Background: Botulinum toxin injections and suction-curettage have been separately shown to be effective in treating axillary hyperhidrosis but have not been compared in the same patients.
Objective: We sought to compare effectiveness of suction-curettage versus neurotoxin for the treatment of axillary hyperhidrosis.
Methods: Each of 20 patients was randomized to receive toxin injections to one axilla and suction-curettage to the contralateral axilla. The primary outcome measure was reduction of sweat rate measured by gravimetry, and the secondary measure was quality of life as measured by a patient-directed questionnaire.
Results: At 3 months posttreatment, toxin injections decreased baseline resting sweat production by 72.1% versus 60.4% (P = .29) for suction-curettage, and baseline exercise-induced sweat production by 73.8% versus 58.8% (P = .10). When patients were stratified into the categories of light and heavy sweaters, there was a difference among heavy sweaters, with exercise-induced sweat production lower by 10.48 mg/min or 34.3% (P = .0025) at toxin-treated sites. Compared with suction-curettage, toxin also resulted in greater improvements in quality of life by 0.80 points (P = .0002) and 0.90 points (P = .0017) at 3 and 6 months posttreatment, respectively, as measured by the patient questionnaire.
Limitations: The follow-up period was limited to 6 months.
Conclusions: By objective measures 3 months after treatment, neurotoxin injections are nominally more effective than suction-curettage in all cases, and markedly more effective in heavy sweaters. Patients have a very significant preference for neurotoxin injections at 3 months, and this is maintained at 6 months.
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http://dx.doi.org/10.1016/j.jaad.2013.02.013 | DOI Listing |
Sci Adv
January 2025
Department of Structural Biochemistry, Max Planck Institute of Molecular Physiology, Otto-Hahn-Str. 11, 44227 Dortmund, Germany.
Tc toxins are pore-forming virulence factors of many pathogenic bacteria. Following pH-induced conformational changes, they perforate the target membrane like a syringe to translocate toxic enzymes into a cell. Although this complex transformation has been structurally well studied, the reaction pathway and the resulting temporal evolution have remained elusive.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Microglia play an important role in immune memory. Lipopolysaccharide (LPS) triggers immune memory and primes microglia, resulting in brain pathologies and brain dysfunction following a second stimulus (1, 2). An increase in the C1q/ PSD95 expressions within microglia and excessively synaptic pruning were observed in mouse model of Alzheimer's disease (3).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA.
Background: Multiple AD risk genes are implicated in lipid metabolism, and plasma and brain lipid levels are altered in AD. Astrocytes are enriched in key lipid-related factors and are likely contributors to altered lipid homeostasis in AD. We hypothesize that APP/Aβ-related pathology and neuroimmune factors modulate astrocytic gene transcription that promote maladaptive changes in lipid pathways, including aberrant astrocytic production and release of lipids that could affect Aβ pathology and neuronal deficits.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Ivane Beritashvili Center of Experimental Biomedicine, Tbilisi, Georgia.
Background: Alzheimer's disease (AD) is a neurodegenerative disease that causes progressive cognitive decline over age 65. Individuals suffering from this disease suffer memory loss, and histological examination of the brains. Okadaic acid (OA), is a potent and selective inhibitor of protein phosphatases 1 and 2A.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Aging microglia accumulate lipid droplets (LDs), secrete pro-inflammatory cytokines, and are defective in phagocytosis. The E4 allele of Apolipoprotein E (APOE) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD) and is associated with increased neuroinflammation and LD accumulation. Here, we aimed to determine if the effects of aging and the E4 allele are synergistic in causing the accumulation of LDs seen in LOAD.
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