Current treatments for chronic hepatitis B are able to provide a sustained suppression of the viral replication (i.e., persistent undetectability of HBV DNA). This leads to improvement of liver fibrosis and reduction of clinical complications. However, hepatitis B surface antigen (HBsAg) persists in most patients, probably justifying a still increased risk of hepatocellular carcinoma. Indeed, obtaining a complete and sterilizing cure with elimination of the covalently closed circular DNA (cccDNA) or silencing its activity is still a holy grail. New molecules are under evaluation to suppress viral replication acting on multiple phases of the HBV cycle or improve specific immune response against HBV. Molecules acting on HBV cycle have already showed encouraging results, such as entry inhibitors, small interfering RNAs (siRNAs), capsid assembly modulators (CAMs), nucleic acid polymers (NAPs). Also, promising results have been observed with immune-modulators, therapeutic vaccines, and other immune-based approaches. Among these, toll-like (TLR) or anti-programmed receptor agonists antibody 1 of the cell death protein (PD1) (e.g., nivolumab) are most promising. This paper describes newer drugs appearing on the horizon, including antiviral drugs targeting different steps of the HBV life cycle and therapeutic approaches based on immune-modulation.

Peritoneal tuberculosis (PTB) is a common type of extrapulmonary tuberculosis; however, due to variety of clinical presentations, diagnostic challenges do occur. The nonspecific features of this disease can lead to diagnostic delays and the development of complications. In addition, PTB can mimic a malignancy, especially in women who present with ascites and elevated cancer antigen (CA) 125 levels. A high index of suspicion is an important factor in an early diagnosis. Moreover, an early diagnosis and the initiation of antituberculous therapy are essential for preventing morbidity and mortality. Fortunately, most of these patients respond very well to standard antituberculous therapy.Here, we have reported the case of a young female patient who presented with chronic ascites, mild abdominal tenderness, and later, scrofula. Ultimately, she was diagnosed with PTB based on her test results. We expect that this case report will contribute to the existing literature on this subject.

Statins are a well-recognized cause of a variety of skeletal myopathic effects, which generally resolve when discontinuing the treatment. Among autoimmune manifestations associated with statins, there is immune-mediated necrotizing myopathy (IMNM).The present article summarizes the main features of statin-related IMNM, describing diagnosis, classification, epidemiology, treatment, and the main autoantibodies detected.Statins are a well-recognized cause of a variety of skeletal myopathic effects, which generally resolve when discontinuing the treatment. Among autoimmune manifestations associated with statins, there is immune-mediated necrotizing myopathy (IMNM).The present article summarizes the main features of statin-related IMNM, describing diagnosis, classification, epidemiology, treatment, and the main autoantibodies detected.Although it is impossible to define the precise number, it evident that more than 550 statin-related IMNM cases have been described in the literature. Among IMNM, two forms must be distinguished: with anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and with anti-signal recognition particle (SRP) antibodies. The differential diagnosis should be made between the IMNM and self-limited statin-related myopathy, drug-induced rhabdomyolysis, and nonautoimmune myopathies.Patients who have failed to normalize high creatine phosphokinase (CPK) after statin withdrawal should be tested for anti-HMGCR antibodies and, if these are positive, undergo muscle biopsy to confirm the diagnosis of IMNM. Pharmacological therapy of IMNM, not yet based on evidence, involves the use of high-dose corticosteroids, immunosuppressant drugs used alone or in combination, intravenous immunoglobulins (IVIg) or plasmapheresis.

BACKGROUND AND AIM: The Rapid Response System (RRS) has been introduced to prevent cardiac arrest, unplanned admissions to the intensive care unit, and death in hospitalized patients. Despite the constant and widespread presence of this system in worldwide hospitals, it remains debated whether its use improves patient outcomes. The aim of this narrative review is to describe the available evidence supporting the effectiveness of RRSs and to discuss the controversies on the lack of level 1 evidence studies.METHODS: The literature search covers the period from 1 January 2000 to 31 March 2016.RESULTS: Studies with different research designs, observational, quasi-experimental with non-randomized control group and experimental, and aggregate data of meta-analyses indicate a statistically significant reduction of in-hospital cardiac arrests and hospital mortality associated with the deployment of RRSs.CONCLUSIONS: A RRS is a complex intervention in a complex system, such as a hospital. This complexity does not allow considering experimental trials only as the most appropriate methodology to answer at research objectives. Furthermore, the benefits of a RRS depend greatly on its proper use. Accumulating evidence suggests the importance to investigate barriers and facilitators that can affect the integration, within a hospital, of this complex intervention.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. Acute exacerbations of COPD (AECOPD) are important events in the natural history of this condition because they negatively impact health status, rate of hospitalization, disease progression, and mortality.Viral and/or bacterial infections are the main cause of exacerbations. The treatments include systemic corticosteroids, bronchodilators, anticholinergics and/or short- or long-acting β2-agonists, and antibiotics in case of bacterial infections. In some cases, oxygen-therapy is indicated.This article focuses on several aspects of AECOPD, including epidemiology, diagnostic approach, i.e. investigations and management of AECOPD.

Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by complex pathophysiology and heterogeneous clinical picture. Belimumab is the first biological therapy licensed for SLE. We report the case of a 24 years old woman affected by a severe form of systemic lupus erythematosus with arthritis, muscle weakness, cervical lymphadenopathy, cutaneous involvement, fever, leukopenia, low complement levels and positivity for anti-dsDNA antibodies. Treatment with high dose steroids, hydroxychloroquine, and mycophenolate mofetil did not induce remission and several disease flares were observed. Therapy with anti-BLys monoclonal antibody belimumab leads to a fast clinical and laboratory response and to stable remission lasting for 30 months allowing steroid tapering to very low maintenance dose.

The article illustrates the case report of a patient, an elderly woman, admitted in the Emergency Department (ED) with acute pulmonary edema, which was quickly solved through a well-timed application of the therapeutic protocols. At first, the course of the treatment was positive, but some complications developed because of the long stay in the hospital, specifically a decubitus ulcer; this condition quickly evolved regardless of the proper treatment, and caused a progressive fall of the general clinical status of the patient. Within the ER, some state-of-the-art clinical apparatus (protocols, unintrusive ventilation) are available for even the treatment of the worst conditions. ED overcrowding – with full occupancy of beds and long waits of patients – is related to greater risk of poor outcomes. One of the risks is to expose the patient to serious complications, that are note related to the reason of admission in hospital, but, paradoxically, are caused by the prolonged hospitalization in ED.