Association between chronic pain and acute coronary syndrome in the older population: a nationwide population-based cohort study.

BACKGROUND: Chronic pain (CP) may increase the risk of acute coronary syndrome (ACS); however, this issue in the older population remains unclear. Therefore, this study was conducted to clarify it. METHODS: We used the Taiwan National Health Insurance Research Database to identify older patients with CP between 2001 and 2005 as the study cohort. Comparison cohort was the older patients without CP by matching age, sex, and index date at 1:1 ratio with the study cohort in the same period. We also included common underlying comorbidities in the analyses. The risk of ACS was compared between the two cohorts by following up until 2015. RESULTS: A total of 17241 older patients with CP and 17241 older patients without CP were included in this study. In both cohorts, the mean age (± standard deviation) and female percentage were 73.5 (± 5.7) years and 55.4%, respectively. Spinal disorders (31.9%) and osteoarthritis (27.0%) were the most common causes of CP. Older patients with CP had an increased risk for ACS compared to those without CP after adjusting for all underlying comorbidities (adjusted sub-distribution hazard ratio [sHR] 1.18; 95% confidence interval: 1.07-1.30). The increasement of risk of ACS was more when the follow-up period was longer (adjusted sHR of < 3 years: 1.8 vs. <2 years: 1.75 vs. <1 year: 1.55). CONCLUSIONS: CP was associated with an increased risk of ACS in the older population, and the association was more prominent when the follow-up period was longer. Early detection and intervention for CP are suggested in this population.

Carpal tunnel syndrome in dentists compared to other populations: A nationwide population-based study in Taiwan.

BACKGROUND: Dentists may be at a higher risk of developing carpal tunnel syndrome (CTS) because of their use of frequent wrist and vibratory instruments at work; however, this issue remains unclear. Therefore, we conducted this study to clarify it. METHODS: Taiwan National Health Insurance Research Database was used for this nationwide population-based study. We identified 11,084 dentists, 74,901 non-dentist healthcare professionals (HCPs), and identical number of age- and sex-matched participants from the general population. Participants who had the diagnosis of CTS before 2007 were excluded. Between 2007 and 2011, the risk of developing CTS among dentists, non-dentist HCPs, and the general population was compared by following their medical histories. RESULTS: The cumulative incidence rate of CTS among dentists was 0.5% during the 5-year follow-up period. In dentists, the risk was higher in women (women: 0.7%; men: 0.4%) and older individuals (≥60 years: 1.0%; <60 years: 0.4%). After adjusting for age, sex, and underlying comorbidities, dentists had a lower risk of CTS than the general population (adjusted odds ratio [AOR]: 0.65, 95% confidence interval [CI]: 0.45-0.92). Dentists had a higher risk for CTS compared with non-dentist HCPs, although the difference was not statistically significant (AOR: 1.21; 95% CI: 0.90-1.64). CONCLUSIONS: In CTS, dentists had a lower risk than the general population and a trend of higher risk than non-dentist HCPs. The difference between dentists and non-dentist HCPs suggests that we should pay attention to dentists for potential occupational risk of this disease. However, further studies are warranted to better clarify it.

Algorithm to Improve Resuscitation Outcomes in Patients With Traumatic Out-of-Hospital Cardiac Arrest.

BACKGROUND: This study proposed an algorithm to improve resuscitation outcomes in the emergency department (ED) for patients with traumatic out-of-hospital cardiac arrest (TOHCA). We also performed a retrospective chart review of patient outcomes before and after implementing the algorithm and sought to define factors that might influence patient outcomes. METHODS: In September 2018, we implemented an algorithm for patients with TOHCA. This algorithm rapidly identifies possible causes of TOHCA and recommends appropriate interventions. We retrospectively reviewed the outcomes of all patients with TOHCA during a five-year period (comprising periods before and after the algorithm) and compared the results before and after the implementation of the algorithm. RESULTS: After this algorithm was implemented, the use of the ED interventions of blood transfusion, placement of a large-bore central venous catheter, and thoracostomy increased significantly. The rate of return of spontaneous circulation (ROSC) also increased (before vs. after: ROSC: 23.6% vs. 41.5%, P = 0.035). Regarding hospital admission and survival to hospital discharge, we observed the trend of increment (hospital admission: 18.2% vs. 24.6%, P = 0.394; survival to hospital discharge: 0.0% vs. 4.6%, P = 0.107). Admitted patients exhibited a higher end-tidal CO2 level during resuscitation than nonadmitted patients [admitted vs. nonadmitted: 41.5 (33.3-52.0) vs. 12.0 (7.5-18.8), P = 0.001]. CONCLUSION: Our algorithm prioritizes the three major treatable causes of TOHCA: impedance of venous return, hypovolemia, and hypoxia. We found that rate of ROSC increased with the increasing implementation of the ED interventions recommended by the algorithm.

Thyroid-stimulating hormone receptor antibodies during follow-up as remission markers in childhood-onset Graves' disease treated with antithyroid drugs.

Graves' disease is uncommon in children. The remission rate after antithyroid drugs (ATD) therapy is lower than in adults. We evaluated the clinical course of ATD therapy in children with Graves' disease in southern Taiwan to determine whether their biochemical markers could be used to predict remission in these patients. We retrospectively reviewed the clinical data of 53 children diagnosed with Graves' disease between 2009 and 2019. Clinical and biochemical parameters were analyzed for predictors of remission. About three-fourths of the patients were female. Their median age at diagnosis was 13 years. No sex differences were found in most clinical characteristics. There was no correlation between thyroid-stimulating hormone receptor antibody (TRAb) levels at diagnosis and thyroid function or adverse reactions to ATD. Relapse occurred in 62% of patients after discontinuation of first-course ATD therapy. Three variables-good initial response to ATD, a decrease in TRAb levels during the first year after diagnosis, and a decrease in TRAb levels during the second year after diagnosis-were significant predictors of remission for more than 18 months. In conclusion, children with Graves' disease who had early ATD-controlled Graves' disease and decreased TRAb levels during the first 2 years are likely to enter remission for more than 18 months.

HSP-70-Mediated Hyperbaric Oxygen Reduces Brain and Pulmonary Edema and Cognitive Deficits in Rats in a Simulated High-Altitude Exposure.

High-mountain sickness is characterized by brain and pulmonary edema and cognitive deficits. The definition can be fulfilled by a rat model of high-altitude exposure (HAE) used in the present study. This study aimed to investigate the protective effect of hyperbaric oxygen therapy (HBO2T) and to determine the underlying mechanisms. Rats were subjected to an HAE (9.7% O2 at 0.47 absolute atmosphere of 6,000 m for 3 days). Immediately after termination of HAE, rats were treated with HBO2T (100% O2 at 2.0 absolute atmosphere for 1 hour per day for 5 consecutive days) or non-HBO2T (21% O2 at 1.0 absolute atmosphere for 1 hour per day for 5 consecutive days). As compared to non-HAE+non-HBO2T controls, the HAE+non-HBO2T rats exhibited brain edema and resulted in cognitive deficits, reduced food and water consumption, body weight loss, increased cerebral inflammation and oxidative stress, and pulmonary edema. HBO2T increased expression of both hippocampus and lung heat shock protein (HSP-70) and also reversed the HAE-induced brain and pulmonary edema, cognitive deficits, reduced food and water consumption, body weight loss, and brain inflammation and oxidative stress. Decreasing the overexpression of HSP-70 in both hippocampus and lung tissues with HSP-70 antibodies significantly attenuated the beneficial effects exerted by HBO2T in HAE rats. Our data provide in vivo evidence that HBO2T works on a remodeling of brain/lung to exert a protective effect against simulated high-mountain sickness via enhancing HSP-70 expression in HAE rats.

Attenuating systemic inflammatory markers in simulated high-altitude exposure by heat shock protein 70-mediated hypobaric hypoxia preconditioning in rats.

BACKGROUND/PURPOSE: The primary goal of this study was to test whether high-altitude exposure (HAE: 0.9% O(2) at 0.47 ATA for 24 hours) was capable of increasing the systemic inflammatory markers as well as the toxic organ injury indicators in rats, with a secondary goal to test whether preinduction of heat shock protein (HSP) 70 by hypobaric hypoxia preconditioning (HHP: 18.3% O(2) at 0.66 ATA for 5 h/day on 5 days consecutively for 2 weeks) attenuated the proposed increased serum levels of both the systemic inflammatory markers and the toxic organ injury indicators. METHODS: Rats were assigned to: (1) non-HHP (21% O(2) at 1.0 ATA)+non-HAE (21% O(2) at 1.0 ATA) group; (2) non-HHP+HAE group; (3) HHP+non-HAE group; (4) HHP+HAE group; and (5) HHP+HSP70 antibodies (Ab)+HAE group. For the HSP70Ab group, a neutralizing HSP70Ab was injected intravenously at 24 hours prior to HAE. All the physiological and biochemical parameters were obtained at the end of HAE or the equivalent time period of non-HAE. Blood samples were obtained for determination of both the systemic inflammatory markers (e.g., serum tumor necrosis factor-α, interleukin-1ß, E-selectin, intercellular adhesion molecule-1, and liver myeloperoxidase activity) and the toxic organ injury indicators (e.g., nitric oxide metabolites, 2,3-dihydroxybenzoic acid, and lactate dehydrogenase). RESULTS: HHP, in addition to inducing overexpression of tissue HSP70, significantly attenuated the HAE-induced hypotension, bradycardia, hypoxia, acidosis, and increased tissue levels of both the systemic inflammatory markers and the toxic organ injury indicators. The beneficial effects of HHP in inducing tissue overexpression of HSP70 as well as in preventing the HAE-induced increased levels of the systemic inflammatory markers and the toxic organ injury indicators could be significantly reduced by HSP70Ab preconditioning. CONCLUSION: These results suggest that HHP may downgrade both the systemic inflammatory markers and the toxic organ injury indicators in HAE by upregulating tissue HSP70.

Carotid blowout syndrome.

Carotid blowout syndrome refers to the rupture of the carotid artery and its branches. Carotid blowout syndrome is a dangerous medical emergency typically resulting from complications of treatments for head and neck cancer. A patient without a prior history of head or neck cancer presented to the emergency department with a painless, enlarging neck mass was reported in this study. The mass progressed to acute airway obstruction during imaging of the lesion and necessitated emergency cricothyrotomy to secure the airway. The patient underwent four endovascular treatments to manage repeated bleeding thus producing the neurological complication of right middle cerebral artery infarction. Clinical manifestations, varied treatments, and common complications of carotid blowout syndrome were discussed.

Hypobaric hypoxia preconditioning attenuates acute lung injury during high-altitude exposure in rats via up-regulating heat-shock protein 70.

HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the expression of HSP70 in lungs prior to the onset of HAE. At 2 weeks after the start of HHP, animals were exposed to a simulated HAE of 6000 m in a hypobaric chamber for 24 h. Immediately after being returned to ambient pressure, the non-HHP animals had higher scores of alveolar oedema, neutrophil infiltration and haemorrhage, acute pleurisy (e.g. increased exudate volume, increased numbers of polymorphonuclear cells and increased lung myeloperoxidase activity), increased pro-inflammatory cytokines [e.g. TNF-α (tumour necrosis factor-α), IL (interleukin)-1ß and IL-6], and increased cellular ischaemia (i.e. glutamate and lactate/pyruvate ratio) and oxidative damage [glycerol, NOx (combined nitrate+nitrite) and 2,3-dihydroxybenzoic acid] markers in the BALF (bronchoalveolar fluid). HHP, in addition to inducing overexpression of HSP70 in the lungs, significantly attenuated HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage in the lungs. The beneficial effects of HHP in preventing the occurrence of HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage was reduced significantly by pretreatment with a neutralizing anti-HSP70 antibody. In conclusion, HHP may attenuate the occurrence of pulmonary oedema, inflammation, and ischaemic and oxidative damage caused by HAE in part via up-regulating HSP70 in the lungs.