Clinical use of percutaneous needle electrolysis in musculoskeletal injuries: A critical and systematic review of the literature

Objective: To review the current scientific evidence for the clinical use of percutaneous needle electrolysis (PNE) in musculoskeletal conditions. Methods: A systematic electronic search was performed in biomedical databases. Only clinical studies on human subjects using PNE on musculoskeletal pathologies were included. Methodological quality and risk of bias were assessed using the methodological index for non-randomized studies (MINORS). Treatment protocols were described, and primary outcomes (pain, injury-related function, and tissue structure) were compared against other treatment modalities or control groups in short (<1 month), mid (1-3 months) and long term (>3 months).ResultsTwenty-one studies met eligibility criteria (14 comparative studies and 7 case series). Sixty-two percent were at moderate to high risk of bias. PNE was applied in a wide range of injury types (mostly tendon-related), and application protocols were heterogeneous in terms of dosage (intensity: 0.35-6mA; time: 9-90sec), frequency (from twice a week to once every 2 weeks) and treatment duration (1-10 weeks). PNE showed moderate effects on pain at short and mid-term compared to active exercise interventions alone and sham needling. There is limited evidence that PNE improves injury-related function compared to other treatment modalities and no evidence of tissue structure improvement after PNE application.ConclusionThere is paucity of high-quality clinical studies about PNE in musculoskeletal conditions and lack of consensus about treatment indications and application protocols. Although a moderate effect on pain at short and mid-term has been documented, further research is needed. (AU)

Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.

BACKGROUND: Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. METHODS: Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated. RESULTS: The percentage of frail mice was significantly lower in the G6PD-Tg than in the WT genotype, especially in 26-month-old mice where 50% of the WT were frail vs. only 13% of the Tg ones (P < 0.001). Skeletal muscle transcriptomic analysis showed an up-regulation of respiratory chain and oxidative phosphorylation (P = 0.009) as well as glutathione metabolism (P = 0.035) pathways in the G6PD-Tg mice. Accordingly, the Tg animals exhibited an increase in reduced glutathione (34.5%, P < 0.01) and a decrease on its oxidized form (-69%, P < 0.05) and in lipid peroxidation (4-HNE: -20.5%, P < 0.05). The G6PD-Tg mice also showed reduced apoptosis (BAX/Bcl2: -25.5%, P < 0.05; and Bcl-xL: -20.5%, P < 0.05), lower levels of the intramuscular adipocyte marker FABP4 (-54.7%, P < 0.05), and increased markers of mitochondrial content (COX IV: 89.7%, P < 0.05; Grp75: 37.8%, P < 0.05) and mitochondrial OXPHOS complexes (CII: 81.25%, P < 0.01; CIII: 52.5%, P < 0.01; and CV: 37.2%, P < 0.05). Energy expenditure (-4.29%, P < 0.001) and the respiratory exchange ratio were lower (-13.4%, P < 0.0001) while the locomotor activity was higher (43.4%, P < 0.0001) in the 20-month-old Tg, indicating a major energetic advantage in these mice. Short-term exercise training in young C57BL76J mice induced a robust activation of G6PD in skeletal muscle (203.4%, P < 0.05), similar to that achieved in the G6PD-Tg mice (142.3%, P < 0.01). CONCLUSIONS: Glucose 6-P dehydrogenase deficiency can be an underestimated risk factor for several human pathologies and even frailty. By overexpressing G6PD, we provide the first molecular model of robustness. Because G6PD is regulated by pharmacological and physiological interventions like exercise, our results provide molecular bases for interventions that by increasing G6PD will delay the onset of frailty.

Allopurinol partially prevents disuse muscle atrophy in mice and humans.

Disuse muscle wasting will likely affect everyone in his or her lifetime in response to pathologies such as joint immobilization, inactivity or bed rest. There are no good therapies to treat it. We previously found that allopurinol, a drug widely used to treat gout, protects muscle damage after exhaustive exercise and results in functional gains in old individuals. Thus, we decided to test its effect in the prevention of soleus muscle atrophy after two weeks of hindlimb unloading in mice, and lower leg immobilization following ankle sprain in humans (EudraCT: 2011-003541-17). Our results show that allopurinol partially protects against muscle atrophy in both mice and humans. The protective effect of allopurinol is similar to that of resistance exercise which is the best-known way to prevent muscle mass loss in disuse human models. We report that allopurinol protects against the loss of muscle mass by inhibiting the expression of ubiquitin ligases. Our results suggest that the ubiquitin-proteasome pathway is an appropriate therapeutic target to inhibit muscle wasting and emphasizes the role of allopurinol as a non-hormonal intervention to treat disuse muscle atrophy.

Alopurinol y su papel en el tratamiento de la sarcopenia / Allopurinol and its role in the treatment of sarcopenia

La xantina oxidasa (XO) es la enzima que cataliza la oxidación de hipoxantina a xantina y de esta a ácido úrico, por lo que desempeña un importante papel en el catabolismo de las purinas. El alopurinol, un análogo de las purinas, es un conocido inhibidor de la XO ampliamente utilizado en la práctica clínica para el tratamiento de la gota. Estudios recientes indican que el alopurinol reduce el estrés oxidativo y mejora la función vascular en diversas enfemedades cardiometabólicas, aumenta el tiempo de ejercicio en pacientes con angina de pecho y mejora la eficiencia de la contractilidad miocárdica en la insuficiencia cardiaca. La XO también ejerce un papel importante en la generación de radicales libres durante la contracción muscular, y por tanto se ha relacionado con el daño muscular asociado al ejercicio físico agotador. Diversos grupos de investigación han demostrado el efecto protector del alopurinol en la prevención de este tipo de daño. Teniendo en cuenta estos antecedentes, en este trabajo nos hemos planteado revisar el posible papel del alopurinol en el tratamiento de la sarcopenia, un síndrome geriátrico caracterizado por la progresiva y generalizada pérdida de masa y fuerza muscular, que supone un aumento del riesgo de discapacidad, baja calidad de vida y muerte (AU)

Xanthine oxidase (XO) is an enzyme that catalyzes the oxidation of hypoxanthine to xanthine and uric acid and plays an important role in purine catabolism. The purine analogue, allopurinol, is a well-known inhibitor of XO widely used in the clinical management of gout and conditions associated with hyperuricemia. More recent data indicate that allopurinol reduces oxidative stress and improves vascular function in several cardiometabolic diseases, prolongs exercise time in angina, and improves the efficiency of cardiac contractility in heart failure. XO also plays an important role in free radical generation during skeletal muscle contraction and thus, it has been related to the muscle damage associated to exhaustive exercise. Several research groups have shown the protective effect of allopurinol in the prevention of this type of damage. Based on this background, a critical overview is presented on the possible role of allopurinol in the treatment of sarcopenia, a geriatric syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength with a risk of adverse outcomes, such as physical disability, poor quality of life and death (AU)

[Allopurinol and its role in the treatment of sarcopenia]. / Alopurinol y su papel en el tratamiento de la sarcopenia.

Xanthine oxidase (XO) is an enzyme that catalyzes the oxidation of hypoxanthine to xanthine and uric acid and plays an important role in purine catabolism. The purine analogue, allopurinol, is a well-known inhibitor of XO widely used in the clinical management of gout and conditions associated with hyperuricemia. More recent data indicate that allopurinol reduces oxidative stress and improves vascular function in several cardiometabolic diseases, prolongs exercise time in angina, and improves the efficiency of cardiac contractility in heart failure. XO also plays an important role in free radical generation during skeletal muscle contraction and thus, it has been related to the muscle damage associated to exhaustive exercise. Several research groups have shown the protective effect of allopurinol in the prevention of this type of damage. Based on this background, a critical overview is presented on the possible role of allopurinol in the treatment of sarcopenia, a geriatric syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength with a risk of adverse outcomes, such as physical disability, poor quality of life and death.

What are obese patients able to eat after Roux-en-Y gastric bypass?

BACKGROUND/AIMS: The goal of this study was to analyze the likelihood of patients undergoing Roux-en-Y gastric bypass (RYGB) to recover a normal daily food intake, and the possible influence of dietary and exercise habits on long-term weight loss. METHODS: The sample included 107 morbidly obese postoperative patients with at least 1 year of follow-up. The data collected included anthropometry, dietary and exercise habits, and information on ingested food. The unpaired Student's t test and the multivariate step-by-step regression were used in the analysis. RESULTS: The mean preoperative BMI was 50.7 ± 11.8 kg/m(2), which had decreased at the moment of survey to 31.7 ± 5.4 kg/m(2). The mean % Excess of BMI Lost (%EBMIL) was 77.4 ± 23.7%. The nutritional components of diet were similar to those for the nonobese population. There were no significant differences in %EBMIL regarding number of meals, social habits, components of diet, or amount of exercise. The daily mean caloric intake (1,364 ± 293 kcal) was the only parameter significantly related to the %EBMIL outcome. More than 30% of the patients had intolerance to certain foods. CONCLUSION: Obese patients undergoing RYGB can establish a postoperative lifestyle and diet similar to the ideal. Only the daily amount of ingested calories demonstrated a statistically significant influence on weight loss over time.

Eponym : Grisel syndrome.

Grisel syndrome or atlantoaxial non-traumatic subluxation is a rare entity, poorly described in pediatric literature, although it is a pathology that usually appears in young children. The typical presentation is a torticollis with a previous surgical antecedent (mainly a surgery of the ear, nose, and throat area like adenoidectomy) or after an upper tract respiratory infection. A prompt diagnosis is essential for a successful evolution, and the treatment in most cases is conservative. We report a case of an 8-year-old girl with a typical evolution of this unusual complication. In our case, the most important element for diagnosis was the 3D CT scanner, and the treatment was conservative with a successful outcome. Pediatricians should be aware of this rare but potentially serious entity to establish the correct treatment and avoid complications.

Repeated muscle biopsies through a single skin incision do not elicit muscle signaling, but IL-6 mRNA and STAT3 phosphorylation increase in injured muscle.

To determine if muscle biopsies can be repeated using a single small (5-6 mm) skin incision without inducing immediate MAPK activation or inflammation in the noninjured areas, the phosphorylation of ERK1/2, p38-MAPK, c-Jun NH(2)-terminal kinases (JNKs), IκBα, IKKα, and signal transducer and activator of transcription 3 (STAT3) was examined concurrent with IL-6 mRNA in six muscle biopsies obtained from the vastus lateralis of five men. Four biopsies were obtained through the same incision (5-6 mm) from the right leg (taken at 0, 30, 123, and 126 min) and another two each from new incisions performed in the left leg (at 31 and 120 min), while the subjects rested supine. The first three biopsies from the right leg were taken ∼3 cm apart from prebiopsied areas. The last biopsy was obtained from the same point from which the second biopsy was sampled. The three biopsies performed through the same skin incision from noninjured muscle areas showed similar levels of ERK1/2, p38-MAPK, JNK, IKKα, IκBα, and STAT3 phosphorylation and similar IL-6 mRNA content. There were no significant differences in the levels of ERK1/2, p38-MAPK, JNK, IKKα, and IκBα phosphorylation between the mean of the three biopsies obtained from the same incision and the sixth biopsy obtained from an injured area. STAT3 phosphorylation was increased by ∼3.5-fold in the sixth biopsy compared with the mean the three biopsies obtained from the same incision (P < 0.05), and IL-6 mRNA content was increased by 1.8-fold (P < 0.05). In summary, repeated muscle biopsies can be performed through a single 5- to 6-mm skin incision without eliciting muscle signaling through cascades responding to cellular stress, inflammation, or muscle damage. STAT3 phosphorylation is an early event in the healing response to muscle injury, probably mediated by the autocrine production of IL-6.

¿Mejora la calidad con la implantación de centros de salud? Una visión desde la hospitalización evitable / Does the development of primary healthcare centers improve quality? The perspective of avoidable hospitalizations

Objetivo: Las hospitalizaciones evitables (HE) son un conjunto de diagnósticos en los que una atención primaria de salud efectiva y adecuada hubiera evitado su ingreso hospitalario. Por tanto, su control sirve como medida del nivel de calidad obtenido en los centros de salud. Pacientes y método: Se realizó un estudio prospectivo individual de todos los pacientes ingresados (1999-2000) en un hospital procedentes de 2 zonas, una con un modelo tradicional de atención primaria (consultorio) y otro con un modelo moderno de centro de salud. El período de seguimiento fue de 2 años. A los pacientes que ingresaron se les pasó una encuesta. Para el estudio se empleó un listado de códigos de HE ya utilizado en otros trabajos. Resultados: La población del consultorio tuvo un 22 por ciento más riesgo de HE ajustado por morbilidad que la correspondiente del centro de salud. La incidencia anual poblacional fue de 10 por 1.000 habitantes. El factor más influyente para la HE fue ser atendido en un consultorio (RRa = 3,3), seguido por ser varón y tener un nivel económico bajo (RRa = 2,8), las edades extremas de la vida (joven y tercera) y la poca accesibilidad del centro (RRa = 2,2). También influyeron, aunque de forma más moderada, la estancia hospitalaria prolongada. No influyó el nivel de satisfacción de los pacientes. Conclusiones: Se demuestra que, conforme se mejoran los centros de atención primaria pasando al nuevo modelo, se reduce el riesgo de HE (AU)