Natalia Khalaf

Coffee and Caffeine Are Associated With Decreased Risk of Advanced Hepatic Fibrosis Among Patients With Hepatitis C

BACKGROUND & AIMS Coffee or caffeine has been proposed to protect against hepatic fibrosis, but few data are available on their effects in patients with chronic hepatitis C virus (HCV) infection. METHODS We conducted a cross-sectional study of veterans with chronic HCV infection to evaluate the association between daily intake of caffeinated and decaffeinated coffee, tea, and soda, and level of hepatic fibrosis, based on the FibroSURE test (BioPredictive, Paris, France) (F0-F3, mild [controls] vs. F3/F4-F4, advanced). Models were adjusted for multiple potential confounders including age, alcohol abuse, and obesity. RESULTS Among 910 patients with chronic HCV infection, 98% were male and 38% had advanced hepatic fibrosis. Daily intake of caffeinated coffee was higher among controls than patients with advanced fibrosis (1.37 vs. 1.05 cups/d; P = .038). In contrast, daily intake of caffeinated tea (0.61 vs. 0.56 cups/d; P = .651) or soda (1.14 vs. 0.95 cans/d; P = .106) did not differ between the groups. A higher percentage of controls (66.0%) than patients with advanced fibrosis (57.9%) consumed 100 mg or more of caffeine daily from all sources (P = .014); controls also received a larger proportion of their caffeine from coffee (50.2% vs. 43.0%; P = .035). Hepatoprotective effects of an average daily intake of 100 mg or more of caffeine (adjusted odds ratio, 0.71; 95% confidence interval, 0.53-0.95; P = .020) and 1 cup or more of caffeinated tea by non-coffee drinkers (adjusted odds ratio, 0.56; 95% confidence interval, 0.34-0.94; P = .028) persisted after adjustment for confounders, including insulin resistance. CONCLUSIONS A modest daily caffeine intake (as little as 100 mg) may protect against advanced hepatic fibrosis in men with chronic HCV infection. Additional research is needed to confirm these findings in women and in people with other chronic liver diseases.

Statin Use Is Associated With a Decreased Risk of Barrett’s Esophagus

BACKGROUND & AIMS Statins have been associated with a reduced risk of esophageal adenocarcinoma, but little is known about their effect on development of Barretts esophagus. We evaluated the association between statins and risk of Barretts esophagus. METHODS We conducted a case-control study among eligible patients scheduled for elective esophagogastroduodenoscopy and patients eligible for screening colonoscopy, recruited from primary care clinics at a Veterans Affairs center. We compared 303 patients with Barretts esophagus with 2 separate sex-matched control groups: 606 elective endoscopy controls and 303 primary care controls without Barretts esophagus. Use of statins and other lipid-lowering medications was ascertained by reviewing filled prescriptions in electronic pharmacy records during a 10-year period before the Barretts esophagus diagnosis date for patients and study endoscopy date for controls. We calculated odds ratios (OR) and 95% confidence intervals (CI) using conditional multivariable logistic-regression models among 276 patients and 828 controls further matched on age. RESULTS A smaller proportion of Barretts esophagus patients filled statin prescriptions (57.4%) than endoscopy controls (64.9%; P = .029) or primary care controls (71.3%; P < .001). Controls had longer durations of statin prescriptions filled than patients (28.6 vs 22.1 months; P = .001). Statin use was associated with a significantly lower risk of Barretts esophagus (adjusted OR = 0.57; 95% CI: 0.38-0.87) compared with the combined control groups. The risk of Barretts esophagus was especially lower with statin use among obese patients (OR = 0.26; 95% CI: 0.09-0.71), as was the risk for Barretts esophagus segments ≥ 3 cm (OR = 0.13; 95% CI: 0.06-0.30). We found no significant association between Barretts esophagus and nonstatin lipid-lowering medications (P = .452). CONCLUSIONS In a case-control study of veterans, statin use was associated with a reduced risk of Barretts esophagus. The greatest level of risk reduction was observed for obese patients and for long-segment Barretts esophagus.

Natural History of Untreated Hepatocellular Carcinoma in a US Cohort and the Role of Cancer Surveillance

BACKGROUND & AIMS: Determining the natural history and predictors of survival in patients with untreated hepatocellular carcinoma (HCC) in the United States is useful to test existing tumor classifications, identify subgroups of patients likely to benefit from treatment, and estimate lead time related to HCC surveillance. METHODS: We identified a national cohort of 518 veterans diagnosed with HCC from 2004 through 2011, with follow‐up ending in 2014, who received no palliative or curative treatment. We examined the association between postdiagnosis survival and patient factors, tumor characteristics, and prediagnosis surveillance. RESULTS: The mean age at HCC diagnosis was 65.7 years and most patients had hepatitis C (60.6%). Almost all patients (99%) died within the observation period; the median overall survival time was 3.6 months and survival times were 13.4, 9.5, 3.4, and 1.6 months for patients of Barcelona Clinic Liver Cancer stages 0/A, B, C, and D, respectively. In addition, model for end‐stage liver disease and levels of &agr;‐fetoprotein were predictive of survival. Nearly 28% received prediagnosis HCC surveillance, which was associated with detection of disease at an earlier stage (Barcelona Clinic Liver Cancer 0/A/B; 26.4% vs 14.4%; P = .0006) and slightly longer survival than patients with no surveillance overall (5.2 months vs 3.4 months; P = .021); there was no difference in survival times of patients with 0/A stage who did versus did not receive surveillance (10.3 months vs 10.5 months). CONCLUSIONS: Patients with HCCs, including those detected through surveillance, survived for short time periods in the absence of treatment, irrespective of their initial stage at diagnosis. Model for end‐stage liver disease scores and levels of &agr;‐fetoprotein were prognostic factors, independent of Barcelona Clinic Liver Cancer stage. The lead time related to detection by surveillance was modest (<2 months) and therefore unlikely to explain the survival benefit associated with surveillance in previous studies.

Nonsteroidal Anti-inflammatory Drugs and the Risk of Barrett's Esophagus

BACKGROUND & AIMS Nonsteroidal anti-inflammatory drugs (NSAIDs) have been suggested to protect against esophageal adenocarcinoma (EAC). This study examined the effect of NSAIDs on the risk of developing Barretts esophagus (BE), the precursor lesion to EAC. METHODS We conducted a case-control study among eligible patients scheduled for either elective esophagogastroduodenoscopy (EGD) or recruited from primary care clinics to undergo a study EGD. We compared 323 patients with BE (296 nondysplastic and 27 dysplastic) with 2 separate control groups: 1347 patients from the elective EGD group (endoscopy controls) and 502 patients from the primary care group (primary care controls) with no endoscopic or histopathologic BE. Use of aspirin products and 23 nonaspirin NSAIDs was ascertained from detailed, self-reported questionnaires. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariable logistic regression models. RESULTS There were no significant differences in self-reported NSAID use between all BE cases and all controls (58.2% vs 54.6%; P = .33); this was seen for aspirin products (43.0% vs 37.4%; P = .08) and nonaspirin NSAIDs (7.7% vs 8.9%; P = .46). These findings persisted in the multivariable model for any NSAIDs (adjusted OR, 0.89; 95% CI, 0.75-1.28), aspirin (adjusted OR, 1.16; 95% CI, 0.90-1.51), and nonaspirin NSAIDs (adjusted OR, 0.88; 95% CI, 0.55-1.39). Use of a combination of aspirin and nonaspirin NSAIDs was reported in 7.4% of cases and 8.3% of controls, and a nonsignificant inverse association with BE was seen (adjusted OR, 0.70; 95% CI, 0.44-1.11). There was no significant association between BE and daily NSAID use (adjusted OR, 1.03; 95% CI, 0.78-1.37). Similar findings were observed for comparisons involving nondysplastic or dysplastic BE cases, and endoscopy or primary care control groups separately or combined. CONCLUSIONS The use of NSAIDs was not associated with a reduced risk of BE. It is likely that the protective mechanism of NSAIDs on EAC occurs subsequent to the development of BE.

Churg-Strauss Syndrome: An Uncommon Cause of Intracerebral Hemorrhage

A58-year-oldmanwithasthma, chronic sinusitis, andnasal polyposis presented with a 1-day history of headache, blurry vision, and vomiting. His blood pressure was 170/88mmHg. Neurological examinationwas significant for right homonymous hemianopsia. Initial laboratory resultswere remarkable for peripheral bloodeosinophilia (25%; normal, 0%-8.5%). A computed tomographic scan of theheadshowedan intracranialhemorrhage in the leftoccipital lobe (Figure1A).Emergentevacuationof the intracranialhemorrhagewas performed, and brain tissue was sent for routine biopsy. On postoperativeday2, hedevelopedcoughand shortness of breath.Oxygen saturation was 90%. A general examination revealed coarse crackles bilaterally on chest auscultation. Diffuse alveolar hemorrhage was noted on a computed tomographic scan of the chest (Figure 1B).Hewas intubated for respiratory failure. Furtherworkup revealed an elevated myeloperoxidase–antineutrophil cytoplasmic antibody (>1000EU; normal, 0-21 EU). Brain tissue pathologic study results showed an intense eosinophilic vasculitis (Figure 2A andB).AdiagnosisofChurg-StraussSyndrome(CSS)wasmade.The patientreceivedpulsecyclophosphamide infusionanda5-daycourse of pulse intravenous methylprednisone (1000 mg/d). His respiratory parameters improved, and he was weaned off the ventilator. Hewasdischargedandprescribedoral prednisoneandmonthly cyclophosphamide infusions. Brain magnetic resonance imaging (Figure 2C) obtained 6weeks later showed a small residual left occipital hematoma,withnoevidenceof chronic ischemic sequelaeor microhemorrhages. At the 3-month follow-up, the patient’s neuro-

Intragastric Balloon in the Emergency Department: An Unusual Cause of Gastric Outlet Obstruction

BACKGROUND Obesity has become a worldwide epidemic and is associated with significant morbidity and mortality. Many strategies to promote weight loss, including medications and surgical techniques, have been developed; however, few have proven effective. As the rates of obesity and associated complications continue to climb, there is growing pressure on the medical community to develop less invasive procedures that can provide lasting weight loss results. OBJECTIVES One surgical treatment for obesity, available in several countries but not yet approved for use in the United States, is the intragastric balloon (IGB). The IGB is a temporary, space-occupying device placed endoscopically into the stomach to decrease gastric volume and provide a sense of early satiety. Our objective is to highlight potential complications of this device that emergency physicians should be familiar with, in particular, gastric outlet obstruction. CASE REPORT We report the case of a morbidly obese 63-year-old Middle Eastern man who presented to an emergency department in Texas with mechanical gastric outlet obstruction 2 months after IGB placement. After three endoscopic attempts, the balloon was successfully removed and the obstruction relieved. CONCLUSION With an increasingly mobile and obese global population, emergency physicians should be aware of weight loss procedures such as the IGB and appropriate time-sensitive management of high-risk complications.

Personal and family history of cancer and the risk of Barrett's esophagus in men

The association between Barretts esophagus (BE) and a personal or family history of cancer other than gastroesophageal remains unknown. To evaluate the effect of personal and family history of certain cancers and cancer treatments on the risk of BE, we analyzed data from a Veterans Affairs case-control study that included 264 men with definitive BE (cases) and 1486 men without BE (controls). Patients with history of esophageal or gastric cancer were excluded. Patients underwent elective esophagogastroduodenoscopy or a study esophagogastroduodenoscopy concurrently with screening colonoscopy to determine BE status. Personal and family history of several types of cancer was obtained from self-reported questionnaires, supplemented and verified by electronic medical-record reviews. We estimated the association between personal and family history of cancer or radiation/chemotherapy, and BE. Personal history of oropharyngeal cancer (1.5% vs. 0.4%) or prostate cancer (7.2% vs. 4.4%) was more frequently present in cases than controls. The association between BE and prostate cancer persisted in multivariable analyses (adjusted odds ratio 1.90; 95% confidence interval 1.07-3.38, P = 0.028) while that with oropharyngeal cancer (adjusted odds ratio 3.63; 95% confidence interval 0.92-14.29, P = 0.066) was attenuated after adjusting for retained covariates of age, race, gastroesophageal reflux disease, hiatal hernia, and proton pump inhibitor use. Within the subset of patients with cancer, prior treatment with radiation or chemotherapy was not associated with BE. There were no significant differences between cases and controls in the proportions of subjects with several specific malignancies in first- or second-degree relatives. In conclusion, the risk of BE in men may be elevated with prior personal history of oropharyngeal or prostate cancer. However, prior cancer treatments and family history of cancer were not associated with increased risk of BE. Further studies are needed to elucidate if there is a causative relationship or shared risk factors between prostate cancer and BE.