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Summary: Background: Non‐alcoholic fatty liver disease (NAFLD) is a major liver disease worldwide. Bile acid dysregulation may be a key feature in its pathogenesis and progression. Aims: To characterise the relationship between bile acid levels and NAFLD at the population level Methods: We conducted a cross‐sectional study in Guatemala in 2016 to examine the prevalence of NAFLD. Participants (n = 415) completed questionnaires, donated blood samples and had a brief medical exam. NAFLD was determined by calculation of the fatty liver index. The levels of 15 circulating bile acids were determined by LC–MS/MS. Adjusted prevalence odds ratios (PORadj) and 95% CI were calculated to examine the relationships between bile acid levels (in tertiles) and NAFLD. Results: Persons with NAFLD had significantly higher levels of the conjugated primary bile acids glycocholic acid (GCA) (PORadj T3 vs T1 = 1.85), taurocholic acid (TCA) (PORadj T3 vs T1 = 2.45) and taurochenodeoxycholic acid (TCDCA) (PORadj T3 vs T1 = 2.10), as well as significantly higher levels the unconjugated secondary bile acid, deoxycholic acid (DCA) (PORadj T3 vs T1 = 1.78) and its conjugated form, taurodeoxycholic acid (TDCA) (PORadj T3 vs T1 = 1.81). Conclusions: The bile acid levels of persons with and without NAFLD differed significantly. Among persons with NAFLD, higher levels of the conjugated forms of CA (i.e. GCA, TCA) and the secondary bile acids that derive from CA (i.e. DCA, TDCA) may indicate there is hepatic overproduction of CA, which may affect the liver via aberrant signalling mediated by the bile acids. [ABSTRACT FROM AUTHOR]

Persons heterozygous for the risk allele have a two-fold higher risk of liver disease, while persons who are homozygous have a greater than threefold risk.3 In Guatemala, we estimate that >30% of NAFLD among adults may be related to rs738409. Definition of liver disease The primary measure of liver disease was an elevated level of ALT or AST, hereafter referred to as elevated ALT/AST. Keywords: genetics; Guatemala; Latinos; NAFLD; PNPLA3 EN genetics Guatemala Latinos NAFLD PNPLA3 1470 1474 5 06/13/22 20220601 NES 220601 INTRODUCTION Spurred by the epidemics of diabetes and obesity, nonalcoholic fatty liver disease (NAFLD) has become one of the most common chronic liver conditions in the world.1 In the Americas, individuals of Latino ancestry experience disproportionate rates of NAFLD and other liver disorders.2 Genetic susceptibility to NAFLD has been identified, with the I149M polymorphism (rs738409) in the patatin-like phospholipase gene I PNPLA3 i found to be most consistently associated. As shown in Table 2, the frequencies of the previously reported risk allele at each loci were: I PNPLA3 i rs738409 G allele = 0.69, I NCAN i rs2228603 T allele = 0.01, I GCKR i rs780094 T allele = 0.39 and I LYPLAL1 i rs12137855 C allele = 0.94. [Extracted from the article]

Background: Previous studies have suggested an association between Helicobacter pylori (H pylori) and nonalcoholic fatty liver disease (NAFLD). The aim of the current study was to examine the association in Guatemala, a region with elevated prevalences of both H pylori and NAFLD. Associations between H pylori and other metabolic conditions were also examined, as were associations between H hepaticus and H bilis and the metabolic conditions. Materials & Methods: The analysis included 424 participants from a cross‐sectional study in Guatemala. H pylori seropositivity was defined as positivity for ≥ 4 antigens. Seropositivities for H bilis and H hepaticus were defined as positivity for ≥ 2 antigens. NAFLD was estimated using the Fatty Liver Index and the Hepatic Steatosis Index. Other conditions examined were obesity, central obesity, hypercholesterolemia, low HDL, diabetes and metabolic syndrome (MetSyn). Prevalence odds ratios (POR) and 95% confidence intervals (CIs) were estimated. Results: No overall associations between H pylori,H hepaticus, or H bilis and NAFLD or related metabolic conditions were found. Seropositivity for H pylori antigens CagA and VacA and H hepaticus antigen HH0713 was each significantly associated with NAFLD, however. In addition, associations were observed between the H pylori antigens HyuA, HP1564, and UreA and specified metabolic conditions. Conclusions: While no overall associations between H pylori or Helicobacter species with NAFLD or related conditions were observed, some selected Helicobacter spp. antigens were associated with NAFLD. Further research is warranted to examine whether H. species are associated with any metabolic condition. [ABSTRACT FROM AUTHOR]

Liver cancer is an emerging global health issue, with rising incidence in both the United States and the economically developing world. Although Guatemala experiences the highest rates of this disease in the Western hemisphere and a unique 1:1 distribution in men and women, few studies have focused on this population. Thus, we determined the prevalence and correlates of aflatoxin B1 (AFB1) exposure and hepatitis virus infection in Guatemalan adults. Healthy men and women aged ≥40 years (n = 461), residing in five departments of Guatemala, were enrolled in a cross-sectional study from May—October of 2016. Serum AFB1-albumin adducts were quantified using isotope dilution mass spectrometry. Multivariate linear regression was used to assess relationships between AFB1-albumin adduct levels and demographic factors. Biomarkers of hepatitis B virus and hepatitis C virus infection were assessed by immunoassay and analyzed by Fisher’s exact test. AFB1-albumin adducts were detected in 100% of participants, with a median of 8.4 pg/mg albumin (range, 0.2–814.8). Exposure was significantly higher (p<0.05) in male, rural, low-income, and less-educated participants than in female, urban, and higher socioeconomic status participants. Hepatitis B and C seropositivity was low (0.9% and 0.5%, respectively). Substantial AFB1 exposure exists in Guatemalan adults, concurrent with low prevalence of hepatitis virus seropositivity. Quantitatively, AFB1 exposures are similar to those previously found to increase risk for liver cancer in Asia and Africa. Mitigation of AFB1 exposure may reduce liver cancer incidence and mortality in Guatemala, warranting further investigation. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Rivera–Andrade et al papers. To view these articles, visit https://doi.org/10.1111/apt.16948 and https://doi.org/10.1111/apt.16962 [ABSTRACT FROM AUTHOR]

Background: Reports suggest that Latin American and Caribbean (LAC) countries have not reduced leukemia mortality compared to high-income countries. However, updated trends remain largely unknown in the region. Given that leukemia is the leading cause of cancer-related death in LAC children, we evaluated mortality trends in children (0-14y) from 15 LAC countries for the period 2000-2017 and predicted mortality to 2030., Methods: We retrieved cancer mortality data using the World Health Organization Mortality Database. Mortality rates (standardized to the world standard SEGI population) were analyzed for 15 LAC countries. We evaluated the average mortality rates for the last 5 years (2013-2017). Joinpoint regression analysis was used to evaluate leukemia mortality trends and provide an estimated annual percent change (EAPC). Nordpred was utilized for the calculation of predictions until 2030., Results: Between 2013 and 2017, the highest mortality rates were reported in Venezuela, Ecuador, Nicaragua, Mexico, and Peru. Upward mortality trends were reported in Nicaragua (EAPC by 2.9% in boys, and EAPC by 2.0% in girls), and Peru (EAPC by 1.4% in both sexes). Puerto Rico experienced large declines in mortality among both boys (EAPC by - 9.7%), and girls (EAPC by - 6.0%). Leukemia mortality will increase in Argentina, Ecuador, Guatemala, Panama, Peru, and Uruguay by 2030., Conclusion: Leukemia mortality is predicted to increase in some LAC countries by 2030. Interventions to prevent this outcome should be tailor to reduce the socioeconomic inequalities and ensure universal healthcare coverage.

Objective: In Guatemala, cirrhosis is among the 10 leading causes of death, and mortality rates have increased lately. The reasons for this heavy burden of disease are not clear as the prevalence of prominent risk factors, such as hepatitis B virus, hepatitis C virus and heavy alcohol consumption, appears to be low. Aflatoxin B 1 (AFB 1 ) exposure, however, appears to be high, and thus could be associated with the high burden of cirrhosis. Whether AFB 1 increases the risk of cirrhosis in the absence of viral infection, however, is not clear., Design: Cirrhosis cases (n=100) from two major referral hospitals in Guatemala City were compared with controls (n=200) from a cross-sectional study. Logistic regression was used to estimate the ORs and 95% CIs of cirrhosis and quintiles of AFB 1 in crude and adjusted models. A sex-stratified analysis was also conducted., Results: The median AFB 1 level was significantly higher among the cases (11.4 pg/mg) than controls (5.11 pg/mg). In logistic regression analyses, higher levels of AFB 1 was associated with cirrhosis (quintile 5 vs quintile 1, OR: 11.55; 95% CI 4.05 to 32.89). No attenuation was observed with adjustment by sex, ethnicity, hepatitis B virus status, and heavy alcohol consumption. A significantly increasing trend in association was observed in both models (p trend <0.01). Additionally, the cirrhosis-AFB 1 association was more prominent among men., Conclusions: The current study found a significant positive association between AFB 1 exposure and cirrhosis. Mitigation of AFB 1 exposure and a better understanding of additional risk factors may be important to reduce the burden of cirrhosis in Guatemala., Competing Interests: Competing interests: None declared., (Re-use permitted under CC BY. Published by BMJ.)