Malformaciones cavernosas cerebrales, presentación de 14 casos y revisión de literatura / Brain cavernous malformations, presentation of 14 cases and literature review

Objetivo: Presentar los resultados de tratamiento quirúrgico obtenidos en una serie de 14 casos de malformación cavernosa, situadas en diferentes localizaciones encefálicas, además de realizar una revisión bibliográfica sobre el tema. Material y métodos: En el periodo de los años 2014-2019, se diagnosticaron y protocolizaron 14 pacientes por medio de la consulta externa de neurocirugía del Hospital Juárez de México. Todos menos 2, fueron intervenidos quirúrgicamente. Resultados: En 12 de los 14 casos que recibieron tratamiento quirúrgico, se documentó mejoría neurológica posterior a la resección total en 10 pacientes, 1 paciente de cavernoma gigante temporal se hizo resección subtotal, en 1 paciente con lesión de localización protuberancial se le realizó únicamente drenaje de hematoma. El déficit preoperatorio tendió a mejorar progresivamente en las lesiones de mayor tamaño y en ningún caso se documentaron complicaciones, las crisis convulsivas se controlaron disminuyendo progresivamente la dosis de fármacos anticonvulsivantes en el periodo postquirúrgico de este grupo de pacientes. Y dos pacientes, uno con lesión mesencefálica y el otro con cavernomatosis solo se sometieron a observación. Conclusiones: La cirugía es el método de elección hoy en día para el tratamiento de las malformaciones cavernosas, siendo los mejores resultados a menor tamaño de la lesión y con localizaciones más superficiales. Los resultados quirúrgicos de nuestros pacientes son similares a lo reportado en la literatura mundial.

Objectives: To present the surgical outcomes obtained in a series of 14 cases of cavernous malformation, located in different brain locations, in addition to conducting a literature review on the subject. Method: Between the years, 2014 and 2019, 14 cases were diagnosed and protocolized in neurosurgery department of Hospital Juárez of México. All patients except two, were surgically treated. Results: In 12 of the 14 cases received surgical treatment, neurological improvement was documented after the total resection in ten patients, one patient with giant temporal cavernoma performed a subtotal resection, other case with a lesion in the pontine location a hematoma drainage was performed. All surgical patients the preoperative clinical deficit tended to improve progressively in larger lesions and no complications were documented. Seizures were controlled by gradually decreasing the dose of anticonvulsant drugs in the post-surgical period of this group of patients. And two patients, one with mesencephalic lesion and another with cavernomatosis, were only observe. Conclusion: Surgery is the method of choice today for the treatment of cavernous malformations, with the best outcome being the smallest size of the lesion and with more superficial locations. The surgical outcomes in our patients are similar to those reported in the world literature

Evaluation of rat liver with ARFI elastography: In vivo and ex vivo study.

OBJECTIVE: The aim of this study was to compare in vivo vs ex vivo liver stiffness in rats with acoustic radiation force impulse (ARFI) elastography using the histological findings as the gold standard. METHODS: Eighteen male Wistar rats aged 16-18 months were divided into a control group (n = 6) and obese group (n = 12). Liver stiffness was measured with shear wave velocity (SWV) using the ARFI technique both in vivo and ex vivo. The degree of fibrosis, steatosis and liver inflammation was evaluated in the histological findings. Pearson's correlation coefficient was applied to relate the SWV values to the histological parameters. RESULTS: The SWV values acquired in the ex vivo study were significantly lower than those obtained in vivo (P < 0.004). A significantly higher correlation value between the degree of liver fibrosis and the ARFI elastography assessment was observed in the ex vivo study (r = 0.706, P < 0.002), than the in vivo study (r = 0.623, P < 0.05). CONCLUSION: Assessment of liver stiffness using ARFI elastography yielded a significant correlation between SWV and liver fibrosis in both the in vivo and ex vivo experiments. We consider that by minimising the influence of possible sources of artefact we could improve the accuracy of the measurements acquired with ARFI.

Sex-dependent differences in the adverse renal changes induced by an early in life exposure to a high-fat diet.

This study examines whether the intake of a high-fat diet very early in life leads to changes in arterial pressure and renal function and evaluates whether the mechanisms involved in these changes are sex-dependent. Experiments were performed in male and female Sprague-Dawley rats fed a normal or high-fat diet from weaning to 4 mo of age. This exposure to a high-fat diet lead to an angiotensin II-dependent elevation in arterial pressure and to significant increments in fat abdominal volume and plasma leptin that were similar in both sexes. In addition, the angiotensin II-induced increment in renal vascular resistance was greater ( P < 0.05) in male (106 ± 14%) and female (97 ± 15%) rats fed a high-fat diet than in rats fed a normal-fat diet (51 ± 8%). However, the high-fat intake during early life induced increments in albuminuria, interleukin-6, and infiltration of CD3 lymphocytes in the renal parenchyma that were greater ( P < 0.05) in male than in female rats. Other sex-dependent differences in response to high-fat intake were that adiponectin levels only decreased in females (21%, P < 0.05), and renal NF-κB expression only increased in males (31%, P < 0.05). In summary, the early exposure to a high-fat diet leads to angiotensin II-dependent arterial pressure elevations and to increments in abdominal fat and in the renal sensitivity to angiotensin II that are similar in both sexes. However, the mechanisms involved in the renal changes associated with early exposure to a high-fat diet are different in males and females.

Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences.

BACKGROUND: A substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may "program" susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases. MATERIALS AND METHODS: This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults. RESULTS: Developmental programming of several diseases is secondary to changes in different mechanisms inducing important alterations in the normal development of several organs that lead to significant changes in birth weight. The different diseases occurring as a consequence of an adverse environment during development are secondary to morphological and functional cardiovascular and renal changes, to epigenetic changes and to an activation of several hormonal and regulatory systems, such as angiotensin II, sympathetic activity, nitric oxide, COX2-derived metabolites, oxidative stress and inflammation. The important sex-dependent differences in the developmental programming of diseases seem to be partly secondary to the effects of sex hormones. Recent studies have shown that the progression of these diseases is accelerated during aging in both sexes. CONCLUSIONS: The cardiovascular, renal and metabolic diseases during adult life that occur as a consequence of several insults during fetal and postnatal periods are secondary to multiple structural and functional changes. Future studies are needed in order to prevent the origin and reduce the incidence and consequences of developmental programmed diseases.