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Sandro Vento

Publications and source records attributed to Sandro Vento.

34 records · Page 2Linked to original sources

Enanthema as the first clinical manifestation of abacavir hypersensitivity reaction: a case report.

Abacavir is a nucleoside analogue reverse transcriptase inhibitor used in combination with other antiretroviral drugs for the treatment of HIV 1-infection. Approximately 3% of patients who receive abacavir develop an idiosyncratic hypersensitivity reaction. The most common symptoms are fever, skin rash and gastrointestinal disorders. Respiratory symptoms occurred in approximately 20% of patients who have hypersensitivity reaction. We describe the first case, to our knowledge, of hypesensitivity reaction characterized by enanthema and fever without skin rash promptly resolved after discontinuation of abacavir

Adult↗

Inflammatory pseudotumor of lymph nodes.

A case of inflammatory pseudotumor in a 22-Year-old man is described. Symptoms and signs showed high fever and prominent cervical lymphadenopathy; laboratory findings were consistent with an acute inflammatory process. Diagnosis was reached through a lymph node biopsy which allowed a definitive diagnosis and ruled out several mimicking pathological processes such as malignant lymphoma, infectious diseases and autoimmune disorders. Inflammatory pseudotumor should be included in the differential diagnosis of patients with persistent fever and lymph node enlargement.

Adult↗

Reactivation of replication of hepatitis B and C viruses after immunosuppressive therapy: an unresolved issue.

The liver is susceptible to the toxic effects of many cytotoxic or immunosuppressive treatments. However, in carriers of hepatitis B virus (HBV) and, less frequently, of hepatitis C virus, liver damage due to reactivation of viral replication can occur after withdrawal of immunosuppressive drugs. These reactivations, which are associated with fulminant forms of hepatitis in up to 25% of cases, are observed both in symptom-free chronic carriers of hepatitis B surface antigen and in patients who have chronic hepatitis B or C and concurrent haematological tumours or solid neoplasms or who have received transplants. HBV-related complications may cause delays or modifications of therapy, and the chance of cure is reduced. In this review, we analyse clinical, biochemical, and serological issues in reactivation of viral replication and examine the role of immune reactions in the pathogenesis and the possible toxicity of immunosuppressive drugs. We emphasise the importance of identifying predictive markers of a clinically relevant reactivation, review difficulties in drug prevention and treatment, indicate studies that are needed to address the key clinical issues, and give practical recommendations to practising physicians and oncologists.

Antiviral Agents↗

Does hepatitis C virus cause severe liver disease only in people who drink alcohol?

Hepatitis C virus (HCV) infects about 170 million people worldwide, and has been portrayed in the media as a silent killer, incorrectly implying that cirrhosis and hepatocellular carcinoma are the certain final outcomes of infection. Results of numerous population-based surveys indicate that chronic HCV infection is highly prevalent in elderly people who, in most instances, do not develop end-stage liver disease. In individuals who do progress to cirrhosis and hepatocellular carcinoma alcohol plays a fundamental part, via mechanisms that result in increased viral replication, enhanced HCV quasispecies complexity, increased liver-cell death, suppression of immune responses, and iron overload. Although overlaps are present in the histological appearance of the liver in patients with hepatitis C who do and do not drink alcohol, histology could be of some help in revealing the role of alcohol in HCV disease progression even in people who deny drinking. Interventions and high-impact, continuous public-health campaigns are needed to persuade doctors and patients infected with HCV of the importance of abstaining from alcohol if risk of progression towards cirrhosis and hepatocellular carcinoma is to be reduced.

Adult↗

Infections and solid organ transplant rejection: a cause-and-effect relationship?

Although evidence is far from being conclusive, several studies have suggested that infections could trigger rejection in different transplant settings. In this review we examine the evidence linking cytomegalovirus (CMV), adenovirus, enterovirus, parvovirus, and herpes simplex virus infections to the vasculopathy leading to cardiac allograft rejection, the association between CMV and chronic kidney, lung, and liver graft rejection, and the association of human herpesvirus 6 reactivation with CMV-related disease in kidney and liver transplant recipients. We also review the numerous antiviral prophylactic or pre-emptive treatments in use to control CMV infection, and suggest that they do not limit immune reactions leading to graft rejection or lower the risk of developing post-transplantation atherosclerosis in allograft recipients. Finally, we emphasise the need for prospective, international studies to clarify the role of infections in transplant rejection, to look at virus-to-virus interactions, and to establish specific therapeutic strategies. Such strategies must not rely exclusively on expensive antiviral agents but also on vaccination or other, innovative approaches, such as the use of agents able to inhibit the activity of natural killer cells, which might have an important role in acute allograft rejection.

Adult↗