Restless leg syndrome (RLS) is a chronic disorder characterized by a compulsive urge to move the legs, accompanied by various subjective symptoms and a distinctive nyctimeral pattern. A negligent entity is drug-induced RLS, which may be challenging to recognize by practitioners due to its rarity. Among various drugs that can induce or exacerbate RLS, metoclopramide is notable; however, the literature primarily describes cases related to its intravenous forms. In this case presentation, a 33-year-old male experienced drug-related gastrointestinal (GI) symptoms after starting semaglutide for weight loss. Semaglutide was discontinued, and oral metoclopramide was administered to manage the GI symptoms. Subsequently, he developed RLS-like symptoms, which resolved within 48 hours of stopping metoclopramide. His family history included chronic RLS. Laboratory tests were normal. The case highlights a potential link between drug administration and transient RLS symptoms. This case suggests that RLS can be a rare, reversible side effect of oral metoclopramide. It emphasizes the need for careful monitoring of RLS symptoms in patients using this drug and highlights the variability of side effects depending on the method of drug administration. The case serves as a reminder of the unpredictable nature of drug reactions and the importance of vigilance in pharmacotherapy.

The prevalence of mental health disorders is high among people with Cystic Fibrosis. The psychological symptoms in CF are associated with poor adherence, worse treatment outcomes, and greater health utilization/cost. Mental health and neurocognitive Adverse Events (AEs) have been reported with all available Cystic Fibrosis Transmembrane conductance Regulator (CFTR) modulators in small groups of patients. We report our experience with a dose reduction strategy in 10 of our patients on elexacaftor/tezacaftor/ivacaftor (7.9% of total number of patients) who self-reported developing intense anxiety, irritability, sleep disturbance and/or mental slowness after initiation of full dose treatment. Standard dose elexacaftor/tezacaftor/ivacaftor resulted in 14.3 points improvement in mean Percent Predicted Forced Expiratory Volume in 1 s (ppFEV1), and a mean difference in sweat chloride of -39.3 mmol/L. We initially discontinued and/or reduced therapy according to the AEs severity, with a subsequent planned dose escalation every 4-6 weeks guided by sustainability of clinical effectiveness, absence of AEs recurrence, and patients\' preferences. Clinical parameters including lung function and sweat chloride were monitored for up to 12 weeks to assess ongoing clinical response to the reduced dose regimen. Dose reduction resulted in resolution of self-reported mental/psychological AEs, without loss of clinical effectiveness (ppFEV1 was 80.7% on standard dose, and 83.4% at 12 weeks on reduced dose; sweat chloride was 33.4 and 34 mmol/L on standard and reduced dose, respectively). Furthermore, in a subgroup of patients who completed 24 weeks of the reduced dose regimen, repeat low dose Computed Tomography imaging showed a significant response when compared to pre-initiation of elexacaftor/tezacaftor/ivacaftor.

The study presents a case of a 64-year-old patient with diagnosed Parkinson\'s disease and coexisting REM sleep disorders (RBD) confirmed in a polysomnographic examination. In this patient, the use of supplementary therapy - quetiapine (50mg/daily) - due to psychotic disorders, resulted in speech disorders with sensory-motor mixed aphasia type. Aphasia occurred on the fourth day after beginning the treatment with atypical neuroleptic. In MRI examination of the head, no \"fresh\" cerebral ischemia was found. No focal status epilepticus was reported in the video EEG trial. Results. Complete cure occurred after discontinuation of quetiapine administration. Conclusions. Due to the above, the side-effects of quetiapine treatment were assumed as the cause of focal neurological disorders.

Voriconazole is a second-generation azole widely used for the prevention and treatment of fungal infection in leukemia patients. We report a case of 9-year-old girl with T-cell acute lymphoblastic leukemia who developed hallucinations and visual disturbance after using voriconazole twice. These symptoms began acutely after treatment with voriconazole and resolved rapidly when the voriconazole was stopped. No specific cause was identified, and thus the symptoms were considered to be the adverse drug reactions (ADRs) of voriconazole. Simultaneous development of hallucinations and visual disturbance caused by voriconazole in children rarely have been reported before and the causes of these ADRs are unknown. Several other cases of hallucinations and (or) visual disturbance caused by voriconazole among 15-81 years old patients have been reported in the literature, and are reviewed. Those patients reminded us of the importance of being aware of hallucinations and visual disturbance associated with voriconazole treatment. In addition, we speculate that the hallucinations and visual disturbance are not related to the dosage form of voriconazole. We emphasize that it is also important to monitor the concentration of voriconazole regularly to avoid potential toxicity.

Amiodarone therapy is widely prescribed in patients with atrial fibrillation. The higher prevalence of this arrhythmic heart disease, and the specific age-related issues of homeostasis in the elderly population, makes this group particularly exposed to its adverse effects. Among the many described side-effects, neurological impairments are the less documented and studied. Because amiodarone can be responsible for severe complications, as described in the case below, a close monitoring is necessary throughout its prescription. Awareness should be brought on the amiodarone-induced neurological side-effects as they could be overlooked.

In forensic settings, the most common indication for clozapine is treatment-resistant schizophrenia (TRS). Clozapine has also been shown to be effective in reducing hostility, aggression and violence in patients with schizophrenia and is of benefit in comorbid substance use disorders. The decision to initiate or to discontinue recently initiated clozapine can have a profound beneficial or detrimental influence on the lives and safety of patients and the staff caring for them. We present a case in which treatment with clozapine proved effective in spite of earlier repeated discontinuation of clozapine out of fear of neuroleptic malignant syndrome (NMS). Elevation of creatine kinase was deemed to be indicative of NMS in the absence of clinical signs of NMS. In somatic medicine, it is well known that creatine kinase elevation has many causes, most of them non-harmful. Collaboration with clinical chemistry was shown to be very useful, if not essential; research in the 1980s found replicated evidence for both sex and race differences in creatine kinase levels. In addition, substantial intra-individual variation has been found over time in healthy individuals. The creatine kinase levels of this patient of African descent were within normal limits for the African population. Baseline creatine kinase assessment and repetition of this assessment after 2 weeks with careful interpretation are recommended in all clozapine-treated patients. The authors advocate the introduction of evidence-based creatine kinase cut-off points that reflect the biological differences between the sexes and among races. More intensive contact between psychiatrists and clinical chemist can facilitate faster diagnosis and better treatment.

Electronic health records (EHR) provide a valuable resource for assessing drug side-effects, but treatments are not randomly allocated in routine care creating the potential for bias. We conduct a case study using the Prior Event Rate Ratio (PERR) Pairwise method to reduce unmeasured confounding bias in side-effect estimates for two second-line therapies for type 2 diabetes, thiazolidinediones, and sulfonylureas.
Primary care data were extracted from the Clinical Practice Research Datalink (n = 41,871). We utilized outcomes from the period when patients took first-line metformin to adjust for unmeasured confounding. Estimates for known side-effects and a negative control outcome were compared with the A Diabetes Outcome Progression Trial (ADOPT) trial (n = 2,545).
When on metformin, patients later prescribed thiazolidinediones had greater risks of edema, HR 95% CI 1.38 (1.13, 1.68) and gastrointestinal side-effects (GI) 1.47 (1.28, 1.68), suggesting the presence of unmeasured confounding. Conventional Cox regression overestimated the risk of edema on thiazolidinediones and identified a false association with GI. The PERR Pairwise estimates were consistent with ADOPT: 1.43 (1.10, 1.83) vs. 1.39 (1.04, 1.86), respectively, for edema, and 0.91 (0.79, 1.05) vs. 0.94 (0.80, 1.10) for GI.
The PERR Pairwise approach offers potential for enhancing postmarketing surveillance of side-effects from EHRs but requires careful consideration of assumptions.

BACKGROUND: Mirtazapine is a noradrenergic and specific serotonergic antidepressant; its pharmacological profile indicates a low risk for dopaminergic adverse effects. To date, there has been only a single case report of Pisa syndrome associated with mirtazapine.
METHODS: The authors report a case involving a 79-year-old woman with bipolar disorder, in whom Pisa syndrome occurred after introduction of mirtazapine, and completely disappeared 3 days after suspension of the drug.
CONCLUSIONS: Aspects of this particular case suggest that Pisa syndrome is a possible side effect of Mirtazapine.

Biologic therapies may cause so-called \"paradoxical side-effects,\" that is, the onset or exacerbation of new symptoms/diseases for which biological treatment should be effective. Among these, psoriatic skin lesions have been described. We report a case series of ten patients with either new onset (seven cases) or worsening (three cases) of psoriasis occurring during a biologic therapy. Six patients were receiving a biologic monotherapy, while four patients were in combination treatment with methotrexate (MTX). Psoriasis remission was observed in two patients who discontinued biologic therapy. In the six patients in whom biologic therapy was not discontinued, a complete disappearance or a partial improvement of skin lesions was achieved following topic steroid therapy in two patients and three patients, respectively. In the remaining patient, psoriasis developed during Adalimumab monotherapy, which completely disappeared when the Infliximab and MTX combination was started. The potential pathogenetic mechanisms were shortly reviewed.

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