Liver involvement in presence of heart disease and heart involvement in presence of liver disease: a conundrum.

Data from literature show a cross-talk between the heart and liver during diseases which primarily involve one of the two organs, but data regarding this relationship are scant. Aim of this study was to investigate this relationship. In this narrative review we critically explored the most recent literature on this topic using PubMed and Medline and examining the most recent studies about liver involvement in heart failure and heart involvement in course of liver disease. Patients with acute and chronic heart failure and those who undergo heart transplatation (HT) manifest various signs of liver damage with a rate of incidence which is higher in candidates for left ventricular assist device. In presence of cardiogenic shock a very marked hepatocellular necrosis may occur while in the setting of chronic heart failure congestive hepatopathy and-or the so-called cardiac cirrhosis are observed. On the other side in presence of chronic liver disease and in case of liver transplantation (LT) heart functions may be altered and cirrhotic cardiomyopathy, which is a syndrome characterized by systolic, diastolic and electrophysiological abnormalities may occur. In this review we have analyzed the relationship between heart and liver disease, even in case of LT and HT. Furthermore we have underscored the effects of chronic alcoholism and of systemic disorders such as hemochromatosis and amyloidosis on both heart and liver.

Alcohol-related diseases: from metabolism to the main effect on the body.

Alcohol consumption can cause, beyond addiction, roughly 200 different diseases and at least fourteen types of cancer. In 2016 the WHO estimated that 29% of alcohol-related deaths were mainly due to oncological diseases, liver cirrhosis (20%), and cardiovascular disorders (19%). The aim of this review was to focus on the absorption and metabolism of ethanol and discuss the main conditions caused by alcohol consumption (i.e., liver and cardiovascular diseases, and tumors). This narrative review is based on a detailed analysis of the scientific literature published before January 31, 2024 (PubMed, Web of Science, Scopus, Google Scholar). Approximately 90% of the absorbed alcohol reaches the liver where it is metabolized to acetaldehyde, a highly reactive and toxic compound. The excessive use of alcohol causes damage to several organs and systems, mainly the liver (e.g., steatosis, steato-hepatitis, fibrosis, and cirrhosis), cardiovascular system (cardiomyopathy, arrythmias, arterial hypertension, and stroke), and significantly contribute to the onset of neoplastic lesions to various organs including the esophagus, liver and breast. Even moderate drinking appears not to reduce mortality risk. Alcohol intake is one of the main risk factors for several pathological conditions and social problems, thus drastically impacting on public health. Proper awareness of the high risk related to alcohol consumption is of crucial importance to reduce the harm to public health.

Driving under the influence of alcohol and alcohol use disorder: the relevance of early identification from an Italian retrospective outpatient study.

INTRODUCTION: Worldwide, almost 1.2 million people drive under the influence of alcohol. However, early identification of alcohol use disorder (AUD) in subjects driving under the influence (DUI) of alcohol is seldom achieved. AIM: The aim of our retrospective study is to investigate the presence of AUD in a population of DUI subjects who had their driving license suspended, and if they were following a specific rehabilitation program. METHODS AND RESULTS: 750 subjects were retrospectively enrolled from 2018 to 2021. DSM-V to assess AUD was used. Forty-eight (6.4%) subjects presented a diagnosis of AUD, after one month they showed a statistically significant reduction of carbohydrate-deficient transferrin (CDT) (p<0.0001); however, none were following a program for the treatment of AUD. CONCLUSIONS: This outpatient setting may be considered a place of primary and secondary prevention where DUI subjects with a diagnosis of AUD may be entrusted to a Centre in order to follow rehabilitation treatment.

Alcohol use disorders and liver fibrosis: an update.

Alcoholic liver disease (ALD) is currently, worldwide, the second most common cause of human fatalities every year. Alcohol use disorders (AUDs) lead to 80% of hepatotoxic deaths, and about 40% of cases of cirrhosis are alcohol-related. An acceptable daily intake (ADI) of ethanol is hard to establish and studies somewhat controversially recommend a variety of dosages of ADI, whilst others regard any intake as dangerous. Steatohepatitis should be viewed as "the rate limiting step": generally, it can be overcome by abstinence, although in some patients, abstinence has little effect, with the risk of fibrosis, leading in some cases to hepatocellular carcinoma (HCC). Chronic alcoholism can also cause hypercortisolism, specifically pseudo-Cushing Syndrome, whose diagnosis is challenging. If fibrosis is spotted early, patients may be enrolled in detoxification programs to achieve abstinence. Treatment drugs include silybin, metadoxine and adenosyl methionine. Nutrition and the proper use of micronutrients are important, albeit often overlooked in ALD treatment. Other drugs, with promising antifibrotic effects, are now being studied. This review deals with the clinical and pathogenetic aspects of alcohol-related liver fibrosis and suggests possible future strategies to prevent cirrhosis.

Use of sodium oxybate for the treatment of alcohol withdrawal syndrome in patients with acute alcohol-associated hepatitis: A 4-patient case report.

INTRODUCTION: During the treatment of alcohol use disorder, alcohol withdrawal syndrome (AWS) can occur. Benzodiazepines remain the "gold standard" for the pharmacological treatment of AWS. However, other drugs have been approved in some European Countries for the treatment of AWS: namely, clomethiazole in Spain and Germany and sodium oxybate in Italy and Austria. Acute alcohol-associated hepatitis (AAH) is a distinct clinical syndrome characterized by the recent onset of jaundice with or without other signs of liver decompensation in patients with ongoing alcohol consumption. RATIONALE: We report 4 paradigmatic clinical cases to analyze the efficacy, safety, and tolerability of the very short half-life (30-45 minutes) sodium oxybate (SO) in the management of AWS with moderate to severe AAH. Compared to SO, "as needed" short-acting benzodiazepines, currently prescribed to treat AWS in patients with AAH, have a much longer half-life (5-25 hours) which increases the risk of drug accumulation. The very short half-life of SO provides a fixed dose approach allowing for a more effective control of AWS than "as needed" therapy throughout the 24 hours. PATIENT CONCERNS: Patients reported anxiety, agitation, diffuse abdominal pain, loss of appetite, and nausea with elevation in serum bilirubin and 2 of them had abdomen distension due to ascites. DIAGNOSIS: Patients were affected by moderate or severe AWS and moderate or severe AAH on alcohol-related liver cirrhosis. INTERVENTIONS: In order to suppress AWS, all patients were treated with oral sodium oxybate at a dose of 25 mg/kg/day, progressively increased to 50 to 100 mg/kg/day, divided into 3 to 5 administrations. OUTCOMES: SO was efficient, safe and tolerable in suppressing AWS even in patients with severe AAH. All treated patients showed a rapid improvement of all symptom (via the Clinical Institute of Withdrawal Assessment for Alcohol Scale) and liver test scores (Model for End-Stage Liver Disease). CONCLUSION: Because of its short half-life, SO can be considered a safe and effective pharmacological option for the AWS in patients with moderate to severe AAH even in comparison to short-acting benzodiazepines, thus avoiding the risk of accumulation. Notably, SO guarantees a fixed approach to cover the possible onset of AWS throughout the 24 hours.

Pyogenic liver abscess caused by Gemella morbillorum / Absceso hepático piógeno causado por Gemella morbillorum

Even though Gemella morbillorum infection (GMI) is rare in humans, it may, nevertheless, cause endocarditis, meningitis, brain abscess, pleural empyema, nephritis, mediastinitis, and - occasionally - liver abscess. We are describing the case of a 64-year-old Caucasian male admitted with fever and abdominal pain. Laboratory parameters revealed inflammation signs, and instrumental examinations showed the presence of diverticula in the ascending colon. Abdominal ultrasound (US) and computer tomography (CT) showed two focal lesions in the right liver lobe. One had the characteristics of a simple cyst; the second was hypoechoic with a low density area, possibly containing necrotic material. US-guided needle biopsy was found negative for neoplastic cells, showing purulent infiltrate. Pus culture was found positive for GMI. Systemic antibiotic therapy, coupled with repeated US-guided needle aspiration, induced the resolution of the hepatic abscess. Few cases have been reported of hepatic abscess caused by GMI in immunocompetent non-cirrhotic subjects.

A pesar de que la infección por Gemella morbillorum (GMI, por el término en inglés) es poco común en seres humanos, puede causar endocarditis, meningitis, absceso cerebral, empiema pleural, nefritis, mediastinitis y en ocasiones, absceso hepático. Describimos el caso de un hombre caucásico de 64 años que ingresó con fiebre y dolor abdominal. Los parámetros de laboratorio revelaron signos de inflamación y los exámenes mostraron la presencia de divertículos en el colon ascendente. La ecografía abdominal (US) y la tomografía computarizada (CT) mostró dos lesiones focales en el lóbulo hepático derecho. Una presentó las características de un quiste simple; la segunda fue hipoecóica con una zona de baja densidad, que posiblemente contenía material necrótico. Biopsia con aguja guiada por US dio un resultado negativo para células neoplásicas, mostrando infiltrado purulento. Cultivo de pus fue encontrado positivo para GMI. Una terapia con antibióticos sistémicos, junto con aspiración repetida con aguja guiada por US indujo a la resolución del absceso hepático. Pocos casos se han reportado de absceso hepático causado por GMI en sujetos inmunocompetentes no cirróticos.

Serum pepsinogen A and pepsin secretion in duodenal ulcer: helicobacter pylori influence

El pepsinageno sérico A (PGA) y la actividad péptica total (PA) en jugo gástrico, son investigados en 87 pacientes con úlcera duodenal. Los resultados indican un significativo aumento del PGA y PA en relación a controles. Los pacientes con úlcera duodenal, Helicobater Pylori positivo muestran el aumento del PGA no habiendo variaciones en el PA. Este contraste puede deberse a varios factores: dado que los dos parámetros son expresión de actividades celulares distintas y el PA en jugo gástrico es expresión del pepsinógeno total. Se puede concluir que el daño del HP sobre la mucosa duodenal es debido a su acción y no a la alteración de la actividad péptica en jugo gástrico (AU)

Serum pepsinogen A and pepsin secretion in duodenal ulcer: helicobacter pylori influence

El pepsinageno sérico A (PGA) y la actividad péptica total (PA) en jugo gástrico, son investigados en 87 pacientes con úlcera duodenal. Los resultados indican un significativo aumento del PGA y PA en relación a controles. Los pacientes con úlcera duodenal, Helicobater Pylori positivo muestran el aumento del PGA no habiendo variaciones en el PA. Este contraste puede deberse a varios factores: dado que los dos parámetros son expresión de actividades celulares distintas y el PA en jugo gástrico es expresión del pepsinógeno total. Se puede concluir que el daño del HP sobre la mucosa duodenal es debido a su acción y no a la alteración de la actividad péptica en jugo gástrico

Gastric chief cell mass in duodenal ulcer

A 25 pacientes ulcerosos duodenales y 40 controles sanos se les calculó la massa de células principales y el Pepsinogeno serico I. Se comparó también con la masa celular parietal y la secreción ácida estimulada. La masa celular principal fue expresada por el índice Zinogenico (IZ) obtenido multiplicando al número de células principales por mm2 por el espesor de la capa glandular. Se encontró una significativa disminución del IZ en pacientes com úlcera duodenal que en controles. El agrupamiento según la edad por encima y debajo de 50 anos, confirma que el IZ disminuye significativamente en ulcerosos duodenales en relación a controles. No hay cambios de IZ en ulcerosos duodenales con gastritis fundica superficial en comparación con aquellos con mucosa fundica normal. El pepsinógeno serico II está aumentado en pacientes ulcerosos con gastritis fundica superficial en relación a los que tienen mucosa normal. Se observa hipopesinogenemia en pacientes con hiperparietolismo y normopepsinogenemia en los pacientes con normoparietolismo. Finalmente no se observa correlación entre índice Zinogenico y Pepsinógeno serico I (AU)

Gastric chief cell mass in duodenal ulcer

A 25 pacientes ulcerosos duodenales y 40 controles sanos se les calculó la massa de células principales y el Pepsinogeno serico I. Se comparó también con la masa celular parietal y la secreción ácida estimulada. La masa celular principal fue expresada por el índice Zinogenico (IZ) obtenido multiplicando al número de células principales por mm2 por el espesor de la capa glandular. Se encontró una significativa disminución del IZ en pacientes com úlcera duodenal que en controles. El agrupamiento según la edad por encima y debajo de 50 anos, confirma que el IZ disminuye significativamente en ulcerosos duodenales en relación a controles. No hay cambios de IZ en ulcerosos duodenales con gastritis fundica superficial en comparación con aquellos con mucosa fundica normal. El pepsinógeno serico II está aumentado en pacientes ulcerosos con gastritis fundica superficial en relación a los que tienen mucosa normal. Se observa hipopesinogenemia en pacientes con hiperparietolismo y normopepsinogenemia en los pacientes con normoparietolismo. Finalmente no se observa correlación entre índice Zinogenico y Pepsinógeno serico I