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1.
Dig Dis Sci ; 68(8): 3451-3457, 2023 08.
Artículo en Inglés | MEDLINE | ID: mdl-37291473

RESUMEN

BACKGROUND: Genetic mutations causing defective VLDL secretion and low LDL cholesterol are associated with hepatic steatosis and nonalcoholic fatty liver disease (NAFLD). AIMS: Determine if low LDL cholesterol (< 5th percentile) was an independent predictor of hepatic steatosis. METHODS: Secondary data analysis of the Dallas Heart study (an urban, multiethnic, probability-based sample), we defined hepatic steatosis utilizing intrahepatic triglyceride (IHTG) analyzed using magnetic resonance spectroscopy in conjunction and available demographic, serological and genetic information. We exclude patients on lipid lowering medications. RESULTS: Of the 2094 subjects that met our exclusion criteria, 86 had a low LDL cholesterol, of whom 19 (22%) exhibited hepatic steatosis. After matching for age, sex, BMI, and alcohol consumption, low LDL cholesterol was not a risk factor for hepatic steatosis compared to those with normal (50-180 mg/dL) or high (> 180 mg/dL) LDL. When analyzed as a continuous variable, we observed lower IHTG in the low LDL group compared to the normal or high LDL groups (2.2%, 3.5%, 4.6%; all pairwise comparisons p < 0.001). Subjects with both hepatic steatosis and low LDL cholesterol exhibited a more favorable lipid profile but similar insulin resistance and hepatic fibrosis risk compared to other subjects with hepatic steatosis. The distribution of variant alleles associated with NAFLD, including PNPLA3, GCKR, and MTTP was indistinguishable between subjects with hepatic steatosis and low versus high LDL cholesterol. CONCLUSION: These findings suggest that low serum LDL levels are not a useful predictor of hepatic steatosis and NAFLD. Moreover, subjects with low LDL exhibit a more favorable lipid profile and lower IHTG.


Asunto(s)
Resistencia a la Insulina , Enfermedad del Hígado Graso no Alcohólico , Humanos , Enfermedad del Hígado Graso no Alcohólico/diagnóstico , Enfermedad del Hígado Graso no Alcohólico/epidemiología , Enfermedad del Hígado Graso no Alcohólico/genética , Factores de Riesgo , Cirrosis Hepática , Triglicéridos , Hígado/diagnóstico por imagen
2.
ACG Case Rep J ; 10(5): e01046, 2023 May.
Artículo en Inglés | MEDLINE | ID: mdl-37180464

RESUMEN

In gastrointestinal-variant Lemierre syndrome, Fusobacterium nucleatum can cause pylephlebitis and liver abscesses. We report a 62-year-old woman presenting with abdominal pain and altered mental status. Abdominal computed tomography showed hepatic lesions and thrombosis in the superior mesenteric and portal veins. Magnetic resonance cholangiopancreatography showed multiple cystic hepatic masses suspicious for abscess vs metastases. Malignancy workup was unrevealing. F. nucleatum grew on both blood and ultrasound-guided liver aspirate cultures. Twelve weeks of antibiotics and anticoagulants resolved her condition. Given the high mortality rates, prompt detection and treatment of gastrointestinal-variant Lemierre syndrome is critical to delivering quality, patient-centered care.

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