Central giant-cell granuloma in a patient with neurofibromatosis type 1: 7 years of follow-up.

Neurofibromatosis type 1 (NF1) is an autosomally dominant tumor suppressor syndrome and multisystem disease. Central giant-cell granulomas (CGCGs) can be seen in patients with NF1. A 21-year-old female was diagnosed with two CGCGs, one in the mandible and then one in the maxilla, in a 7-year period. Increased incidence of CGCGs in NF1 patients was thought to be caused by an underlying susceptibility to developing CGCG-like lesions in qualitatively abnormal bone, such as fibrous dysplasia. However, germline and somatic truncating second-hit mutations in the NF1 gene have been detected in NF1 patients with CGCGs, validating that they are NF1-associated lesions. Oral manifestations in patients with NF1 are very common. Knowledge of these manifestations and the genetic link between NF1 and CGCGs will enhance early detection and enable optimal patient care.

Prepubertal castration eliminates sex differences in lifespan and growth trajectories in genetically heterogeneous mice.

Sex differences in aging and longevity have been widely observed, with females consistently outliving males across human populations. However, the mechanisms driving these disparities remain poorly understood. In this study, we explored the influence of post-pubertal testicular effects on sex differences in aging by prepubertally castrating genetically heterogeneous (UM-HET3) mice, a unique mouse model that emulates human sex differences in age-related mortality. Prepubertal castration eliminated the longevity disparity between sexes by reducing the elevated early- to mid-life mortality rate observed in males and extending their median lifespan to match that of females. Additionally, castration extended the duration of body weight growth and attenuated the inverse correlation between early-age body weight and lifespan in males, aligning their growth trajectories with those of females. Our findings suggest that post-pubertal testicular actions in genetically diverse mice are primarily responsible for sex differences in longevity as well as growth trajectories. These findings offer a foundation for further investigation into the fundamental mechanisms driving sex-specific aging patterns and the development of potential pro-longevity interventions.

Lifespan benefits for the combination of rapamycin plus acarbose and for captopril in genetically heterogeneous mice.

Mice bred in 2017 and entered into the C2017 cohort were tested for possible lifespan benefits of (R/S)-1,3-butanediol (BD), captopril (Capt), leucine (Leu), the Nrf2-activating botanical mixture PB125, sulindac, syringaresinol, or the combination of rapamycin and acarbose started at 9 or 16 months of age (RaAc9, RaAc16). In male mice, the combination of Rapa and Aca started at 9 months and led to a longer lifespan than in either of the two prior cohorts of mice treated with Rapa only, suggesting that this drug combination was more potent than either of its components used alone. In females, lifespan in mice receiving both drugs was neither higher nor lower than that seen previously in Rapa only, perhaps reflecting the limited survival benefits seen in prior cohorts of females receiving Aca alone. Capt led to a significant, though small (4% or 5%), increase in female lifespan. Capt also showed some possible benefits in male mice, but the interpretation was complicated by the unusually low survival of controls at one of the three test sites. BD seemed to produce a small (2%) increase in females, but only if the analysis included data from the site with unusually short-lived controls. None of the other 4 tested agents led to any lifespan benefit. The C2017 ITP dataset shows that combinations of anti-aging drugs may have effects that surpass the benefits produced by either drug used alone, and that additional studies of captopril, over a wider range of doses, are likely to be rewarding.

Canagliflozin extends life span in genetically heterogeneous male but not female mice.

Canagliflozin (Cana) is an FDA-approved diabetes drug that protects against cardiovascular and kidney diseases. It also inhibits the sodium glucose transporter 2 by blocking renal reuptake and intestinal absorption of glucose. In the context of the mouse Interventions Testing Program, genetically heterogeneous mice were given chow containing Cana at 180 ppm at 7 months of age until their death. Cana extended median survival of male mice by 14%. Cana also increased by 9% the age for 90th percentile survival, with parallel effects seen at each of 3 test sites. Neither the distribution of inferred cause of death nor incidental pathology findings at end-of-life necropsies were altered by Cana. Moreover, although no life span benefits were seen in female mice, Cana led to lower fasting glucose and improved glucose tolerance in both sexes, diminishing fat mass in females only. Therefore, the life span benefit of Cana is likely to reflect blunting of peak glucose levels, because similar longevity effects are seen in male mice given acarbose, a diabetes drug that blocks glucose surges through a distinct mechanism, i.e., slowing breakdown of carbohydrate in the intestine. Interventions that control daily peak glucose levels deserve attention as possible preventive medicines to protect from a wide range of late-life neoplastic and degenerative diseases.

Hyperadrenocorticism of calorie restriction contributes to its anti-inflammatory action in mice.

Calorie restriction (CR), which lengthens lifespan in many species, is associated with moderate hyperadrenocorticism and attenuated inflammation. Given the anti-inflammatory action of glucocorticoids, we tested the hypothesis that the hyperadrenocorticism of CR contributes to its attenuated inflammatory response. We used a corticotropin-releasing-hormone knockout (CRHKO) mouse, which is glucocorticoid insufficient. There were four controls groups: CRHKO mice and wild-type (WT) littermates fed either ad libitum (AL) or CR (60% of AL food intake), and three experimental groups: (a) AL-fed CRHKO mice given corticosterone (CORT) in their drinking water titrated to match the integrated 24-hr plasma CORT levels of AL-fed WT mice, (b) CR-fed CRHKO mice given CORT to match the 24-hr CORT levels of AL-fed WT mice, and (c) CR-fed CHRKO mice given CORT to match the 24-hr CORT levels of CR-fed WT mice. Inflammation was measured volumetrically as footpad edema induced by carrageenan injection. As previously observed, CR attenuated footpad edema in WT mice. This attenuation was significantly blocked in CORT-deficient CR-fed CRHKO mice. Replacement of CORT in CR-fed CRHKO mice to the elevated levels observed in CR-fed WT mice, but not to the levels observed in AL-fed WT mice, restored the anti-inflammatory effect of CR. These results indicate that the hyperadrenocorticism of CR contributes to the anti-inflammatory action of CR, which may in turn contribute to its life-extending actions.

Hydrogen sulfide ameliorates aging-associated changes in the kidney.

Aging is associated with replacement of normal kidney parenchyma by fibrosis. Because hydrogen sulfide (H2S) ameliorates kidney fibrosis in disease models, we examined its status in the aging kidney. In the first study, we examined kidney cortical H2S metabolism and signaling pathways related to synthesis of proteins including matrix proteins in young and old male C57BL/6 mice. In old mice, increase in renal cortical content of matrix protein involved in fibrosis was associated with decreased H2S generation and AMPK activity, and activation of insulin receptor (IR)/IRS-2-Akt-mTORC1-mRNA translation signaling axis that can lead to increase in protein synthesis. In the second study, we randomized 18-19 month-old male C57BL/6 mice to receive 30 µmol/L sodium hydrosulfide (NaHS) in drinking water vs. water alone (control) for 5 months. Administration of NaHS increased plasma free sulfide levels. NaHS inhibited the increase in kidney cortical content of matrix proteins involved in fibrosis and ameliorated glomerulosclerosis. NaHS restored AMPK activity and inhibited activation of IR/IRS-2-Akt-mTORC1-mRNA translation axis. NaHS inhibited age-related increase in kidney cortical content of p21, IL-1ß, and IL-6, components of the senescence-associated secretory phenotype. NaHS abolished increase in urinary albumin excretion seen in control mice and reduced serum cystatin C levels suggesting improved glomerular clearance function. We conclude that aging-induced changes in the kidney are associated with H2S deficiency. Administration of H2S ameliorates aging-induced kidney changes probably by inhibiting signaling pathways leading to matrix protein synthesis.

Lifelong reduction in complex IV induces tissue-specific metabolic effects but does not reduce lifespan or healthspan in mice.

Loss of SURF1, a Complex IV assembly protein, was reported to increase lifespan in mice despite dramatically lower cytochrome oxidase (COX) activity. Consistent with this, our previous studies found advantageous changes in metabolism (reduced adiposity, increased insulin sensitivity, and mitochondrial biogenesis) in Surf1-/- mice. The lack of deleterious phenotypes in Surf1-/- mice is contrary to the hypothesis that mitochondrial dysfunction contributes to aging. We found only a modest (nonsignificant) extension of lifespan (7% median, 16% maximum) and no change in healthspan indices in Surf1-/- vs. Surf1+/+ mice despite substantial decreases in COX activity (22%-87% across tissues). Dietary restriction (DR) increased median lifespan in both Surf1+/+ and Surf1-/- mice (36% and 19%, respectively). We measured gene expression, metabolites, and targeted expression of key metabolic proteins in adipose tissue, liver, and brain in Surf1+/+ and Surf1-/- mice. Gene expression was differentially regulated in a tissue-specific manner. Many proteins and metabolites are downregulated in Surf1-/- adipose tissue and reversed by DR, while in brain, most metabolites that changed were elevated in Surf1-/- mice. Finally, mitochondrial unfolded protein response (UPRmt )-associated proteins were not uniformly altered by age or genotype, suggesting the UPRmt is not a key player in aging or in response to reduced COX activity. While the changes in gene expression and metabolism may represent compensatory responses to mitochondrial stress, the important outcome of this study is that lifespan and healthspan are not compromised in Surf1-/- mice, suggesting that not all mitochondrial deficiencies are a critical determinant of lifespan.

Hyperpolarized [1-13C]-Pyruvate Magnetic Resonance Spectroscopic Imaging of Prostate Cancer In Vivo Predicts Efficacy of Targeting the Warburg Effect.

Purpose: To evaluate the potential of hyperpolarized [1-13C]-pyruvate magnetic resonance spectroscopic imaging (MRSI) of prostate cancer as a predictive biomarker for targeting the Warburg effect.Experimental Design: Two human prostate cancer cell lines (DU145 and PC3) were grown as xenografts. The conversion of pyruvate to lactate in xenografts was measured with hyperpolarized [1-13C]-pyruvate MRSI after systemic delivery of [1-13C] pyruvic acid. Steady-state metabolomic analysis of xenograft tumors was performed with mass spectrometry and steady-state lactate concentrations were measured with proton (1H) MRS. Perfusion and oxygenation of xenografts were measured with electron paramagnetic resonance (EPR) imaging with OX063. Tumor growth was assessed after lactate dehydrogenase (LDH) inhibition with FX-11 (42 µg/mouse/day for 5 days × 2 weekly cycles). Lactate production, pyruvate uptake, extracellular acidification rates, and oxygen consumption of the prostate cancer cell lines were analyzed in vitro LDH activity was assessed in tumor homogenates.Results: DU145 tumors demonstrated an enhanced conversion of pyruvate to lactate with hyperpolarized [1-13C]-pyruvate MRSI compared with PC3 and a corresponding greater sensitivity to LDH inhibition. No difference was observed between PC3 and DU145 xenografts in steady-state measures of pyruvate fermentation, oxygenation, or perfusion. The two cell lines exhibited similar sensitivity to FX-11 in vitro LDH activity correlated to FX-11 sensitivity.Conclusions: Hyperpolarized [1-13C]-pyruvate MRSI of prostate cancer predicts efficacy of targeting the Warburg effect. Clin Cancer Res; 24(13); 3137-48. ©2018 AACR.

Moderate lifelong overexpression of tuberous sclerosis complex 1 (TSC1) improves health and survival in mice.

The tuberous sclerosis complex 1/2 (TSC1/2) is an endogenous regulator of the mechanistic target of rapamycin (mTOR). While mTOR has been shown to play an important role in health and aging, the role of TSC1/2 in aging has not been fully investigated. In the current study, a constitutive TSC1 transgenic (Tsc1 tg ) mouse model was generated and characterized. mTORC1 signaling was reduced in majority of the tissues, except the brain. In contrast, mTORC2 signaling was enhanced in Tsc1 tg mice. Tsc1 tg mice are more tolerant to exhaustive exercises and less susceptible to isoproterenol-induced cardiac hypertrophy at both young and advanced ages. Tsc1 tg mice have less fibrosis and inflammation in aged as well as isoproterenol-challenged heart than age-matched wild type mice. The female Tsc1 tg mice exhibit a higher fat to lean mass ratio at advanced ages than age-matched wild type mice. More importantly, the lifespan increased significantly in female Tsc1 tg mice, but not in male Tsc1 tg mice. Collectively, our data demonstrated that moderate increase of TSC1 expression can enhance overall health, particularly cardiovascular health, and improve survival in a gender-specific manner.

Rapamycin Increases Mortality in db/db Mice, a Mouse Model of Type 2 Diabetes.

We examined the effect of rapamycin on the life span of a mouse model of type 2 diabetes, db/db mice. At 4 months of age, male and female C57BLKSJ-lepr (db/db) mice (db/db) were placed on either a control diet, lacking rapamycin or a diet containing rapamycin and maintained on these diets over their life span. Rapamycin was found to reduce the life span of the db/db mice. The median survival of male db/db mice fed the control and rapamycin diets was 349 and 302 days, respectively, and the median survival of female db/db mice fed the control and rapamycin diets was 487 and 411 days, respectively. Adjusting for gender differences, rapamycin increased the mortality risk 1.7-fold in both male and female db/db mice. End-of-life pathological data showed that suppurative inflammation was the main cause of death in the db/db mice, which is enhanced slightly by rapamycin treatment.

The mammalian target of rapamycin modulates the immunoproteasome system in the heart.

The mammalian target of rapamycin (mTOR) plays an important role in cardiac development and function. Inhibition of mTOR by rapamycin has been shown to attenuate pathological cardiac hypertrophy and improve the function of aging heart, accompanied by an inhibition of the cardiac proteasome activity. The current study aimed to determine the potential mechanism(s) by which mTOR inhibition modulates cardiac proteasome. Inhibition of mTOR by rapamycin was found to reduce primarily the immunoproteasome in both H9c2 cells in vitro and mouse heart in vivo, without significant effect on the constitutive proteasome and protein ubiquitination. Concurrent with the reduction of the immunoproteasome, rapamycin reduced two important inflammatory response pathways, the NF-κB and Stat3 signaling. In addition, rapamycin attenuated the induction of the immunoproteasome in H9c2 cells by inflammatory cytokines, including INFγ and TNFα, by suppressing NF-κB signaling. These data indicate that rapamycin indirectly modulated immunoproteasome through the suppression of inflammatory response pathways. Lastly, the role of the immunoproteasome during the development of cardiac hypertrophy was investigated. Administration of a specific inhibitor of the immunoproteasome ONX 0914 attenuated isoproterenol-induced cardiac hypertrophy, suggesting that the immunoproteasome may be involved in the development of cardiac hypertrophy and therefore could be a therapeutic target. In conclusion, rapamycin inhibits the immunoproteasome through its effect on the inflammatory signaling pathways and the immunoproteasome could be a potential therapeutic target for pathological cardiac hypertrophy.

Litiasis biliar en el niño, diez años de experiencia / Ten years of experience in treatomg biliary lithiasis in the child

Introducción: hasta hace pocos años, la litiasis biliar en la infancia se consideraba una enfermedad poco frecuente y se asociaba fundamentalmente a enfermedades hemolíticas. Con el advenimiento del ultrasonido abdominal, el hallazgo y diagnóstico de esta enfermedad aumentó. El espectro clínico descrito es muy amplio, y varía desde casos asintomáticos hasta la presencia de cuadros de colecistitis aguda.Objetivo: caracterizar clínica y quirúrgicamente a pacientes en edad pediátrica con litiasis vesicular operados en el Hospital Universitario Pediátrico Centro Habana.Métodos: se realizó un estudio descriptivo, longitudinal, retro y prospectivo, en 182 pacientes con diagnóstico de litiasis biliar, intervenidos quirúrgicamente en el Servicio de Cirugía del hospital, desde junio de 2003 a junio de 2013.Resultados: la litiasis biliar se evidenció con más frecuencia en el sexo femenino (52,7 por ciento), y en el grupo de edades de 11 a 15 años. Los principales factores de riesgo fueron el sobrepeso (28 por ciento) y la obesidad (21,4 por ciento). La forma clínica predominante fue el dolor abdominal recurrente en hipocondrio derecho (69,7 por ciento). El ultrasonido abdominal mostró predominio de cálculos únicos (54,9 por ciento). La videolaparoscopia fue la vía de acceso de elección (98,9 por ciento). La incidencia de complicaciones fue mínima (0,5 por ciento), y el hallazgo anatomopatológico más frecuente fue la colecistitis crónica litiásica (89,6 por ciento). El 92,9 por ciento tuvo corta estadía. No hubo fallecidos.Conclusiones: se considera que la litiasis biliar no es rara en Pediatría, sobre todo en niñas con exceso de peso, que su forma de presentación más frecuente es el dolor abdominal recurrente, y el acceso laparoscópico ofrece excelentes resultados(AU)

Litiasis biliar en el niño, diez años de experiencia / Ten years of experience in treatomg biliary lithiasis in the child

INTRODUCCIÓN: hasta hace pocos años, la litiasis biliar en la infancia se consideraba una enfermedad poco frecuente y se asociaba fundamentalmente a enfermedades hemolíticas. Con el advenimiento del ultrasonido abdominal, el hallazgo y diagnóstico de esta enfermedad aumentó. El espectro clínico descrito es muy amplio, y varía desde casos asintomáticos hasta la presencia de cuadros de colecistitis aguda. OBJETIVO: caracterizar clínica y quirúrgicamente a pacientes en edad pediátrica con litiasis vesicular operados en el Hospital Universitario Pediátrico Centro Habana. MÉTODOS: se realizó un estudio descriptivo, longitudinal, retro y prospectivo, en 182 pacientes con diagnóstico de litiasis biliar, intervenidos quirúrgicamente en el Servicio de Cirugía del hospital, desde junio de 2003 a junio de 2013. RESULTADOS: la litiasis biliar se evidenció con más frecuencia en el sexo femenino (52,7 %), y en el grupo de edades de 11 a 15 años. Los principales factores de riesgo fueron el sobrepeso (28 %) y la obesidad (21,4 %). La forma clínica predominante fue el dolor abdominal recurrente en hipocondrio derecho (69,7 %). El ultrasonido abdominal mostró predominio de cálculos únicos (54,9 %). La videolaparoscopia fue la vía de acceso de elección (98,9 %). La incidencia de complicaciones fue mínima (0,5 %), y el hallazgo anatomopatológico más frecuente fue la colecistitis crónica litiásica (89,6 %). El 92,9 % tuvo corta estadía. No hubo fallecidos. CONCLUSIONES: se considera que la litiasis biliar no es rara en Pediatría, sobre todo en niñas con exceso de peso, que su forma de presentación más frecuente es el dolor abdominal recurrente, y el acceso laparoscópico ofrece excelentes resultados.

INTRODUCTION: till a few years ago, biliary lithiasis in childhood was considered as an uncommon disease mainly linked to hemolytic illnesses. With the advent of the abdominal ultrasound, the diagnosis and findings of this disease became more frequent. The clinical spectrum is very broad and ranges from asymptomatic cases to acute cholecystitis. OBJECTIVE: to characterize clinically and surgically the pediatric patients with gallbladder lithiasis operated on at the university pediatric hospital of Centro Habana. METHODS: prospective, retrospective, longitudinal and descriptive study of 182 patients diagnosed with biliary lithiasis. They had been operated on at the surgical service of this hospital from June 2003 through June 2013. RESULTS: biliary lithiasis was more frequently observed in girls (52.7 %) and in the 11-15 years-old group. The main risk factors were overweight (28 %) and obesity (21.4 %). The predominant clinical form was recurrent abdominal pain in the right hypochondrium (69.7 %). The abdominal ultrasound mostly showed single calculi (54.9 %). Video-assisted laparoscopy was the access way of choice (98.9 %). The incidence of complications was minimal (0.5 %) and the common anatomical and pathological finding was chronic lithiasic cholecystitis (89.6 %). The length of stay at hospital was short, with 92.9 %. There was not a single death. CONCLUSIONS: it is considered that biliary lithiasis is not a rare entity in pediatrics, mainly in overweighed girl; the most common form of presentation is recurrent abdominal pain and the laparoscopic access offers the best results.

Rapamycin-induced metabolic defects are reversible in both lean and obese mice.

The inhibition of mTOR (mechanistic target of rapamycin) by the macrolide rapamycin has many beneficial effects in mice, including extension of lifespan and reduction or prevention of several age-related diseases. At the same time, chronic rapamycin treatment causes impairments in glucose metabolism including hyperglycemia, glucose intolerance and insulin resistance. It is unknown whether these metabolic effects of rapamycin are permanent or whether they can be alleviated. Here, we confirmed that rapamycin causes glucose intolerance and insulin resistance in both inbred and genetically heterogeneous mice fed either low fat or high fat diets, suggesting that these effects of rapamycin are independent of genetic background. Importantly, we also found that these effects were almost completely lost within a few weeks of cessation of treatment, showing that chronic rapamycin treatment does not induce permanent impairment of glucose metabolism. Somewhat surprisingly, chronic rapamycin also promoted increased accumulation of adipose tissue in high fat fed mice. However, this effect too was lost when rapamycin treatment was ended suggesting that this effect of rapamycin is also not permanent. The reversible nature of rapamycin's alterations of metabolic function suggests that these potentially detrimental side-effects might be managed through alternative dosing strategies or concurrent treatment options.

Regulation of motor function and behavior by atypical chemokine receptor 1.

Atypical Chemokine Receptor 1 (ACKR1), previously known as Duffy Antigen Receptor for Chemokines, stands out among chemokine receptors for high selective expression on cerebellar Purkinje neurons. Although ACKR1 ligands activate Purkinje cells in vitro, evidence for ACKR1 regulation of brain function in vivo is lacking. Here we demonstrate that Ackr1 (-/-) mice have markedly impaired balance and ataxia on a rotating rod and increased tremor when injected with harmaline, which induces whole-body tremor by activating Purkinje cells. Ackr1 (-/-) mice also exhibited impaired exploratory behavior, increased anxiety-like behavior and frequent episodes of marked hypoactivity under low-stress conditions. Surprisingly, Ackr1 (+/-) had similar behavioral abnormalities, indicating pronounced haploinsufficiency. The behavioral phenotype of Ackr1 (-/-) mice was the opposite of mouse models of cerebellar degeneration, and the defects persisted when Ackr1 was deficient only on non-hematopoietic cells. Together, the results suggest that normal motor function and behavior may partly depend on negative regulation of Purkinje cell activity by Ackr1.

Sudor compensador, un efecto no deseado secundario al tratamiento quirúrgico de la hiperhidrosis primaria infantil / Compensatory sweating, an unwanted effect secondary to the surgical treatment of primary infant hyperhidrosis

Introducción: la hiperhidrosis idiopática infantil se caracteriza por sudoración desproporcionada en manos, axilas y pies fundamentalmente, y ocasiona problemas sociales a los que la padecen. El sudor compensador es un efecto no deseado que puede aparecer después de la cirugía torácica en los pacientes. Objetivo: evaluar la presencia del sudor compensador en niños operados de hiperhidrosis palmar y axilar idiopática. Métodos: se realizó un estudio de una serie de casos compuesta por 61 niños operados y seguidos de forma consecutiva por hiperhidrosis idiopática, con edades comprendidas de 11 a 18 años, en el Hospital Universitario Pediátrico Centro Habana, desde enero de 2011 a octubre de 2013. Las variables analizadas fueron: edad, sexo, localización de la hiperhidrosis, presencia de sudor compensador y sus localizaciones más frecuentes, así como evolución a corto y mediano plazo. Resultados: fueron 42 niñas (68,9 por ciento) y 19 varones (31,1 por ciento), todos intervenidos mediante la técnica simpaticolisis videotoracoscópica bilateral sincrónica, por un solo puerto. Presentaron sudor compensador 17 pacientes (27,9 por ciento), de ellos, 14 pacientes de forma ligera y 3 moderada. No hubo significación en relación con la localización de la hiperhidrosis y el desarrollar sudor compensador. En la espalda fue donde con mayor frecuencia se presentó el sudor compensador, en 6 casos (9,8 por ciento). Hubo mejoría en el tiempo o desapareció en el 70,4 por ciento de los pacientes. Conclusiones: los pacientes que presentaron sudor compensador evalúan su situación de satisfactoria, pues resolvieron la parte molesta de las manos, y consideraron oportuno el tratamiento quirúrgico al que fueron sometidos(AU)

Introduction: infantile idiopathic hyperhidrosis is characterized by disproportionate sweating in hands, axillae and feet fundamentally, and brings social problems to those suffering it. Compensatory sweating is unwanted effect that may occur after thoracic surgery. Objective: to evaluate the presence of compensatory sweating in children operated on from idiopathic hyperhidrosis in hands and axillae. Methods: a study of a case series of sixty one 11-18 years-old children operated on from idiopathic hyperhidrosis and subsequently followed-up in university pediatric hospital of Centro Habana from January 2011 to October 2013. The variables were age, sex, location of hyperhidrosis, presence of compensatory sweating and its most common locations as well as its short-and medium-term evolution. Results: forty two girls (68.9 percent) and 19 boys (31.1 percent) were all operated through synchronic bilateral thoracoscopic sympathicholysis technique using one access port. Seventeen patients (27.9 percent) presented with compensatory sweating, 14 in its slight form and 3 in its moderate form. There was no significant difference as to the location of hyperhidrosis and occurrence of compensatory sweating. The most common location was the back in 6 cases (9.8 percent). This effect improved as time went by or disappeared in 70.4 percent of patients. Conclusions: the patients who had compensatory sweating regarded their present situation as satisfactory because they overcame discomfort in their hands, and they also considered that the surgical treatment was timely(AU)

Sudor compensador, un efecto no deseado secundario al tratamiento quirúrgico de la hiperhidrosis primaria infantil / Compensatory sweating, an unwanted effect secondary to the surgical treatment of primary infant hyperhidrosis

INTRODUCCIÓN: la hiperhidrosis idiopática infantil se caracteriza por sudoración desproporcionada en manos, axilas y pies fundamentalmente, y ocasiona problemas sociales a los que la padecen. El sudor compensador es un efecto no deseado que puede aparecer después de la cirugía torácica en los pacientes. OBJETIVO: evaluar la presencia del sudor compensador en niños operados de hiperhidrosis palmar y axilar idiopática. MÉTODOS: se realizó un estudio de una serie de casos compuesta por 61 niños operados y seguidos de forma consecutiva por hiperhidrosis idiopática, con edades comprendidas de 11 a 18 años, en el Hospital Universitario Pediátrico Centro Habana, desde enero de 2011 a octubre de 2013. Las variables analizadas fueron: edad, sexo, localización de la hiperhidrosis, presencia de sudor compensador y sus localizaciones más frecuentes, así como evolución a corto y mediano plazo. RESULTADOS: fueron 42 niñas (68,9 %) y 19 varones (31,1 %), todos intervenidos mediante la técnica simpaticolisis videotoracoscópica bilateral sincrónica, por un solo puerto. Presentaron sudor compensador 17 pacientes (27,9 %), de ellos, 14 pacientes de forma ligera y 3 moderada. No hubo significación en relación con la localización de la hiperhidrosis y el desarrollar sudor compensador. En la espalda fue donde con mayor frecuencia se presentó el sudor compensador, en 6 casos (9,8 %). Hubo mejoría en el tiempo o desapareció en el 70,4 % de los pacientes. CONCLUSIONES: los pacientes que presentaron sudor compensador evalúan su situación de satisfactoria, pues resolvieron la parte molesta de las manos, y consideraron oportuno el tratamiento quirúrgico al que fueron sometidos.

INTRODUCTION: infantile idiopathic hyperhidrosis is characterized by disproportionate sweating in hands, axillae and feet fundamentally, and brings social problems to those suffering it. Compensatory sweating is unwanted effect that may occur after thoracic surgery. OBJECTIVE: to evaluate the presence of compensatory sweating in children operated on from idiopathic hyperhidrosis in hands and axillae. METHODS: a study of a case series of sixty one 11-18 years-old children operated on from idiopathic hyperhidrosis and subsequently followed-up in university pediatric hospital of Centro Habana from January 2011 to October 2013. The variables were age, sex, location of hyperhidrosis, presence of compensatory sweating and its most common locations as well as its short-and medium-term evolution. RESULTS: forty two girls (68.9 %) and 19 boys (31.1 %) were all operated through synchronic bilateral thoracoscopic sympathicholysis technique using one access port. Seventeen patients (27.9 %) presented with compensatory sweating, 14 in its slight form and 3 in its moderate form. There was no significant difference as to the location of hyperhidrosis and occurrence of compensatory sweating. The most common location was the back in 6 cases (9.8 %). This effect improved as time went by or disappeared in 70.4 % of patients. CONCLUSIONS: the patients who had compensatory sweating regarded their present situation as satisfactory because they overcame discomfort in their hands, and they also considered that the surgical treatment was timely.