Search

Objectives: Cytokines are thought to contribute to the pathogenesis of psychiatric symptoms by kynurenine pathway activation. Kynurenine metabolites affect neurotransmission and can cause neurotoxicity. We measured inflammatory markers in patients with bipolar disorder (BD) and studied their relation to kynurenine metabolites and mood. Methods: Patients with BD suffering from an acute mood episode were assigned to the depressive (n = 35) or (hypo)manic (n = 32) subgroup. Plasma levels of inflammatory markers [cytokines, C‐reactive protein] and kynurenine metabolites [tryptophan (TRP), kynurenine (KYN), 3‐hydroxykynurenine (3‐HK), quinolinic acid (QA), kynurenic acid (KYNA)] were measured on 6 time points during 8 months follow‐up. Biological marker levels in patients were compared to controls (n = 35) and correlated to scores on mood scales. Spearman correlations and linear mixed models were used for statistical analysis. Results: Twenty patients of the manic subgroup, 29 of the depressive subgroup, and 30 controls completed the study. The manic subgroup had a rapid remission of mood symptoms, but in the depressive subgroup subsyndromal symptoms persisted. No differences in inflammation were found between groups. A strong correlation between tumor necrosis factor‐α and KYN, KYN/TRP, 3‐HK and QA (ρ > 0.60) was specific for the manic group, but only at baseline (during mania). The depressive subgroup had a lower neuroprotective ratio (KYNA/3‐HK, P =.0004) and a strong association between interferon‐y and kynurenine pathway activation (P <.0001). KYNA was low in both patient groups versus controls throughout the whole follow‐up (P =.0008). Conclusions: Mania and chronic depressive symptoms in BD are accompanied by a strong interaction between inflammation and a potentially neurotoxic kynurenine metabolism. [ABSTRACT FROM AUTHOR]

Background: In 2015, the World Health Organization recommended that all people living with HIV begin antiretroviral treatment (ART) regardless of immune status, a policy known as 'Treat-All to end AIDS', commonly referred to as Treat-All. Almost all low- and middle-income countries adopted this policy by 2019. This study describes how linkage to treatment of newly diagnosed persons changed between 2015 and 2018 and how complementary policies may have similarly increased linkage for 13 African countries. These countries adopted and implemented Treat-All policies between 2015 and 2018 and were supported by the U.S. Government's President's Emergency Plan for AIDS Relief (PEPFAR). The focuses of this research were to understand 1) linkage rates to ART initiation before and after the adoption of Treat-All in each country; 2) how Treat-All implementation differed across these countries; and 3) whether complementary policies (including same-day treatment initiation, task-shifting, reduced ART visits, and reduced ART pickups) implemented around the same time may have increased ART linkage., Methods: HIV testing and treatment data were collected by PEPFAR country programs in 13 African countries from 2015 to 2018. These countries were chosen based on the completeness of policy data and availability of program data during the study period. Program data were used to calculate proxy linkage rates. These rates were compared relative to the Treat All adoption period and the adoption of complementary policies., Results: The 13 countries experienced an average increase in ART linkage of 29.3% over the entire study period. In examining individual countries, all but two showed increases in linkage to treatment immediately after Treat All adoption. Across all countries, those that had adopted four or more complementary policies showed an average increased linkage of 39.8% compared to 13.9% in countries with fewer than four complementary policies., Conclusions: Eleven of 13 country programs examined in this study demonstrated an increase in ART linkage after Treat-All policy adoption. Increases in linkage were associated with complementary policies. When exploring new public health policies, policymakers may consider which complementary policies might also help achieve the desired outcome of the public health policy., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Introduction: Nodding Syndrome (NS), an unexplained illness characterized by spells of head bobbing, has been reported in Sudan and Tanzania, perhaps as early as 1962. Hypothesized causes include sorghum consumption, measles, and onchocerciasis infection. In 2009, a couple thousand cases were reportedly in Northern Uganda., Methods: In December 2009, we identified cases in Kitgum District. The case definition included persons who were previously developmentally normal who had nodding. Cases, further defined as 5- to 15-years-old with an additional neurological deficit, were matched to village controls to assess risk factors and test biological specimens. Logistic regression models were used to evaluate associations., Results: Surveillance identified 224 cases; most (95%) were 5-15-years-old (range = 2-27). Cases were reported in Uganda since 1997. The overall prevalence was 12 cases per 1,000 (range by parish = 0·6-46). The case-control investigation (n = 49 case/village control pairs) showed no association between NS and previously reported measles; sorghum was consumed by most subjects. Positive onchocerciasis serology [age-adjusted odds ratio (AOR1) = 14·4 (2·7, 78·3)], exposure to munitions [AOR1 = 13·9 (1·4, 135·3)], and consumption of crushed roots [AOR1 = 5·4 (1·3, 22·1)] were more likely in cases. Vitamin B6 deficiency was present in the majority of cases (84%) and controls (75%)., Conclusion: NS appears to be increasing in Uganda since 2000 with 2009 parish prevalence as high as 46 cases per 1,000 5- to 15-year old children. Our results found no supporting evidence for many proposed NS risk factors, revealed association with onchocerciasis, which for the first time was examined with serologic testing, and raised nutritional deficiencies and toxic exposures as possible etiologies.

Background: Nodding syndrome is an unexplained illness characterised by head-bobbing spells. The clinical and epidemiological features are incompletely described, and the explanation for the nodding and the underlying cause of nodding syndrome are unknown. We aimed to describe the clinical and neurological diagnostic features of this illness., Methods: In December, 2009, we did a multifaceted investigation to assess epidemiological and clinical illness features in 13 parishes in Kitgum District, Uganda. We defined a case as a previously healthy child aged 5-15 years with reported nodding and at least one other neurological deficit. Children from a systematic sample of a case-control investigation were enrolled in a clinical case series which included history, physical assessment, and neurological examinations; a subset had electroencephalography (EEG), electromyography, brain MRI, CSF analysis, or a combination of these analyses. We reassessed the available children 8 months later., Findings: We enrolled 23 children (median age 12 years, range 7-15 years) in the case-series investigation, all of whom reported at least daily head nodding. 14 children had reported seizures. Seven (30%) children had gross cognitive impairment, and children with nodding did worse on cognitive tasks than did age-matched controls, with significantly lower scores on tests of short-term recall and attention, semantic fluency and fund of knowledge, and motor praxis. We obtained CSF samples from 16 children, all of which had normal glucose and protein concentrations. EEG of 12 children with nodding syndrome showed disorganised, slow background (n=10), and interictal generalised 2·5-3·0 Hz spike and slow waves (n=10). Two children had nodding episodes during EEG, which showed generalised electrodecrement and paraspinal electromyography dropout consistent with atonic seizures. MRI in four of five children showed generalised cerebral and cerebellar atrophy. Reassessment of 12 children found that six worsened in their clinical condition between the first evaluation and the follow-up evaluation interval, as indicated by more frequent head nodding or seizure episodes, and none had cessation or decrease in frequency of these episodes., Interpretation: Nodding syndrome is an epidemic epilepsy associated with encephalopathy, with head nodding caused by atonic seizures. The natural history, cause, and management of the disorder remain to be determined., Funding: Division of Global Disease Detection and Emergency Response, US Centers for Disease Control and Prevention., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Objective: To evaluate the use of routine laboratory monitoring in terms of clinical outcomes among patients receiving antiretroviral therapy (ART) in Uganda., Design: Randomised clinical trial, Setting: A home based ART programme in rural Uganda., Participants: All participants were people with HIV who were members of the AIDS Support Organisation. Participants had CD4 cell counts <250 cells × 10(6)/L or World Health Organization stage 3 or 4 disease., Interventions: Participants were randomised to one of three different monitoring arms: a viral load arm (clinical monitoring, quarterly CD4 counts, and viral load measurements), CD4 arm (clinical monitoring and CD4 counts), or clinical arm (clinical monitoring alone)., Main Outcome Measures: Serious morbidity (newly diagnosed AIDS defining illness) and mortality., Results: 1094 participants started ART; median CD4 count at baseline was 129 cells × 10(6)/L. Median follow-up was three years. In total, 126 participants died (12%), 148 (14%) experienced new AIDS defining illnesses, and 61(6%) experienced virological failure, defined as two consecutive viral loads >500 copies/mL occurring more than three months after the start of ART. After adjustment for age, sex, baseline CD4 count, viral load, and body mass index, the rate of new AIDS defining events or death was higher in the clinical arm than the viral load arm (adjusted hazard ratio 1.83, P = 0.002) or the CD4 arm (1.49, P = 0.032). There was no significant difference between the CD4 arm and the viral load arm (1.23, P = 0.31)., Conclusion: In patients receiving ART for HIV infection in Uganda, routine laboratory monitoring is associated with improved health and survival compared with clinical monitoring alone. Trial registration Clinical Trials NCT00119093.

Background: Up to 20% of people initiating antiretroviral therapy (ART) in sub-Saharan Africa die during the first year of treatment. Understanding the clinical conditions associated with mortality could potentially lead to effective interventions to prevent these deaths., Methods: We examined data from participants aged ≥18 years in the Home-Based AIDS Care project in Tororo, Uganda, to describe mortality over time and to determine clinical conditions associated with death. Survival analysis was used to examine variables associated with mortality at baseline and during follow-up., Results: A total of 112 (9.4%) deaths occurred in 1132 subjects (73% women) during a median of 3.0 years of ART. Mortality was 15.9 per 100 person-years during the first 3 months and declined to 0.3 per 100 person-years beyond 24 months after ART initiation. Tuberculosis (TB) was the most common condition associated with death (21% of deaths), followed by Candida disease (15%). In 43% of deaths, no specific clinical diagnosis was identified. Deaths within 3 months after ART initiation were associated with World Health Organization clinical stage III or IV at baseline, diagnosis of TB at baseline, a diagnosis of a non-TB opportunistic infection in follow-up and a body mass index ≤17 kg/m² during follow-up. Mortality after 3 months of ART was associated with CD4 cell counts <200 cells per microliter, a diagnosis of TB or other opportunistic infection, adherence to therapy <95%, and low hemoglobin levels during follow-up., Conclusion: Potentially remediable conditions and preventable infections were associated with mortality while receiving ART in Uganda.

Background: The World Health Organization (WHO) recommends the discontinuation of oral poliovirus vaccine after eradication of wild poliovirus. Studies assessing inactivated poliovirus vaccine (IPV) immunogenicity in tropical countries, using the WHO Expanded Programme on Immunization (EPI) schedule, have been limited., Methods: We conducted a randomized clinical trial in Ponce, Puerto Rico. Infants were assigned to 1 of 2 study arms: those in the EPI arm received IPV at 6, 10, and 14 weeks of age, and those in the US arm received IPV at 2, 4, and 6 months of age. Neutralizing antibody titers against poliovirus types 1, 2, and 3 were tested on serum specimens obtained before administration of the first dose of IPV and 28-45 days after administration of the last dose of IPV., Results: Seroconversion rates for the EPI (n=225) and US (n=230) arms, respectively, were 85.8% and 99.6% for poliovirus type 1 (P<.001), 86.2% and 100% for poliovirus type 2 (P<.001), and 96.9% and 99.1% for poliovirus type 3 (P=.08). Seroconversion rates were lower among infants in the EPI arm who had high maternal antibody levels for all 3 poliovirus types (P<.001)., Conclusions: The EPI schedule resulted in lower seroconversion rates for poliovirus types 1 and 2. These results are relevant for tropical countries planning to use IPV in a posteradication environment.

Context: The last case of poliomyelitis in the United States due to indigenously acquired wild poliovirus occurred in 1979; however, as a consequence of oral poliovirus vaccine (OPV) use that began in 1961, an average of 9 cases of vaccine-associated paralytic poliomyelitis (VAPP) were confirmed each year from 1961 through 1989. To reduce the VAPP burden, national vaccination policy changed in 1997 from reliance on OPV to options for a sequential schedule of inactivated poliovirus vaccine (IPV) followed by OPV. In 2000, an exclusive IPV schedule was adopted., Objective: To review the epidemiology of paralytic poliomyelitis and document the association between the vaccine schedule changes and VAPP in the United States., Design and Setting: Review of national surveillance data from 1990 through 2003 for cases of confirmed paralytic poliomyelitis., Main Outcome Measures: Number of confirmed paralytic poliomyelitis cases, including VAPP, and ratio of VAPP cases to number of doses of OPV distributed that occurred before, during, and after implementation of policy changes., Results: From 1990 through 1999, 61 cases of paralytic poliomyelitis were reported; 59 (97%) of these were VAPP (1 case per 2.9 million OPV doses distributed), 1 case was imported, and 1 case was indeterminate. Thirteen cases occurred during the 1997-1999 transitional policy period and were associated with the all-OPV schedule; none occurred with the IPV-OPV schedule. No cases occurred after the United States implemented the all-IPV policy in 2000. The last imported poliomyelitis case occurred in 1993 and the last case of VAPP occurred in 1999., Conclusion: The change in polio vaccination policy from OPV to exclusive use of IPV was successfully implemented; this change led to the elimination of VAPP in the United States.

Setting: Health care workers and medical students in the United States subject to annual tuberculin skin testing., Objective: To use skin testing with Mycobacterium avium sensitin (MAS) to determine contemporary rates of infection with non-tuberculous mycobacteria (NTM) and their effect on reactions to M. tuberculosis purified protein derivative (PPD)., Design: Dual skin testing was performed with PPD and MAS on 784 health care workers and medical students in the northern and southern US. MAS reactions that were > or = 5 mm and also > or = 3 mm larger than the PPD reaction were defined as MAS dominant and due to NTM., Results: MAS reactions were > or = 5 mm in 40% and > or = 15 mm in 18% of subjects; 95% were MAS dominant. MAS dominant reactions were more common in the south than the north (P < 0.001). PPD reactions were > or = 15 mm in 3% of subjects. PPD reactions > or = 15 mm were more common among males, foreign born subjects and subjects with BCG immunization (all P < 0.001). MAS dominant reactions were found in 82% of subjects with 5-9 mm PPD reactions and 50% with 10-14 mm PPD reactions; these reactions were more common among whites (P = 0.046), US-born (P = 0.038) and subjects without BCG immunization (P = 0.004)., Conclusions: Infections with NTM are responsible for the majority of 5-14 mm PPD reactions among US-born health care workers and medical students subject to annual tuberculin testing.

Disseminated Mycobacterium avium complex disease remains a substantial cause of morbidity and mortality among patients with acquired immunodeficiency syndrome. From 1985 through 2000, we studied 1458 consecutive patients at Grady Memorial Hospital, Atlanta, with disseminated M. avium complex disease. There was a peak of 198 patients in the 1995, which decreased to 66 patients in 2000. In 1997, significantly more patients than in 1991 or 1994 were female (P<.001) or black (P<.001) and significantly fewer had acquired human immunodeficiency virus through homosexual contact (P<.001). In 1997, 50 (51%) of 99 of patients acquired M. avium complex disease despite receiving antimicrobial prophylaxis, but 32 (89%) of 36 patients did not adhere to the prophylaxis regimen. The median duration of survival of patients in 1991 was 110 days, whereas in 1994 it was 185 days, and in 1997 it was 339 days (P<.001). Prolonged survival was associated with receiving therapy that included clarithromycin and receiving combination antiretroviral therapy that included a protease inhibitor.

ESAT-6 (for 6-kDa early secreted antigenic target) is a secreted antigen found almost exclusively in organisms of the Mycobacterium tuberculosis complex. We compared in vitro gamma interferon (IFN-gamma) responses by peripheral blood mononuclear cells to this antigen in patients with pulmonary disease due to either Mycobacterium avium complex (MAC) or Mycobacterium tuberculosis with those in healthy, skin test-negative, control subjects. Significant IFN-gamma responses to ESAT-6 were detected in 16 (59%) of 27 M. tuberculosis pulmonary disease patients, 0 (0%) of 8 MAC disease patients, and 0 (0%) of 8 controls. Significant IFN-gamma responses to M. tuberculosis purified protein derivative were detected in 23 (85%) of 27 M. tuberculosis disease patients, 2 (25%) of 8 MAC disease patients, and 5 (63%) of 8 healthy controls. M. avium sensitin was recognized in 24 (89%) of 27 M. tuberculosis disease patients, 4 (50%) of 8 MAC disease patients, and 1 (13%) of 8 controls. IFN-gamma responses to ESAT-6 are specific for disease due to M. tuberculosis and are not observed in patients with MAC disease or in healthy controls.

Background: Although endoscopic evaluation of the gastrointestinal tract is commonly performed to evaluate iron deficiency, little data is available regarding the underlying causes, yield of evaluation, and long-term outcome for those in whom gastrointestinal and systemic symptoms and signs are absent., Methods: In- or out-patients seen by the gastroenterology consultative service at a large inner-city hospital over a 56-month period were considered eligible for the study when iron deficiency (serum ferritin <50 ng/mL) was documented. Exclusion criteria included: any gastrointestinal or systemic symptoms/signs, radiographic or endoscopic examinations of the gastrointestinal tract within 3 and 5 years, respectively, or obvious source of blood loss. Patients underwent colonoscopy and if no lesions other than carcinoma were found, upper endoscopy was then performed with a pediatric colonoscope., Results: Fifty-two patients were evaluated (mean age, 66 +/- 13 years; range, 20 to 89 years; 32 men/20 women). At the time of evaluation, the mean (+/-SD) hematocrit was 25% +/- 7% (range, 14% to 42%). Overall, 23 patients (44%; 95% CI 30% to 59%) had an identifiable gastrointestinal lesion considered the cause of iron deficiency, including: colonic carcinoma, 11 (21%); colonic and/or esophagogastric/duodenal vascular ectasias, 9 (17%); and gastric carcinoma, colonic polyposis, and colonic ulcers in 1 patient each. Long-term follow-up (median 24 months, range 2 to 63 months) identified only 1 patient with a cause found (colonic carcinoma), and in this patient, complete colonoscopy was not technically possible at the time of initial evaluation. There were no clinical or laboratory features that distinguished patients with an etiology for iron deficiency to the idiopathic group., Conclusions: Approximately half of patients with iron deficiency in whom gastrointestinal or systemic signs or symptoms are absent have an underlying gastrointestinal lesion. Nevertheless, despite a thorough endoscopic evaluation, some patients will have no etiology found; the prognosis for these patients is excellent.

To evaluate the association between nonsteroidal antiinflammatory drug (NSAID) use and upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB), we performed a prospective case-control study at a large inner-city hospital over a 28-month period evaluating 461 consecutive patients hospitalized for UGIB and 105 with LGIB. During the same period, 1895 in-patients evaluated by our gastroenterology consultative service served as controls. At the time of initial evaluation, all patients were asked about the use of any prescription or over-the-counter NSAID product within one week of admission. Endoscopic examination was performed in most patients with bleeding. NSAID use was almost equivalent in patients with UGIB and LGIB (60%) and significantly greater than controls [34%; P < 0.001; odds ratio (OR) 3.0; 95% CI, 2.4-3.6]. The age, race, and gender adjusted risk for LGIB associated with NSAID use was significant [adjusted OR (AOR) 2.6; 95% CI 1.7-3.9], although less than UGIB (AOR 3.2; P = 0.34). The risk associated with diverticular bleeding (N = 53, AOR 3.4; 95% CI 1.9-6.2) was higher than duodenal ulcer bleeding although not significantly (N = 97, AOR 3.0). We conclude that NSAID use is strongly associated with LGIB and from lesions not considered associated with mucosal ulceration such as diverticulosis.

Thalidomide appears to be highly effective for oropharyngeal apthous ulcers in HIV-infected patients. However, there are limited data regarding the use of this drug for the treatment of HIV-associated idiopathic esophageal ulcer(s) (IEU). Twelve HIV-infected patients with esophageal symptoms and IEU as defined by previously proposed criteria were studied prospectively. Two of these patients had failed oral corticosteroid treatment, and two others had a previous history of IEU. Patients were treated with thalidomide (200 mg/day orally) for 28 days in an open label fashion. Clinical evaluation was performed weekly with endoscopic reexamination performed at the completion of treatment. After therapy, patients were followed clinically with endoscopy recommended for recurrent esophageal symptoms. Of the 12 treated patients, 11 (92%) had a complete symptomatic response; endoscopy in 11 patients at the completion of treatment showed 9 with complete ulcer healing, 1 partially healed, and 1 with no response. All responders were asymptomatic by day 28. The partial responder received an additional 1 month of thalidomide at 300 mg/day, resulting in complete endoscopic healing. The patient failing therapy received prednisone, but died prior to completing this therapy. On follow-up to 20 months, six patients have died with no recurrence of IEU. Three patients had relapse of IEU, two of whom had a prior history of multiple recurrences of IEU; both of these patients relapsed within 2 months of completing thalidomide treatment. The drug was well tolerated without significant side effects. Thalidomide appears to be an effective and well-tolerated alternative to prednisone for the treatment of IEU.

Background: Although hematochezia is well recognized to occur in patients with upper GI hemorrhage (UGIH), its prevalence, clinical presentation, causes, and outcome in these patients are not well defined., Methods: Consecutive patients evaluated for UGIH by the gastroenterology service at a large inner city hospital from August 1, 1990, through September 31, 1994, were prospectively identified. Vital signs and stool color were recorded on admission to the emergency department. Endoscopy was performed in all patients, usually within 48 h of admission. The cause of bleeding was determined by endoscopy, surgery, or autopsy., Results: Over the 50-month study period, 727 patients with UGIH meeting the inclusion criteria were evaluated, with 104 (14%) presenting with hematochezia (18 with bright red blood and 86 with maroon blood). The most common causes of bleeding were duodenal ulcer (44%) and gastric ulcer (20%). In comparison with patients with melena (N = 441), patients with hematochezia were older (55 vs 50 yr, p < 0.01) and more likely to present with duodenal ulcer bleeding (43 vs 25%, p < 0.01); no differences in vital signs, including prevalence of shock, or admission Hb concentration were found. However, transfusion requirements (5.4 vs 4.0 units, p = 0.01), need for surgery (11.7 vs 5.7%, p = 0.03), and mortality (13.6 vs 7.5%, p = 0.05) were significantly higher in patients with hematochezia than in those with melena, suggesting more severe bleeding and a worse outcome., Conclusions: Hematochezia is common in patients with UGIH, and the presenting features are similar to those of patients with melena. Duodenal ulcer is the most common cause of bleeding associated with hematochezia. Patients with UGIH and hematochezia seem to have a worse prognosis.

Purpose: To determine the etiologies of esophageal symptoms in human immunodeficiency virus (HIV)-infected patients failing antifungal treatment., Methods: Between August 1, 1990 and December 31, 1994, all HIV-infected patients seen at a large inner-city hospital who had esophageal complaints despite being on antifungal therapy were prospectively evaluated for the cause of symptoms. Thus, the population studied included patients given empiric antifungal therapy for esophageal symptoms and patients who developed symptoms while on long-term antifungal therapy. Endoscopy was performed in all patients. The cause of symptoms was determined by the clinical, endoscopic, and pathologic findings, and follow-up after treatment., Results: Over the 53-month study period, 74 patients failing empiric antifungal therapy were identified. The majority (77%) of these patients had esophageal ulcers; 25 patients had idiopathic ulcers and 24 had cytomegalovirus. In 2 patients, Candida was present with other causes of ulcerative esophagitis. Candida esophagitis alone was diagnosed in only 3 patients. No endoscopic abnormalities were observed in 14 patients (19%). An additional 24 patients developed esophageal symptoms while receiving antifungal therapy; endoscopic findings in these patients included ulceration in 16 (67%), Candida esophagitis alone in 2, and normal in 6. Empirically treated patients in whom odynophagia was not the only symptom, those with dysphagia alone, and those with a CD4 count > 100/mm3 were less likely to have an endoscopic diagnosis., Conclusions: Esophageal ulceration is the most common cause of esophageal symptoms in HIV-infected patients failing empiric antifungal therapy and those developing symptoms while receiving antifungal agents. Given these findings, endoscopy should be the test of choice for these nonresponders, rather than escalating the dose of antifungal agent, adding other empiric treatments, or performing barium esophagography.

Objective: To determine prospectively the causes of upper GI hemorrhage (UGIH) in alcoholics, focusing on the prevalence of alcoholic gastropathy, and to compare the etiology of bleeding in patients who drink alcohol to that of nondrinkers., Methods: From August 1, 1990 through September 9, 1994, all patients evaluated by the gastroenterology consultative service at a large inner-city hospital presenting with UGIH were prospectively identified. Patients had to have a subnormal hematocrit on or within 12 h of admission or a fall of at least 5 points from a previous baseline determination to be included. Upper GI endoscopy was performed in all patients within 48 h of admission. Alcohol use was quantitated as chronic (80 g or more per day for at least 1 month), binge, occasional, or none., Results: Over the 4-yr study period, 727 patients met the inclusion criteria, and of these, 212 (29%) were classified as chronic alcohol users. Overall, peptic ulcer disease was the most common cause of bleeding (60%). Gastropathy (diffuse subepithelial hemorrhage) was considered etiological in only 32 patients (4%). The most common causes of gastropathy were portal hypertension in 22 patients and nonsteroidal anti-inflammatory drug use in five. Only three patients were identified in whom alcoholic gastropathy was considered etiological; in these patients, bleeding was mild and self-limited. When the causes of bleeding were compared between drinkers and nondrinkers, drinkers were more likely to bleed from varices (p = 0.024) or other portal hypertension-related causes (p < 0.01), whereas peptic ulcer was more common in nondrinkers compared with chronic users (67 vs 53%; p < 0.01). Esophagitis (p = 0.95) and Mallory-Weiss tear (p = 0.15) prevalences were not significantly different between the two groups., Conclusion: In the actively drinking patient, the most common causes of UGIH are peptic ulcer and disorders related to portal hypertension. Alcoholic gastropathy appears to be a rare and previously overemphasized cause of bleeding.

There are many options as to the accuracy of a patient's subjective localization of an obstructing esophageal lesion. However, there are few studies specifically examining this issue. Over a 35-month period, all patients evaluated by our gastroenterology service undergoing endoscopy for dysphagia were prospectively identified. The patient's subjective localization for the level of obstruction was evaluated by an investigator blinded to the results of prior barium esophagography and recorded on a schematic of the bony skeleton. At the time of endoscopy, the most proximal level of the obstructing lesion was documented. In all, 139 patients with dysphagia and an esophageal stricture were evaluated. Barium esophagograms were performed prior to endoscopy in all but nine patients (6.5%). The most common lesions causing dysphagia were carcinoma (34.5%), gastroesophageal reflux disease (22.3%), and a Schatzki's ring (15.8%). The level of obstruction was localized exactly in 30 patients (21.6%), within +/- 2 cm in 72 (52%), and within +/- 4 cm in 31 additional patients (74%). Eight patients (15%) with a distal esophageal lesion localized the obstruction to the proximal esophagus, whereas only two patients (5%) with a lesion in the proximal esophagus localized the level of obstruction to the distal esophagus. Overall, patients with distal obstructing lesions were more likely to have referral > 6 cm proximally than proximal lesions with referral to the distal esophagus (P = 0.003). There were no significant differences in accuracy based on the cause of dysphagia. In conclusion, a patient's subjective localization of the level of an esophageal stricture is highly accurate. Patients appear to be most accurate in localizing proximal rather than distal lesions.