Hypercoagulable states, also called thrombophilia, can either be congenital or acquired. Congenital thrombophilia, associated mainly with venous thrombosis, is either secondary to coagulation-inhibitor deficiencies, i.e., antithrombin, protein C and Protein S, or gain of function mutations, i.e., factor V Leiden and prothrombin G20210A mutations. Despite the relative frequency of these two mutations, they have not been associated with venous thrombosis recurrence. Most prevalent thrombophilia have a limited impact and usually does not change indications for duration of antithrombotic treatment or prophylaxis compared to decisions based on clinical factors. However, rare inherited thrombophilia such as antithrombin deficiency could justify a long-term anticoagulation. The main acquired thrombophilia, the Antiphospholipid syndrome (APS), is associated with both arterial and venous thrombosis. Its impact on patient management is significant: choice of the anticoagulant (DOAC vs. warfarin), duration of anticoagulation, screening of any organ involvement and systemic autoimmune disease, introduction of immunosuppressive therapy.

Cancer-associated venous thromboembolism (CAT) is common in patients with cancer and associated with significant morbidity and mortality. The incidence of CAT continues to rise, complicating patient care and burdening healthcare systems. Patients with cancer experiencing VTE face poorer prognoses, making prevention and effective management imperative. This narrative review synthesizes evidence on thromboprophylaxis in ambulatory patients with cancer receiving systemic therapy and acute treatment strategies for CAT. Risk assessment models (e.g., Khorana score) aid in identifying high-risk patients who may benefit from thromboprophylaxis. Pharmacological thromboprophylaxis with low molecular weight heparins (LMWHs) and direct oral anticoagulants (DOACs) has been shown to reduce the risk of CAT without significantly increasing the risk of bleeding complications. However, implementation of risk-based strategies remains limited in clinical practice. For acute CAT management, LMWHs have been the standard of care, but DOACs are increasingly favored due to their convenience and efficacy. However, challenges persist, including bleeding risks and drug interactions. Emerging therapies targeting Factor XI inhibitors present promising alternatives, potentially addressing current limitations in anticoagulation management for CAT.

Venous thromboembolism (VTE) presents a notable healthcare burden, particularly among the elderly, who experience increased risks and more severe complications. This review aims to use the extensive data from the RIETE registry, a comprehensive database on consecutive patients with VTE. We examine the clinical features, therapeutic approaches, and patient outcomes of VTE in elderly patients, compared to younger patients, offering a comprehensive understanding of management challenges and emphasizing the need for strategies that accommodate the unique challenges of this population.

Risk stratification of patients with acute pulmonary embolism (PE) assists with the selection of appropriate initial therapy and treatment setting. Patients with acute symptomatic PE that present with arterial hypotension or shock have a high risk of death, and treatment guidelines recommend strong consideration of reperfusion in this setting. For haemodynamically stable patients with PE, the combination of a negative clinical prognostic score and the absence of computed tomography-assessed right ventricle enlargement may accurately identify those at low-risk of short-term complications after the diagnosis of PE, and such patients might benefit from an abbreviated hospital stay or outpatient therapy. Some evidence suggests that the accumulation of factors indicating worse outcomes from PE on standard anticoagulation identifies the more severe stable patients with acute PE who might benefit from intensive monitoring and recanalization procedures, particularly if haemodynamic deterioration occurs. Current risk classifications have several shortcomings that might adversely affect clinical and healthcare decisions. Ongoing initiatives aim to address many of those shortcomings, and will hopefully help optimize risk stratification algorithms and treatment strategies.

Straightforward, accurate diagnostic management in patients presenting with clinically suspected pulmonary embolism (PE) is essential, since starting anticoagulant treatment may give important adverse effects of bleeding, while false exclusion of the disease may lead to recurrent VTE, with associated morbidity and mortality. In the past three decades, considerable improvement in the diagnostic management of PE has been made. Computed tomography pulmonary angiography (CTPA) has largely replaced conventional pulmonary angiography and ventilation-perfusion lung scanning as the imaging methods of choice. Several diagnostic algorithms, all able to minimize the need for radiological imaging have been developed and validated. Lastly, within the diagnostic algorithms, varying d-dimer cut-off levels have successfully been introduced to further downsize the need for radiological imaging.

Only few years after the first report on diagnosing acute pulmonary embolism (PE) with pulmonary angiography, studies began to investigate the effectiveness and safety of thrombolytic therapy for achieving early reperfusion. In 1992, Guy Meyer demonstrated the fast improvement of pulmonary haemodynamics after alteplase administration; this drug has remained the mainstay of thrombolysis for PE over almost 35 years. In the meantime, algorithms for PE risk stratification continued to evolve. The landmark Pulmonary Embolism International Thrombolysis (PEITHO) trial, led by Guy Meyer, demonstrated the clinical efficacy of thrombolysis for intermediate-risk PE, albeit at a relatively high risk of major, particularly intracranial bleeding. Today, systemic thrombolysis plays an only minor role in the real-world treatment of acute PE in the United States and Europe, but major trials are underway to test safer reperfusion regimens. Of those, the PEITHO-3 study, conceived by Guy Meyer and other European and North American experts, is an ongoing randomised, placebo-controlled, double-blind, multinational academic trial. The primary objective is to assess the efficacy of reduced-dose intravenous thrombolytic therapy against the background of heparin anticoagulation in patients with intermediate-high-risk PE. In parallel, trials with similar design are testing the efficacy and safety of catheter-directed local thrombolysis or mechanical thrombectomy. Increasingly, focus is being placed on long-term functional and patient-reported outcomes, including quality of life indicators, as well as on the utilization of health care resources. The pioneering work of Guy Meyer will thus continue to have a major impact on the management of PE for years to come.

Venous thromboembolism (VTE) is a common, serious condition that requires anticoagulation for at least three months to prevent recurrence and long-term complications. After this initial period, the decision to continue or stop anticoagulation depends on the balance between the risk of recurrent VTE and the risk of bleeding. Established guidelines suggest short-term anticoagulation for VTE caused by transient factors and indefinite anticoagulation for recurrent or cancer-associated VTE. However, for a first unprovoked VTE, decision-making remains challenging. Current predictive scores for recurrence and bleeding are not sufficiently reliable, and the safety and efficacy of reduced-dose anticoagulation remain unclear. In the future, precision and patient-centred medicine may improve treatment decisions in this area.

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.

Neuropathic pain continues to be a significant problem that lacks effective solutions for every single patient. In 2015, international guidelines (NeuPSIG) were published, while the French recommendations were updated in 2020. The purpose of this minireview is to provide an update on the process of developing evidence-based recommendations and explore potential changes to the current recommendations. Primary treatments for neuropathic pain include selective serotonin-norepinephrine reuptake inhibitors (SNRIs) such as duloxetine and venlafaxine, gabapentin, tricyclic antidepressants, as well as topical lidocaine and transcutaneous electrical nerve stimulation, which are specifically suggested for focal peripheral neuropathic pain. Pregabalin is a first line treatment according to international guidelines but second-line in the more recent French guidelines, due to lower efficacy seen in more recent studies and misuse risk. Additionally, tramadol, combination therapies, and psychotherapy as adjuncts are proposed second line; high-concentration capsaicin patches, and botulinum toxin A are proposed specifically for focal peripheral neuropathic pain. In cases where primary and secondary treatments prove insufficient, third-line options come into play. These include high-frequency repetitive transcranial magnetic stimulation (rTMS) targeting the motor cortex, spinal cord stimulation, and the use of strong opioids when no alternative is available. To ensure optimal management of neuropathic pain in real-life situations, it is imperative to disseminate these recommendations widely and secure the acceptance of practitioners. By doing so, we can bridge the gap between theory and practice, and enhance the overall care and treatment of individuals suffering from neuropathic pain.

Diabetic neuropathy is a frequent and severe degenerative complication of diabetes. The diagnosis is easily performed in painful symptomatic patients. Sensitivity disorders responsible for numbness, tingling, and loss of feeling are part and parcel of diabetic foot syndrome and require investigation in view of preventing trophic ulcers. To date, there exists no specific treatment for diabetic neuropathy possibly preventable by careful control of metabolic disorder. Effective management of diabetic patients would make it possible to limit the dramatic consequences of diabetic neuropathy while at the same time acting on other complications.

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.

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.

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.

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.