Background: Dissecting cellulitis of the scalp (DCS) is a rare, chronic neutrophilic dermatosis that is often refractory to conventional therapies. Case report: We present a 29-year-old male with treatment-resistant DCS who achieved rapid and sustained remission following off-label use of tofacitinib, a Janus kinase (JAK) inhibitor. Previous therapies, including antibiotics, corticosteroids, and isotretinoin, had failed. After 9 weeks of tofacitinib 10 mg daily, the patient showed marked improvement and maintained remission for 6 months without side effects. Conclusion: This case supports JAK inhibitors as a promising therapeutic strategy in refractory DCS, highlighting their potential role in managing challenging inflammatory dermatoses.

Acute hepatic failure is a rare but critical complication of Crimean‐Congo hemorrhagic fever (CCHF). This case presents acute hepatic failure with liver enzyme elevation and thrombocytopenia. The patient responded well to treatment that included ribavirin, lactulose, rifaximin, and supportive therapies. This case highlights the importance of early management in CCHF cases, and recovery even in dire clinical scenarios.

Hypertrophic cardiomyopathy (HCM) is the most prevalent hereditary cardiovascular disorder characterized by unexplained left ventricular hypertrophy, sarcomeric hypercontractility, and dynamic left ventricular outflow tract (LVOT) obstruction in approximately 70% of patients. Current therapies predominantly offer symptomatic relief through indirect modulation of cardiac function, leaving the underlying molecular pathophysiology unaddressed. Mavacamten, a first-in-class, selective allosteric inhibitor of β-cardiac myosin ATPase, exemplifies a precision pharmacological approach by directly targeting the sarcomeric hypercontractility fundamental to obstructive HCM (oHCM). This review synthesizes extensive clinical and preclinical evidence delineating mavacamten’s mechanism of action, pharmacokinetics influenced by CYP2C19 genotype variability, and its demonstrated efficacy and long-term safety in improving functional capacity, symptom burden, and cardiac remodeling. Landmark trials, including EXPLORER-HCM and MAVERICK-HCM, underscore mavacamten’s ability to reduce LVOT gradients, enhance diastolic function, and lower cardiac biomarkers, heralding a paradigm shift from symptomatic management to disease-modifying therapy. Despite current knowledge gaps in long-term outcomes and diverse population responses, mavacamten establishes a critical foundation for molecularly targeted therapeutics in HCM and broader cardiomyopathies.

Early recognition of atypical Wilson disease (WD) presentations, such as isolated stiffness, is essential to avoid misdiagnosis and facilitate timely intervention. A comprehensive evaluation, including advanced imaging and biochemical analysis, can help differentiate WD in cases where common neurological symptoms are absent, thus preventing progression to severe neurological impairment.

Aims: Viloxazine is a serotonin–norepinephrine modulatory agent that was recently approved by the U.S. Food and Drug Administration for the treatment of attention‐deficit/hyperactivity disorder (ADHD) in children, adolescents, and adults. This review aims to summarize the regulatory history, pharmacology, pharmacokinetics, clinical efficacy, safety, and current therapeutic role of viloxazine, while also highlighting gaps in the evidence and future research directions. Methods: A narrative literature review was conducted using PubMed, Google Scholar, and FDA regulatory documents. Relevant peer‐reviewed articles, including clinical trials, reviews, meta‐analyses, and prescribing information, were screened for data on viloxazine's historical antidepressant use, mechanism of action, pharmacokinetics, efficacy in ADHD, safety profile, drug interactions, and comparative effectiveness. Non‐peer‐reviewed sources were excluded. Results: Viloxazine was originally marketed in Europe in the 1970s as an antidepressant and showed a favorable safety profile over decades of use. Its pharmacological profile includes moderate norepinephrine reuptake inhibition with additional serotonergic activity, particularly 5‐HT2C agonism and 5‐HT2B antagonism, which supported its repurposing as an extended‐release formulation for ADHD. Multiple randomized, placebo‐controlled trials demonstrated that viloxazine extended‐release significantly improves ADHD symptoms in pediatric, adolescent, and adult populations. Reported effect sizes were generally smaller than those of stimulants but comparable to atomoxetine. The most common adverse events were somnolence, headache, nausea, decreased appetite, and insomnia. Viloxazine also has a pharmacokinetic profile compatible with once‐daily dosing, although clinically relevant drug interactions may occur through CYP1A2 inhibition. Conclusion: Viloxazine expands the range of non‐stimulant treatment options for ADHD and represents a successful example of drug repurposing in neuropsychiatry. Current evidence supports its efficacy and acceptable tolerability across the lifespan, particularly for patients who do not tolerate or respond adequately to stimulants. Nevertheless, evidence for its use beyond ADHD remains limited, and future studies should focus on head‐to‐head comparisons with other ADHD therapies, long‐term safety and efficacy, predictors of response, and potential off‐label psychiatric applications.