Presse Medicale最新文献

Neuropathic pain occurs in people experiencing lesion or disease affecting the somatosensorial system. It is present in 7 % of the general population and may not fully respond to first- and second-line treatments in up to 40 % of cases. Neuromodulation approaches are often proposed for those not tolerating or not responding to usual pharmacological management. These approaches can be delivered surgically (invasively) or non-invasively. Invasive neuromodulation techniques were the first to be employed in neuropathic pain. Among them is spinal cord stimulation (SCS), which consists of the implantation of epidural electrodes over the spinal cord. It is recommended in some guidelines for peripheral neuropathic pain. While recent studies have called into question its efficacy, others have provided promising data, driven by advances in techniques, battery capabilities, programming algorithms and software developments. Deep brain stimulation (DBS) is another well-stablished neuromodulation therapy routinely used for movement disorders; however, its role in pain management remains limited to specific research centers. This is not only due to variable results in the literature contesting its efficacy, but also because several different brain targets have been explored in small trials, compromising comparisons between these studies. Structures such as the periaqueductal grey, posterior thalamus, anterior cingulate cortex, ventral striatum/anterior limb of the internal capsule and the insula are the main targets described to date in literature. SCS and DBS present diverse rationales for use, mechanistic backgrounds, and varying levels of support from experimental studies. The present review aims to present their methodological details, main mechanisms of action for analgesia and their place in the current body of evidence in the management of patients with neuropathic pain, as well their particularities, effectiveness, safety and limitations.

Neuropathic pain, defined as pain arising as a consequence of a lesion or disease affecting the somatosensory nervous system, requires precise diagnostic assessment. Different diagnostic tools have been devised for the diagnosis of neuropathic pain. This review offers insights into the diagnostic accuracy of screening questionnaires and different tests that investigate the somatosensory nervous system, in patients with suspected neuropathic pain. Thus, it illustrates how these tools can aid clinicians in accurately diagnosing neuropathic pain.

Neuropathic pain poses a significant challenge due to its complex mechanisms, necessitating specific treatments. In recent decades, significant progress has been made in the clinical research of neuropathic pain, marking a shift from empirical strategies to evidence-based medicine in its management. This review outlines both pharmacological and non-pharmacological interventions. Antidepressants (tricyclic and serotonin-noradrenaline reuptake inhibitors), antiepileptics (gabapentin, pregabalin), and topical agents constitute the main pharmacological treatments. These approaches target peripheral or central mechanisms associated with neuropathic pain. Noninvasive neurostimulation, including transcutaneous electrical nerve stimulation (TENS) and repetitive transcranial magnetic stimulation (rTMS), provides non-pharmacological alternatives. However, challenges persist in effectively targeting existing medications and developing drugs that act on novel targets, necessitating innovative therapeutic strategies.

This review proposes to look at the evolution of cardiomyopathy treatments in the light of advances in diagnostic techniques, which have enabled to move from a mechanistic to a phenotypic and then etiological approach. The article goes beyond the ejection fraction approach, and look at new therapies that target the pathophysiological pathways of cardiomyopathies, either by targeting the phenotype, or by targeting the etiology. The evolution of HCM treatments is detailed, culminating in the latest etiological treatments such as mavacamten in sarcomeric HCM, tafamidis in transthyretin cardiac amyloidosis and migalastat in Fabry disease. Myosin stimulators are reviewed in the treatment of DCM, before opening perspectives for gene therapy, which proposes direct treatment of the culprit mutation.

Fibrosis is a pathological manifestation in which connective tissue replaces normal one. It can affect many tissues from the skin to internal organs such as the lungs. Manifestations of pulmonary involvement can be pulmonary arterial hypertension or pulmonary fibrosis. The latter one is currently the leading cause of death in various autoimmune diseases, including systemic sclerosis.

Our study group consists of 50 patients with systemic sclerosis: 24 with limited cutaneous form and 26 with diffuse cutaneous form. This cohort was compared to 50 healthy controls (age and sex matched); our aim is to explore the distribution of TH17 cells (TH17) as well as regulatory T cells (TREG) and study their correlation with the disease's progress. Our results show an increase for IL17A in patients compared to controls and that this increase is correlated with a specific clinical involvement: Pulmonary fibrosis. This correlation suggests a crucial role of IL17A in fibrosis especially in systemic sclerosis. In addition, we have shown that the percentages of TH17 cells are higher in patients; however, the percentages of TREG cells are similar between patients and controls. A study of TREG cell activity showed that TREG lost suppressive activity by inactivating the FOXP3 transcription factor. This proves that despite their presence, TREG does not adequately carry out their regulatory activity. Finally, we analyzed the correlation between TH17/TREG and clinical damage; the results show a positive correlation with pulmonary involvement proving the role of TH17/TREG balance in induced fibrosis in systemic sclerosis. No significative difference was observed, for all the parameters, between the two different forms of the disease.

In conclusion, the results associated with the TH17/TREG scale and their correlations with fibrosis in systemic sclerosis open a way for new tools to manage this autoimmune disease, which up to today has neither treatment nor accurate diagnosis.

Vasoactive intestinal peptide secreting tumor (VIPoma) is a rare mostly malignant neuroendocrine tumor that is characterized by watery diarrhea, hypokalemia and achlorhydria due to the nonregulated increased secretion of VIP. VIPomas ar diagnosed by the presence of the most common symptoms, laboratory analysis of blood and stool, radiological imaging and immunohistochemical findings. Primary treatment includes fluid replacement, electrolyte balance correction, pharmacological treatment with somatostatin analogs, surgical resection and chemotherapy. This review aims to provide an insight into the latest research on VIPoma epidemiology, pathophysiology, diagnostics and treatment.

Background and objectives

Because of its severity, prevalence, and medical economic importance, heart failure is a chronic disease that is the subject of intense medical research. The aim of this article was to review the therapeutic innovations of the last decade that have been incorporated into the latest international recommendations for the treatment of heart failure.

Method

Review of literature and current guidelines.

Conclusion

The results of the clinical trials reviewed here represent major advances that will have a significant impact on quality of life, survival, rehospitalisation and, for certain treatments, a beneficial joint effect on commonly associated comorbidities such as diabetes and chronic renal failure.