Hepatitis C, systemic inflammation and oxidative stress: correlations with metabolic diseases

Introduction: Hepatitis C chronic infection has long been correlated with numerous systemic diseases, such as diabetes mellitus and hepatic steatosis. Recent studies have also revealed an association with atherosclerosis. Areas covered: An analysis is presented on the mechanisms through which the hepatitis C viral infection can lead to a systemic increase in pro-inflammatory markers, especially tumor necrosis factor-a and interleukin-6. The immunological imbalance created may, through different mechanisms, act on the metabolic pathways that contribute to the development of insulin resistance, the accumulation of lipids in the liver, and even the formation of atherosclerotic plaques. Moreover, an additional contributing factor to the above-mentioned metabolic derangements is the unopposed oxidative stress observed in chronic hepatitis C viral infection. The virus itself contributes to the formation of oxidative stress, through alterations in the trace metal homeostasis and its effect on pro-inflammatory cytokines, such as tumor necrosis factor-a. Expert opinion: The scope of this review is to emphasize the importance of the metabolic manifestations of hepatitis C viral infection and to elucidate the pathophysiological mechanisms behind their emergence. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group

Fatal Streptococcus pseudoporcinus disseminated infection in decompensated liver cirrhosis: a case report

Background: Streptococcus pseudoporcinus (S. pseudoporcinus) was first identified in 2006. It cross-reacts with Lancefield group B antigen agglutination reagents and has been misidentified as S. agalactiae. Sites of S. pseudoporcinus isolation include the female genitourinary tract, urine, wounds, and dairy products. The prevalence of vaginal colonization is reportedly between 1 and 5.4%. Two uneventful cases of soft tissue infection caused by S. pseudoporcinus were reported in the past. However, since late 2019, six cases of invasive S. pseudoporcinus infections have emerged in the literature, one of which was fatal. Case presentation: We describe a fatal case of a Caucasian male with spontaneous bacterial peritonitis associated with bacteremia due to a multidrug-resistant S. pseudoporcinus strain in a patient with decompensated liver cirrhosis. Despite the patient’s good general condition and stable blood test results when he had visited the outpatient clinic for large-volume paracentesis a few days before admission, this time he presented to the emergency department with a rapidly worsening clinical condition and with laboratory features consistent with multiple-organ dysfunction syndrome, and succumbed within a short period. Conclusions: Contrary to what was thought until recently, multidrug-resistant S. pseudoporcinus may cause invasive, disseminated, fatal disease in humans. According to current limited data, vancomycin, linezolid, daptomycin, levofloxacin, clindamycin, and tetracycline seem to be the most effective antimicrobial agents against multidrug-resistant strains, and should be the empirical choice in cases of disseminated S. pseudoporcinus infection until laboratory antimicrobial susceptibility results are available. Improvements and new approaches for bacterial identification in routine clinical microbiology laboratories may reveal the real spectrum of S. pseudoporcinus infections in humans, which is currently believed to be underestimated. SS. pseudoporcinus could emerge as a serious medical problem in the near future, similar to other β-hemolytic streptococci. © 2021, The Author(s)

Pituitary non-secreting macroadenoma apoplexy in an adolescent. Patient report and review of the literature

Pituitary macroadenomas are rare in children and adolescents, and when encountered are usually hormone secreting. Symptomatic pituitary non-secreting macroadenoma apoplexy in an adolescent is rare and potentially life-threatening. A 15 year-old patient is described, hospitalized due to headache, fever and photophobia 4 days prior to admission. A meningeal syndrome was postulated, based on clinical examination and cerebrospinal fluid testing. However, clinical examination and hormone testing revealed partial failure of the anterior pituitary. Computed tomography of the brain demonstrated a space-occupying lesion of the pituitary. Magnetic nuclear resonance imaging suggested the presence of a pituitary macroadenoma. Hypophysectomy was performed. Histological examination revealed an extensive infarction of a pituitary adenoma. Hormonal substitution with thyroxine and corticosteroids was administered. This report emphasizes that pituitary non-secreting macroadenoma apoplexy may rarely be the cause of headache and fever in an adolescent, thus causing difficulties in differential diagnosis from acute meningitis

Bacterial translocation markers in liver cirrhosis

Bacterial translocation (BT) is an important mechanism in the development of infection in liver cirrhosis. The migration and colonization of bacteria and/or bacterial products from the bowel to mesenteric lymph nodes is a controlled process in healthy persons. Increased intestinal permeability, bacterial overgrowth and defect of gut-associated lymphatic tissue promote impaired BT in cirrhotics. We reviewed the reports on markers used for the evaluation of BT published between 1987 and 2016. We focused on the clinical consequences of BT in cirrhosis, as indicated by the values of the BT markers. Patients with cirrhosis are reported to have elevated levels of surrogate markers associated with BT compared with controls. The most widely used BT parameters are C-reactive protein, procalcitonin, bacterial DNA, endotoxin or lipopolysaccharide, lipopolysaccharide binding protein, calprotectin, and bactericidal/permeability increasing protein. High levels of these factors in serum and/or ascitic fluid in humans may be associated with advanced liver disease, hemodynamic instability, high levels of proinflammatory cytokines, susceptibility to the development of severe or recurrent infections, acute-on-chronic liver failure, hepatic encephalopathy, hepatorenal syndrome and poor prognosis during follow up. In conclusion, high levels of BT markers are associated with a high inflammatory response, increased complications of liver cirrhosis and occasionally high fatality rates. © 2017 Hellenic Society of Gastroenterolog

Cirrhotic cardiomyopathy: The interplay between liver and cardiac muscle. how does the cardiovascular system react when the liver is diseased?

It is widely known that liver cirrhosis, regardless of the etiologies is accompanied by severe hemodynamic changes. The principal pathophysiological mechanisms are the hyperdynamic circulation with increased cardiac output, heart rate along with reduced systemic vascular resistance. Thus, counteractive mechanisms may develop that eventually lead to systolic as well as diastolic dysfunction and rhythm disturbances, in order to keep a steady homeostasis in the human body. Literally, blunted contractile responsiveness to physical or pharmacological stress, impaired diastolic relaxation and electrophysiological changes, primarily QT interval prolongation, do occur progressively in a cirrhotic patient with no known preexisting cardiac disease. This condition is identified as cirrhotic cardiomyopathy (CCM), an entity different from that seen in alcoholic cardiac muscle disease. For the past decades, clinicians did study and attempt to understand the pathophysiology and clinical significance of this process. Indeed, various factors have been identified acting at the molecular and cellular level. Electrocardiography, echocardiography and various serum biomarkers are the main tools that help healthcare practitioners to point to the correct diagnosis. Noteworthy, the subjects that suffer from cirrhotic cardiomyopathy may progress to heart failure during invasive procedures such as surgery, insertion of a transjugular intrahepatic portosystemic shunting (TIPS) and liver transplantation. Besides, several studies have illustrated that CCM is a contributing factor, or even a precipitant, of hepatorenal syndrome (HRS), a conceivable reversible kidney failure in patients with liver cirrhosis and ascites. The treatment is the same as it is in the patients with liver cirrhosis and heart failure and there is no particular treatment for cirrhotic cardiomyopathy. Hence, it is of utmost importance to clearly comprehend the pathophysiology of this disease in order to design more accurate diagnostic tools and definitive treatments in a way to prevent the complications of cirrhosis and overt heart failure. The objective of this review is to describe in a comprehensive way the pathological alterations that occur in the cardiovascular system of cirrhotic patients. It will also point the limitations that remain in the diagnosis and treatment strategies and more importantly, this review will alert the clinicians in the modern era to further observe and record additional pathological changes in this subset of patients. © 2021 Bentham Science Publishers

Pleural effusion and pulmonary injury as an unusual complication to chemotherapy in non-small cell lung cancer patients

We report the appearance of pleural effusion, or pulmonary failure after chemotherapy, followed by tumor reduction, in a small number of patients. Five hundred and fifty-four patients with lung cancer have undergone chemotherapy at our Institute during the last ten years. Three patients with non-small cell lung cancer (NSCLC), with locally advanced disease, exhibited an unusual consequence following cytotoxic drug treatment. Two patients with NSCLC had pleural effusion which improved within 2-3 weeks, together with tumor reduction, which allowed the continuation of treatment. One patient had pulmonary failure with pleural effusion and recovered within two weeks. Two of the three patients had positive cytology for cancer cells in the fluid. All three patients achieved partial remission with no repetition of the complication. The patients' recovery, response to treatment and the tumor reduction suggest that this complication was not due to disease progression

Simultaneous development of diabetic ketoacidosis and Hashitoxicosis in a patient treated with pegylated interferon-alpha for chronic hepatitis C

Classical interferon-alpha has been shown to be correlated with the development of a variety of autoimmune disorders. A 38 year-old female patient developed simultaneously diabetic ketoacidosis and hyperthyroidism 5 mo following initiation of treatment with pegylated interferon-α and ribavirin for chronic hepatitis C. High titers of glutamic acid decarboxylase, antinuclear and thyroid (thyroid peroxidase and thyroglobulin) antibodies were detected. Antiviral treatment was withdrawn and the patient was treated with insulin for insulin-dependent diabetes mellitus and propranolol for hyperthyroidism. Twelve months after cessation of pegylated interferon-α therapy the patient was euthyroid without any medication but remained insulin-dependent. © 2007 The WJG Press. All rights reserved