Preeclampsia is a severe pregnancy hypertensive disorder characterized by arterial hypertension and multiorgan involvement, most frequently affecting the renal, hepatic, and neurological systems. While its typical manifestations include headaches, visual disturbances, and/or epigastric pain, atypical presentations may occur and may lead to life-threatening complications. We report the case of a 33-year-old multiparous woman who developed sudden left-sided hemiparesis, hemisensory loss, homonymous hemianopia, and rightward conjugate gaze deviation within 24 hours after a cesarean delivery. Blood pressure was 169/103 mmHg. Laboratory tests revealed moderate anemia, elevated LDH, low haptoglobin, and significant proteinuria (4.84 g/24h). Brain MRI demonstrated ischemic lesions in the right fronto-parieto-insular cortico-subcortical regions, consistent with a subacute infarction. The diagnosis of preeclampsia complicated by ischemic stroke was established. The patient was treated with acetylsalicylic acid, levetiracetam, and antihypertensive therapy (methyldopa and nicardipine). She progressively improved and achieved full neurological recovery within six weeks. Prophylaxis with low-dose aspirin and low molecular weight heparin was recommended for future pregnancies. This case highlights the importance of considering preeclampsia as a potential underlying cause of postpartum ischemic stroke. Early recognition of neurological symptoms and timely neuroimaging are critical to prevent severe maternal morbidity.

The coexistence of uterine fibroids and gestational hypertension (GH) presents a high-risk obstetric scenario associated with adverse maternal-fetal outcomes. We present the case of a 27-year-old primigravida diagnosed with a 22 × 28 mm anterior uterine fibroid at 8 weeks' gestation, which enlarged to 52 × 48 mm by 29 weeks. At 21 weeks' gestation, she developed new-onset GH (blood pressure 150/98 mmHg) without proteinuria. Her management included prophylactic low-dose aspirin (75 mg daily), methyldopa (250 mg twice daily), and structured home blood pressure monitoring. When her blood pressure rose to 155/100 mmHg at 34 weeks, the methyldopa dosage was increased to three times daily, which successfully restored control. Following induction of labor at 40 weeks, the patient had an uncomplicated vaginal delivery of a healthy 3.3 kg neonate with an APGAR score of 9. The postpartum course was unremarkable, and the fibroid regressed significantly. This case illustrated that a proactive, guideline-based strategy uniting early prophylaxis, adaptive pharmacotherapy guided by home monitoring, and anticipatory care can successfully navigate the compounded risks of this clinical dyad, leading to a favorable outcome.

Advanced Parkinson's disease (PD) is marked by motor fluctuations and dyskinesias that progressively lose responsiveness to optimized oral therapy, making continuous dopaminergic delivery an essential therapeutic strategy. This narrative review examines infusion-based treatments for advanced PD, focusing on their clinical rationale, efficacy, safety, and practical implementation. Currently available infusion therapies include continuous subcutaneous apomorphine infusion (CSAI), intrajejunal levodopa-carbidopa gel (LCIG), intrajejunal levodopa-carbidopa-entacapone gel (LECIG), and subcutaneous foslevodopa- -foscarbidopa (LDp/CDp) infusion. These modalities provide more continuous dopaminergic stimulation than oral therapy, substantially reducing daily OFF time and increasing ON time without disabling dyskinesias, thereby improving quality of life (QoL). Their use may, however, be limited by adverse effects (AEs), including infusion-site reactions (ISR) (CSAI, LDp/CDp), the risk of hallucinations with LDp/CDp, and their invasive nature, as well as potential device-related complications or polyneuropathy associated with LCIG. Levodopa-carbidopa-entacapone gel offers improved levodopa bioavailability and a more user- -friendly device design compared with LCIG. A fully subcutaneous levodopa-carbidopa (LD/CD) infusion (ND0612) is also under investigation, with preliminary results suggesting acceptable safety-to-adverse-events risk ratio and clinical benefit. Despite increasing availability of infusion therapies in recent years, their utilization in clinical practice remains markedly lower than the estimated proportion of eligible patients, underscoring persistent systemic barriers. Further efforts aimed at optimizing qualification pathways, decentralizing access, and enhancing the integration of device-aided therapies (DAT) into routine advanced PD management are warranted.

Emerging contaminants can accumulate in water, soils, and crops; however, little is known about the potential exposure to honeybees. Using samples collected surrounding arable farming in Great Britain and nontarget techniques, we identified 119 suspect chemicals in hives. On average, each hive contained 6.8 (±3.01) active ingredients, these included human pharmaceuticals (64%), industrial chemicals (10%), surfactants (8%), and plasticizers (5%). Elevated concentrations of the anti-inflammatory flurandrenolide (582.3 ± 348.4 ng/g), the nonsteroidal anti-inflammatorydrug aspirin (358.2 ± 390.1 ng/g), the fungicide azoxystrobin (298.5 ± 159.9 ng/g), the antihypertensive methyldopa (123.4 ± 60 ng/g), and the anticonvulsant carbamazepine (79.97 ± 54.2 ng/g) were identified. Elevated concentrations of human-origin contaminants of emerging concern (CECs), and their increased frequency in arable areas, indicate that the reuse of contaminated fertilizers contributes to accumulation in hives across English landscapes. Critically, most of these contaminants lack toxicity data for honeybees, making it impossible to assess their acute or chronic risks.

Parkinson's disease (PD) has been associated with some types of food and drugs. Here, we query PubMed for the association of PD with foods and drugs, using a list of 217,776 compounds derived from the Human Metabolome Database (HMDB). To calculate associations, a Python script was developed to query PubMed for co-citations of PD with each compound, and adjust this count for compound abundance. Notably, PD is found to be associated with small-molecule drugs, adjunctive therapies, contraindicated drugs, diagnostic agents, biomarkers, conditional essential molecules, and inducers. Drugs include L-dopa (49%), carbidopa (63%), benserazide (50%), entacapone (74%), tolcapone (56%), rasagiline (76%), selegiline (46%), pargyline (4%), ropinirole (61%), pramipexole (56%), lisuride (27%), cabergoline (16%), bromocriptine (12%), and zonisamide (9%). Adjunctive therapies include droxidopa (33%), trihexyphenidyl (28%), biperiden (17%), amantadine (24%), memantine (7%), rivastigmine (13%), donepezil (6%), galantamine (4%), domperidone (6%), clonazepam (4%), tetrabenazine (16%), mazindol (13%), quetiapine (6%), and clozapine (4%). Contraindicated drugs include haloperidol (4%), sulpiride (3%), and methyldopa (6%). Diagnostic agents include FP-CIT (60%) and beta-CIT (43%). Biomarkers include 3-methoxytyrosine (48%) and homovanillic acid (12%). Endogenous cofactors include tetrahydrobiopterin (4%) and Coenzyme Q10 (4%). Chemical inducers of PD include 6-hydroxydopamine (40%), N-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 78%), tetrahydropyridine (77%), probenecid (4%), quinolinic acid (4%), 1,2,3,4-tetrahydroisoquinoline (TIQ, 16%), salsolinol (32%), rotenone (25%), and β-Methylamino-L-alanine (BMAA, 29%). Notably, our study highlights conditional essential endogenous cofactors associated with PD and emphasizes rational directions for investigation in PD.

Autoimmune hepatitis triggered by Herpes Zoster infection is a relatively rare condition and a diagnosis of exclusion, as there are other more common causes of autoimmune hepatitis. While evaluating a patient with suspected autoimmune hepatitis, common causes such as viral hepatitis, Epstein-Barr virus, and medications like amoxicillin-clavulanic acid, statins, nitrofurantoin and methyldopa must be ruled out. Furthermore, autoimmune processes like thyroiditis, type 1 diabetes mellitus, rheumatoid arthritis, and ulcerative colitis should be considered. Herpes Zoster virus is known to cause diseases such as post-herpetic neuralgia, meningitis, meningoencephalitis, myelitis, cranial neuropathies, keratitis, uveitis, scleritis, and vision loss. Rarely, it can also trigger an autoimmune process in the body, causing hepatitis. A major dilemma that can be encountered while evaluating a patient with suspected autoimmune hepatitis precipitated by Herpes Zoster infection is drug-induced liver injury, especially if the patient had been managed with a medication known to cause liver injury. Both drug-induced liver injury and Herpes Zoster hepatitis have overlapping clinical, laboratory and histological pictures that can pose a significant diagnostic challenge. We report a case of autoimmune hepatitis in an elderly female precipitated by Herpes Zoster infection. She was observed with findings typical of cholestatic liver disease, and an extensive workup, including imaging and liver biopsy, was done to determine the cause of liver injury. Her clinical presentation, laboratory and Imaging findings favored Herpes Zoster virus as the likely culprit for autoimmune hepatitis.