Context and Objectives: Interferon Beta (IFNβ) is a well-established first-line treatment for patients with multiple sclerosis (RRMS) and remains the most represented agent in sclerosis. Atypical hemolytic uremic syndrome (AHUS) represents a rare but serious adverse effect (AE) that can occur even after many years from the beginning of IFNβ therapy. ECULIZUMAB is currently approved for the treatment of Ahus and recently for the NEUROMYELITE OPTICA SPECTRUM SPECTRUM (NMOSD) with Aquaporin-4 antibodies (AQP4-IGG). In this article, we report the case of the appearance of IFNβ-related IFNβ experienced by an MS patient and we briefly examine the literature on this subject.
Methods: We conducted a systematic review of literature using PubMed and we conducted a retrospective analysis of RRMS patients who received IFNβ-1A in our center and developed thrombotic microangiopathy (TMA). From this search, we have identified only one patient.
Results: In the published literature, we have identified 24 member patients who have received the IFNβ as a treatment modifying the disease (DMT), then developed thrombotic microangiopathy with kidney injury. The Ahus was diagnosed in 6, all IFNβ-1a received and the last appearance was after 15 years. We report a case of a 39-year-old man who has assumed IFNβ-1A since 1999. In July 2018, he has developed an Ahus related to IFNβ. After the failure of the plasma exchange, it has undergone an Eculizumab, with an improvement in the glomerular filtration rate and without new signs of MS activity.
Conclusion: To our knowledge, this case represents the last appearance of IFNβ-related Ahus in patients with SEP. So far, there are no literary reports on the possibility of reintroducing a DMT as a complementary therapy to Eculizumab.
Effectiveness of interferon pegylated monotherapy in the treatment of chronic infection of virus hepatitis: a meta-analysis
An HDV chronic infection is often associated with an aggressive form of liver disease with respect to chronic mono-infection of HBV. However, chronic HDV treatment is difficult because there is currently no approved scheme for affected patients. While standard interferon with / without nucleos (t) IDE analogs were lower than pegylated interferon (peginterferon) as HDV treatment based on some randomized clinical trials. This meta-analysis will summarize the results of studies on the effectiveness of peginterferon as an HDV treatment plan. An electronic search was performed using PubMed databases, Cochrane Library, Research Door and Medline.
Studies involving patients who received peginterfer therapy for at least 48 weeks and followed for 24 weeks after therapy were included. All analyzes were conducted using Review Manager 5.3 designed for Cochrane Critics. The main efficiency endpoint was the virological response (VR) or HDV-RNA negativity at the end of the tracking period, while the endpoints of secondary efficiency were a biochemical response (BR or a clearance of ALT and an HBSAG authorization with seroconversion at the end of the follow-up period. The data has been summarized by 13 relevant studies with a total of 475 patients treated with PEGINTERFERON ALPHA-2A or -2B.
At the end of the post-treatment of 24 weeks, the grouped RV was carried out in 29% of patients with 95% of CI [24%; 34%], BR was reached in 33% of patients [95% CI 27%; 40%] and HBSAC clearance with anti-HBS seroconversion was obtained in 1% of patients with 95% CI [-0.02; 0.05]. In conclusion, this study showed that peginterferon has limited efficacy in HDV treatment, since a third of patients with chronic HDV reached viral clearance and standard Alt levels. In addition, HBSAG clearance with anti-HBS seroconversion has rarely been observed in patients with chronic HDV.
A case report of late-onset atypical Hemolytic Uremic Syndrome during interferon beta in multiple sclerosis: Open issues in literature review
New perspectives on the persistence of hepatitis D: the role of the response of interferon and implications for future therapies
Chronic Hepatitis (CHD), a global health problem, manifests itself as the most serious form of viral hepatitis. The causative agent, the hepatitis D virus (HDV), is the smallest known human virus reproduces its RNA genome with a circular slide in the hepatocyte core. HDV requires hepatitis B virus coded envelope proteins (HBV) for diffusion and NOVO cell input. However, HDV can also spread through cell division. After the NTCP mediated input in hepatocytes, the replica intermediates of HDV RNA are detected by the MDA5 pattern recognition receiver, resulting in an induction IFN-β / λ. This response from the IFN strongly suppresses the spread of HDV genomes with mediation by cell division, but only slightly affects RNA replication HDV in hepatocytes already infected, at rest. In patients, the mono-therapy with IFN-α / λ shows efficiency but rarely leads to an HDV authorization.
Recent molecular information on key determinants of HDV persistence and accelerated development of specifically acting antivirals interfering with the replication cycle, opens a new promising therapeutic perspective. In this report, we soon summarize our knowledge about the replication / persistence of HDV and newly discovered HDV agents, HDV interaction with IFN response and its consequences for persistence. Finally, we discuss the possible role of IFNS in combination with new upcoming therapies for HDV healing. Multiple sclerosis (MS) is an inflammatory self-immunoum disorder in the human central nervous system. The recombinant beta interferon (IFN-β) decreases the number of relapses and repels the progression of the disability of the sp.
However, up to 50% of patients treated with interferon beta are continuing to live relapses and / or aggravate disability. Simple nucleotide polymorphisms of different genes have been known to show significant associations with a response to IFN-β in patients with SEP. In the current work, we examined the potential role of the genes of TrainR1 and GRIA3 genes on the response to IFN-β therapy in patients with Iranian MS. The DNA was extracted from blood samples with standard procedures of 73 patients diagnosed with multiple sclerosis that were responded to IFN-β or not.
Ricardo
