Therapeutic Advances in Chronic Disease最新文献

Sensitization of dorsal horn ganglion sensory neuron plays a crucial role in the maintenance of chronic pain disorder. Multiple interventions targeting dorsal horn ganglion can provide considerable relief of pain, including selective nerve root block, pulsed radiofrequency, and electrical nerve stimulation technique. It remains controversial about the superiority of neuromodulation mentioned above due to distinct pattern of analgesic mechanism. Here, we reported one 71-year-old male presenting at our pain clinic with severe, unilateral lower limb pain caused by postherpetic neuralgia. An implantable stimulator with dual neuromodulation mode, combining pulsed radiofrequency with electrical nerve stimulation, was then placed into the lateral epidural space adjacent to dorsal root ganglion at L4 level. Standard stimulation programing was performed with technicians to achieve satisfactory control of pain, with numerical rating scale decreasing from 8 to 2 postoperatively. This novel dual function neuromodulation strategy may provide an alternative option for pain management for those with intractable neuropathic pain.

Cystic fibrosis (CF), a life-limiting chronic disease caused by mutations in the cystic fibrosis transmembrane regulator (CFTR) gene, affects more than 90,000 people worldwide. Until recently, the only available treatments were directed to symptom control, but they failed to change the course of the disease. New drugs developed in the last decade have the potential to change the expression, function, and stability of CFTR protein, targeting the basic molecular defect. The authors seek to provide an update on the new drugs, with a special focus on the most promising clinical trials that have been carried out to date. These newly approved drugs that target specific CFTR mutations are mainly divided into two main groups of CFTR modulators: potentiators and correctors. New therapies have opened the door for potentially disease-modifying, personalized treatments for patients with CF.

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which may lead to uncontrolled immune activation and cytokine response in some. The pattern of pro-inflammatory cytokines is similar to that which has been observed to be involved in rheumatic diseases and target treatments. Viral arthritis is common with a wide variety in spectrum ranging from arthralgia to spurious and chronic arthritis. However, recent studies have demonstrated a correlation with endemic coronaviruses and increased risk of developing rheumatoid arthritis (RA). Cases are being identified that describe a post-COVID reactive; however, to date, no report has been published describing the onset of psoriasis and concomitant development of psoriatic arthritis after COVID-19 infection. We report an interesting case of psoriatic arthritis in a post-COVID-19 infection patient with review of the current literature.

Noncommunicable disease now contributes to the World Health Organization top 10 causes of death in low-, middle- and high-income countries. Particular examples include stroke, coronary heart disease, dementia and certain cancers. Research linking clinical and lifestyle risk factors to increased risk of noncommunicable disease is now well established with examples of confirmed risk factors, including smoking, physical inactivity, obesity and hypertension. However, despite a need to target our resources to achieve risk reduction, relatively little work has examined the overlap between the risk factors for these main noncommunicable diseases. Our high-level review draws together the evidence in this area. Using a systematic overview of reviews, we demonstrate the likely commonality of established risk factors having an impact on multiple noncommunicable disease outcomes. For example, systematic reviews of the evidence on physical inactivity and poor diet found each to be associated with increased risk of cancers, coronary heart disease, stroke, diabetes mellitus and dementia. We highlight the potential for targeted risk reduction to simultaneously impact multiple noncommunicable disease areas. These relationships now need to be further quantified to allow the most effective development of public health interventions in this area.

Despite significant therapeutic advances, patients with chronic heart failure (HF) remain at high risk for HF progression and death. Sacubitril/valsartan (previously known as LCZ696) is a first-in-class medicine that contains a neprilysin (NEP) inhibitor (sacubitril) and an angiotensin II (Ang-II) receptor blocker (valsartan). NEP is an endopeptidase that metabolizes different vasoactive peptides including natriuretic peptides, bradykinin and Ang-II. In consequence, its inhibition increases mainly the levels of both, natriuretic peptides (promoting diuresis, natriuresis and vasodilatation) and Ang-II whose effects are blocked by the angiotensin receptor blocker, valsartan (reducing vasoconstriction and aldosterone release). Results from the 8442 patient PARADIGM-HF study showed in patients with New York Heart Association (NYHA) class II-IV and reduced ejection fraction treated with LCZ696 (versus enalapril), the following benefits: reduction of the risk of death from cardiovascular causes by 20%; reduction of HF hospitalizations by 21%; reduction of the risk of all-cause mortality by 16%. Overall there was a 20% risk reduction on the primary endpoint, composite measure of cardiovascular (CV) death or time to first HF hospitalization. PARADIGM-HF was stopped early after a median follow up of 27 months. Post hoc analyses of PARADIGM-HF as well as the place in therapy of sacubitril/valsartan, including future directions, are included in the present review.