Amantadine can Ameliorate Lower Urinary Tract Dysfunction and Nocturnal Polyuria in Patients with Parkinson Disease and Vascular Parkinsonism

Background:Amantadine is a drug used for patients with Parkinson\u27s disease (PD) and vascular parkinsonism (VP). These patients often have lower urinary tract symptoms (LUTS) and nocturnal polyuria (NP). Thus, we investigated the effect of amantadine on these in parkinsonian patients.Methods:Twenty-two patients with LUTS, including 13 with PD and nine with VP, were recruited. We performed a urinary questionnaire, frequency-volume chart, and residual urine (RU) measurement before and after daily administration of 150 mg and 300 mg amantadine.Results:Before amantadine administration, mean daytime urinary frequency was 9.07(standard error [SE], 0.64), nighttime urinary frequency 2.89 (0.24), urinary urgency per week 24.2 (6.69), urge incontinence per month 15.1( 9.94), urine volume per void 145.6( 12.6) mL, and residual urine volume 12.5( 6.30) mL. After daily 150 mg amantadine administration, mean daytime and nighttime urinary frequency, urinary urgency, and urge incontinence decreased to 6.9( 0.42), 1.97( 0.21), 13.0( 3.58), and 14.2( 10.2), respectively, and urine volume per void increased to 174.1( 11.3) mL. NP( N=8) was ameliorated in six patients. No patient had side effects. After daily 300 mg amantadine administration( N=8), mean daytime and nighttimeurinary frequency, urinary urgency, and urge incontinence decreased to 6.90 (0.33), 1.69 (0.10), 5.88 (1.61), and 2.31 (0.61), respectively, and urine volume per void increased to180.2 (15.0) mL. NP (N=4) was ameliorated in two patients. One patient developed hallucination, and two patients developed flashing sensation.Conclusion:Amantadine has beneficial effects on LUTS and NP in patients with VP and PD

Influenza vaccine effectiveness against influenza A in children based on the results of various rapid influenza tests in the 2018/19 season.

During influenza epidemics, Japanese clinicians routinely conduct rapid influenza diagnostic tests (RIDTs) in patients with influenza-like illness, and patients with positive test results are treated with anti-influenza drugs within 48 h after the onset of illness. We assessed the vaccine effectiveness (VE) of inactivated influenza vaccine (IIV) in children (6 months-15 years old, N = 4243), using a test-negative case-control design based on the results of RIDTs in the 2018/19 season. The VE against influenza A(H1N1)pdm and A(H3N2) was analyzed separately using an RIDT kit specifically for detecting A(H1N1)pdm09. The adjusted VE against combined influenza A (H1N1pdm and H3N2) and against A(H1N1)pdm09 was 39% (95% confidence interval [CI], 30%-46%) and 74% (95% CI, 39%-89%), respectively. By contrast, the VE against non-A(H1N1)pdm09 influenza A (presumed to be H3N2) was very low at 7%. The adjusted VE for preventing hospitalization was 56% (95% CI, 16%-77%) against influenza A. The VE against A(H1N1)pdm09 was consistently high in our studies. By contrast, the VE against A(H3N2) was low not only in adults but also in children in the 2018/19 season

STAT3-dependent reactive astrogliosis in the spinal dorsal horn underlies chronic itch

Chronic itch is an intractable symptom of inflammatory skin diseases, such as atopic and contact dermatitis1,2,3. Recent studies have revealed neuronal pathways selective for itch4,5,6,7,8, but the mechanisms by which itch turns into a pathological chronic state are poorly understood. Using mouse models of atopic and contact dermatitis, we demonstrate a long-term reactive state of astrocytes in the dorsal horn of the spinal segments that corresponds to lesioned, itchy skin. We found that reactive astrogliosis depended on the activation of signal transducer and activator of transcription 3 (STAT3). Conditional disruption of astrocytic STAT3 suppressed chronic itch, and pharmacological inhibition of spinal STAT3 ameliorated the fully developed chronic itch. Mice with atopic dermatitis exhibited an increase in scratching elicited by intrathecal administration of the itch-inducer gastrin-releasing peptide (GRP)4, and this enhancement was normalized by suppressing STAT3-mediated reactive astrogliosis. Moreover, we identified lipocalin-2 (LCN2) as an astrocytic STAT3-dependent upregulated factor that was crucial for chronic itch, and we demonstrated that intrathecal administration of LCN2 to normal mice increased spinal GRP-evoked scratching. Our findings indicate that STAT3-dependent reactive astrocytes act as critical amplifiers of itching through a mechanism involving the enhancement of spinal itch signals by LCN2, thereby providing a previously unrecognized target for treating chronic itch