Psoriasis is an inflammatory skin disorder characterized by epithelial hyperplasia and infiltration of inflammatory cells. Several immunological therapies have been developed for its treatment, including IL-17 inhibitors such as secukinumab, ixekizumab and bimekizumab. The safety profile of IL-17 inhibitors includes infectious diseases, gastrointestinal disorders, headaches, and cutaneous conditions such as eczema. Here, we report the first case of vitiligo, a depigmenting skin disorder characterized by the selective loss of melanocytes, occurring during treatment with bimekizumab. This case involved a 42-year-old man who achieved complete skin clearance of psoriasis plaques under bimekizumab therapy. After 11 months of treatment, he developed vitiligo patches on his face. These lesions resolved following discontinuation of bimekizumab, minipulse therapy and ruxolitinib cream application. Vitiligo occurrence has been previously observed with other IL-17 inhibitors, including secukinumab and ixekizumab (11 other cases). Although IL-17 is believed to play a role in the pathophysiology of vitiligo, its exact mechanism remains unclear. Paradoxal vitiligo may represent a class effect of IL-17 inhibitors, particularly in patients with psoriasis. This potential adverse effect should be considered, especially in patients with a personal or family history of vitiligo or other depigmentation disorders. Interestingly, stability or even repigmentation has been observed in patients who continued anti-IL-17 therapy, regardless of whether they received symptomatic treatment. Given the efficacy of anti-IL17 inhibitors in psoriasis, the risk-benefit balance should be carefully discussed in this context.

We report the case of a 14-year-old boy who developed motor and vocal tics following sublingual immunotherapy with OSIRIS Acariens mix for allergic rhinitis. The tics resolved upon temporary discontinuation and reappeared upon rechallenge. To our knowledge, this is the first report of such an adverse event associated with this allergen extract. We discuss the potential link between allergic diseases, immunotherapy, and tic disorders, highlighting the need for careful monitoring of unexpected adverse events.

Buprenorphine therapy is widely used in the treatment of opioid use disorder, and the use of its long-acting formulations is increasing. This raises concerns among healthcare professionals when analgesic management becomes necessary, due to its pharmacological properties. This article provides a synthesis of current pharmacological evidence and its implications for the management of acute and chronic pain, whether planned or unplanned. Practical landmarks are proposed according to the type of pain, the formulation used (buccal or subcutaneous), and the clinical context. Available data support the continuation of buprenorphine in most situations, including surgical settings, and suggest that a rational use of multimodal analgesia enables safe and effective pain management. Discontinuation of buprenorphine, long recommended to allow conventional analgesia with full opioid agonists, now appears to be a minority option, reserved for exceptional and anticipated cases. The management of patients receiving buprenorphine should not be viewed as a constraint, but rather as a pharmacological adaptation scenario grounded in well-established principles.

Severe cutaneous adverse drug reactions (SCARs), comprising mainly Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms, acute generalized exanthematous pustulosis, generalized bullous fixed drug eruption (GBFDE), are rare adverse reactions to drugs, hampered by a significant morbidity and mortality. Due to their unpredictable nature, they completely disrupt the benefit-risk balance of drug prescription. Nonetheless, a partial predictability is emerging. Firstly, all drugs do not carry the same risk for SCARs. Drugs carrying the higher risk are allopurinol, carbamazepine, lamotrigine, iodinated contrast media, and antibiotics, particularly sulfonamides and aminopenicillins. In addition, main risk factors comprise genetic polymorphisms of the HLA system and increased drug dosage. A targeted HLA genetic screening together with drug avoidance in case of high risk allowed to reduce the incidence of SCARs associated with carbamazepine and allopurinol. Similarly, a progressive titration of lamotrigine dose allowed to reduce the incidence of SCARs associated with lamotrigine. Pharmacovigilance databases allow the quick identification of culprit drugs, together with the implementation of whistle-blowing policies. Nonetheless, they present with quantitative and qualitative limitations and their own particular biases. Pharmacoepidemiologic databases allow the computation of SCAR incidences and confirm previously identified associations between drugs and SCARs. They may also allow help to identify the main clinical risk factors, e.g., chronic renal disease and Asian ethnicity for allopurinol. Nonetheless, they are limited by measure bias and lack of clinical and biological data. Ultimately, clinical and pharmacogenomic databases allow the identification of more precise risk factors, comprising precise genetic polymorphisms, drug dosage and impaired metabolism. The combination of all allows to establish a personalized risk stratification across SCARs subtypes and drug prescriptions. Ultimately, this allows the establishment of prescribing policies and the decrease of SCARs incidence.

In 2024, the therapeutic drug monitoring and treatment personalization working group of the Société française de pharmacologie et de thérapeutique (French Society of Pharmacology and Therapeutics) drew up a white paper, the aim of which is to present the current state of the biological pharmacology discipline, describe the skills required to exercise the profession, define the scope of professional activity, identify the discipline's current strengths and areas for improvement, with the ultimate aim of proposing changes to the profession of biological pharmacologist. This document is divided into several parts: a preamble outlining the panorama of biological pharmacology in France; a review of the current situation, outlining what a pharmacological biologist is, his or her missions, the strengths and weaknesses of the profession, and the prerequisites in terms of training; a reference framework of competencies for the pharmacological biologist; and, finally, the prospects and new missions of the pharmacological biologist. The purpose of this document is to serve as a term of reference, to help define the profession of pharmacological biologist, and to structure the discipline so that it can evolve into a profession at the interface between biology and the clinic.

Pruritus (itch) is defined as an unpleasant sensation provoking the urge to scratch and can be understood both as a symptom and, when lasting more than six weeks, as a disease entity termed chronic pruritus (CP). CP is characterized by complex neurobiological changes and can persist independently of the initial trigger, significantly impairing quality of life. Advances since the 1990s in understanding itch pathophysiology have led to the development of numerous targeted therapies, although many treatments remain off-label. Pruritus is classified into dermatological, systemic, neuropathic, and psychogenic categories, often with overlapping etiologies. Effective management prioritizes identifying and treating the underlying cause. Pathophysiologically, itch originates from specialized peripheral sensory neurons (pruriceptors), which transmit signals through histaminergic and non-histaminergic pathways. While histamine plays a role mainly in urticaria, chronic itch is largely mediated by non-histaminergic mechanisms involving cytokines, neuropeptides, proteases, transient receptor potential (TRP) channels, and Mas-related G-protein-coupled receptors (MRGPRs). Keratinocytes, mast cells, and immune mediators such as IL-31, IL-4, and IL-13 actively participate in itch signaling, creating neuroimmune feedback loops. Peripheral and central sensitization, spinal disinhibition, and altered pain-itch interactions sustain chronic itch and the itch-scratch cycle, particularly in chronic prurigo (CPG), a distinct disease model for CP. Therapeutic strategies target multiple levels of itch processing. Traditional treatments include antihistamines, topical anesthetics, calcineurin inhibitors, antidepressants, gabapentinoids, and immunosuppressants, though efficacy varies. Recent breakthroughs include biologics targeting TH2 pathways (dupilumab, nemolizumab), JAK inhibitors, κ-opioid receptor agonists (difelikefalin), and IBAT inhibitors (for cholestatic pruritus). Novel targets under investigation include MRGPRs, PARs, KIT receptors, OX-40, and sodium channels.