5 research outputs found
Botulinum Toxin A and B for Palmoplantar Hyperhidrosis
Introduction - Hyperhidrosis is characterized by unpredictable, uncontrollable and excessive sweating. It occurs at rest and is not related to temperature. Hyperhidrosis is a common disorder that has a negative impact on quality of life (QoL). The aim of this quality assurance study was to investigate how treatment of palmoplantar hyperhidrosis with botulinum toxin A (BTX-A) and botulinum toxin B (BTX-B) led to improvement of patient reported outcome measures related to QoL.
Methods - A total of 35 patients with palmar and/or plantar hyperhidrosis who had received BTX-A (Dysport®) and BTX-B (NeuroBloc®) for palmar hyperhidrosis and BTX-B for plantar hyperhidrosis were included in this study. In total, palms were injected with a median dose (low to high) of 400 (100–550) units BTX-A and a median dose (low to high) of 200 (200–500) units. BTX-B was used in the thenar and hypothenar areas to avoid muscle weakness. In the soles a total median dose (low to high) of 600 (475–1000) units BTX-B was injected.
Results - At follow-up 2 weeks post-treatment, patients’ Dermatology Life Quality Index (DLQI) score improved from 13 to 2 (p 
Conclusion - We found that BTX-A and BTX-B treatment for palmar hyperhidrosis and BTX-B treatment for plantar hyperhidrosis led to a substantial improvement of QoL
Causes of inferior relative survival after testicular germ cell tumor diagnosed 1953–2015: A population-based prospective cohort study
Background
Testicular germ cell tumor (TGCT) patients and survivors have excess mortality compared to the general male population, but relative survival (RS) has been scarcely studied. We investigated causes of excess mortality and their impact on RS among men diagnosed with TGCT in Norway, 1953–2015.
Methods and findings
Using registry data (n = 9541), standardized mortality ratios (SMRs) and RS were calculated. By December 31st, 2015, 816 testicular cancer (TC) and 1508 non-TC deaths had occurred (non-TC SMR: 1.36). Within five years of TGCT diagnosis, 80% were TC deaths. Non-TC second cancer (SC) caused 65% of excess non-TC deaths, of which 34% from gastric, pancreatic or bladder cancer. SC SMRs remained elevated ≥26 years of follow-up. In localized TGCT diagnosed >1979, SC SMRs were only elevated after seminoma. Cardiovascular disease caused 9% and other causes 26% of excess non-TC deaths, of which 58% from gastrointestinal and genitourinary disorders. RS continuously declined with follow-up. TGCT patients diagnosed >1989 had superior five-year TC-specific RS (98.3%), lower non-TC SMR (1.21), but elevated SMRs for several SCs, infections, Alzheimer’s disease, genitourinary disease and suicide. A limitation was lack of individual treatment data.
Conclusions
RS declines mainly from TC deaths <5 years after TGCT diagnosis. Later, excess SC mortality becomes particularly important, reducing RS even ≥26 years. Radiotherapy; standard adjuvant seminoma treatment 1980–2007, is likely an important contributor, as are chemotherapy and possibly innate susceptibilities. Vigilant long-term follow-up, including psychosocial aspects, is important. Further research should focus on identifying survivor risk groups and optimizing treatment
Causes of inferior relative survival after testicular germ cell tumor diagnosed 1953–2015: A population-based prospective cohort study
Background
Testicular germ cell tumor (TGCT) patients and survivors have excess mortality compared to the general male population, but relative survival (RS) has been scarcely studied. We investigated causes of excess mortality and their impact on RS among men diagnosed with TGCT in Norway, 1953–2015.
Methods and findings
Using registry data (n = 9541), standardized mortality ratios (SMRs) and RS were calculated. By December 31st, 2015, 816 testicular cancer (TC) and 1508 non-TC deaths had occurred (non-TC SMR: 1.36). Within five years of TGCT diagnosis, 80% were TC deaths. Non-TC second cancer (SC) caused 65% of excess non-TC deaths, of which 34% from gastric, pancreatic or bladder cancer. SC SMRs remained elevated ≥26 years of follow-up. In localized TGCT diagnosed >1979, SC SMRs were only elevated after seminoma. Cardiovascular disease caused 9% and other causes 26% of excess non-TC deaths, of which 58% from gastrointestinal and genitourinary disorders. RS continuously declined with follow-up. TGCT patients diagnosed >1989 had superior five-year TC-specific RS (98.3%), lower non-TC SMR (1.21), but elevated SMRs for several SCs, infections, Alzheimer’s disease, genitourinary disease and suicide. A limitation was lack of individual treatment data.
Conclusions
RS declines mainly from TC deaths <5 years after TGCT diagnosis. Later, excess SC mortality becomes particularly important, reducing RS even ≥26 years. Radiotherapy; standard adjuvant seminoma treatment 1980–2007, is likely an important contributor, as are chemotherapy and possibly innate susceptibilities. Vigilant long-term follow-up, including psychosocial aspects, is important. Further research should focus on identifying survivor risk groups and optimizing treatment