disease genes in patients with drug-associated torsades de pointes.

BACKGROUND: DNA variants appearing to predispose to drug-associated "acquired" long-QT syndrome (aLQTS) have been reported in congenital long-QT disease genes. However, the incidence of these genetic risk factors has not been systematically evaluated in a large set of patients with aLQTS. We have previously identified functionally important DNA variants in genes encoding K+ channel ancillary subunits in 11% of an aLQTS cohort. METHODS AND RESULTS: The coding regions of the genes encoding the pore-forming channel proteins KvLQT1, HERG, and SCN5A were screened in (1) the same aLQTS cohort (n=92) and (2) controls, drawn from patients tolerating QT-prolonging drugs (n=67) and cross sections of the Middle Tennessee (n=71) and US populations (n=90). The frequency of three common nonsynonymous coding region polymorphisms was no different between aLQTS and control subjects, as follows: 24% versus 19% for H558R (SCN5A), 3% versus 3% for R34C (SCN5A), and 14% versus 14% for K897T (HERG). Missense mutations (absent in controls) were identified in 5 of 92 patients. KvLQT1 and HERG mutations (one each) reduced K+ currents in vitro, consistent with the idea that they augment risk for aLQTS. However, three SCN5A variants did not alter I(Na), which argues that they played no role in the aLQTS phenotype. CONCLUSIONS: DNA variants in the coding regions of congenital long-QT disease genes predisposing to aLQTS can be identified in approximately 10% to 15% of affected subjects, predominantly in genes encoding ancillary subunits.

Inherited sodium channelopathies: a continuum of channel dysfunction.

Voltage-gated sodium channels are transmembrane proteins that produce the ionic current responsible for the rising phase of the cardiac action potential and play a fundamental role in the initiation, propagation, and maintenance of normal cardiac rhythm. Inherited mutations in SCN5A, the gene encoding the pore-forming subunit of the cardiac Na+ channel, have been associated with distinct cardiac rhythm syndromes: the congenital long QT syndrome, Brugada syndrome, and isolated conduction disease. Electrophysiologic characterization of heterologously expressed mutant Na+ channels have revealed gating defects that, in many cases, can explain the distinct phenotype associated with the rhythm disorder. However, recent studies have revealed significant overlap between aberrant rhythm phenotypes, and single mutations have been identified that evoke multiple rhythm disorders with common gating lesions. These new insights enhance understanding of the structure-function relationships of voltage-gated Na+ channels, and also highlight the complexities involved in linking single mutations, ion-channel behavior, and cardiac rhythm.

Establishing the link between hepatitis B virus infection and colorectal adenoma.

BACKGROUND: Chronic hepatitis B (CHB) infection has been associated with malignancy, most notably hepatocellular carcinoma. Previous research has shown that hepatitis C is associated with increased colorectal adenomas and neoplasia. Currently, there are no studies on the association of CHB and colorectal adenomas. We aimed to identify a possible link between CHB and colorectal adenoma. METHODS: A retrospective chart review was performed on 588 consecutive patients undergoing screening or diagnostic colonoscopy that were previously screened or diagnosed with hepatitis B. Comparisons between categorical variables were analyzed with Chi Square test and t-test for continuous variables. Unconditional logistic regression was used to generate age-, gender-and race-adjusted odds ratios and their 95% confidence intervals (CI) comparing medication users with non-users. Statistical analyses were performed with SAS 9.3 software. RESULTS: A total of 487 patients were analyzed in the control group vs. 71 in the hepatitis B group. The adenoma detection rate was 23.9% in hepatitis B vs. 15.9% in the non-hepatitis B group for all cause colonoscopy; however this did not reach statistical significance. There was a significantly higher number of adenomas present in the distal colon compared to control (OR =2.16; 95% CI, 1.06-4.43; P=0.04). There were no significant findings between hepatitis B infection with size, multiplicity or presence of proximal adenomas. There was a significant difference noted in regards to smoking history, BMI and age between two groups. CONCLUSIONS: Although the adenoma detection rate was higher in hepatitis B population vs. the non-hepatitis B group this did not reach statistical significance. However, we did find an association between CHB infection and the presence of distal colorectal adenomas. Larger prospective studies are needed to strengthen our findings along with future studies examining hepatitis B virus (HBV) and mechanisms inducing colorectal carcinogenesis.

Ethnic disparities in the risk of colorectal adenomas associated with lipid levels: a retrospective multiethnic study.

BACKGROUND: Although data exists showing that uncontrolled lipid levels in white and black patients is associated with colorectal adenomas, there are currently no studies looking only at the Hispanic population. PURPOSE: With the rapid increase in the Hispanic population, we aimed to look at their risk of colorectal adenomas in association with lipid levels. METHODS: We retrospectively analyzed 1473 patients undergoing colonoscopy from 2009 to 2011 at a community hospital. Statistical analysis was performed using Chi-squared for categorical variables and t test for continuous variables with age-, gender-, and race-adjusted odds ratios. Unconditional logistic regression model was used to estimate 95 % confidence intervals (CI). SAS 9.3 software was used to perform all statistical analysis. RESULTS: In our general population, there was an association with elevated triglyceride levels greater than 150 and presence of multiple colorectal adenomas with odds ratio (OR) 1.60 (1.03, 2.48). There was an association with proximal colon adenomas and cholesterol levels between 200 and 239 with OR 1.57 (1.07, 2.30), and low-density lipoprotein (LDL) levels of greater than 130 with OR 1.54 (1.04, 2.30). There was no association between high-density lipoproteins (HDL) levels and colorectal adenomas. The Hispanic population showed no statistical correlation between elevated triglycerides, cholesterol, or LDL with the presence, size, location, or multiplicity of colorectal adenomas. CONCLUSIONS: We found a significant correlation between elevated lipid levels and colorectal adenomas in white and black patients; however, there was no such association in the Hispanic population. This finding can possibly be due to environmental factors such as dietary, colonic flora, or genetic susceptibility, which fosters further investigation and research.

Low bone mineral density linked to colorectal adenomas: a cross-sectional study of a racially diverse population.

BACKGROUND: Epidemiologic studies suggest that lower bone mineral density (BMD) is associated with an increased risk for colorectal adenoma/cancer, especially in postmenopausal women. The aim of this study is to investigate the association between osteopenia and/or osteoporosis and colorectal adenomas in patients from a New York community hospital. METHODS: We performed a cross-sectional observational study on 200 patients who underwent screening colonoscopies and bone density scan (dual-energy X-ray absorptiometry) at Nassau University Medical Center from November 2009 to March 2011. Among these, 83 patients were identified as osteoporosis (T score of -2.5 or below) and 67 were osteopenia (T score between -1.0 and -2.5). Logistic regression model was performed to assess the association between osteopenia and/or osteoporosis and colorectal adenomas. RESULTS: Among the patients with osteopenia and osteoporosis, the mean ages were 59.1 years [standard deviation (SD) =8.9] and 61.5 (SD =8.9), respectively. There were 94.0%, 85.1% and 74.7% women, respectively, in normal BMD, osteopenia and osteoporosis groups. The prevalence of colorectal adenomas was 17.9% and 25.3% in the osteopenia and osteoporosis groups, respectively, and 18.0% in the normal BMD group. After adjustment for potential confounders including age, sex, race, body mass index (BMI), tobacco use, alcohol use, history of diabetes, hypertension, or dyslipidemia, osteoporosis was found to be associated with presence of colorectal adenomas more than 2, compared to the normal BMD group. No significant associations were found for the prevalence, size, and location of adenomas. CONCLUSIONS: Our study suggests that osteoporosis is significantly associated with the presence of multiple colorectal adenomas. Prospective studies with a larger sample size are warranted in the future.