ABSTRACT
Etiología. La neuropatía diabética dolorosa afecta aproximadamente al 25% de los pacientes diabéticos, aquellos tratados con insulina y/o hipoglucemiantes orales, y se caracteriza por presentarse como una neuropatía distal simétrica asociada a dolor crónico. Fisiopatología. Generalmente es de causa vascular, que provoca lesión de los nervios sensitivos primarios por hipoxia neuronal y déficit de nutrientes. Síntomas. El inicio suele ser bilateral en dedos y pies. En los casos de origen asimétrico, la progresión es hacia la bilateralidad. Puede progresar gradualmente a pantorrillas y rodillas, en cuyo caso los pacientes pueden notar síntomas álgicos y/o parestesias de forma conjunta en manos y pies (patrón de «guante-calcetín»). Síntomas. El dolor lo describen con diversos términos: urente, eléctrico, profundo. La alodinia y la hiperalgesia son menos comunes. La intensidad del dolor suele empeorar por la noche. Síntomas. Otros síntomas: claudicación vascular, signos disautonómicos (color de la piel y temperatura anormal, sudoración), depresión y ansiedad, trastornos del sueño. Hallazgos físicos. Es característico el déficit sensitivo en «guante-calcetín» y la pérdida o disminución del reflejo aquíleo, aunque algunos pacientes que solo tienen afectación de fibras nerviosas pequeñas pueden tener preservados los reflejos y la sensibilidad vibratoria. Diagnóstico. Es clínico. No hay necesidad de realizar estudios electrofisiológicos cuando la historia y los hallazgos físicos son consistentes con el diagnóstico de neuropatía diabética dolorosa. Historia natural. La historia natural de la neuropatía diabética dolorosa es variable y su curso clínico, impredecible. En algunos pacientes, el dolor puede mejorar después de meses o años, mientras que en otros persiste y empeora. Tratamiento. Debido a la gran variedad de factores causales y contribuyentes en la patogenia de la neuropatía diabética, no existe un tratamiento único satisfactorio. El mantenimiento de una hemoglobina glicosilada entre 6,5 y 7,5% puede enlentecer e incluso prevenir la progresión de la neuropatía. Tratamiento. En la actualidad las recomendaciones de tratamiento de la neuropatía diabética dolorosa se pueden observar en la tabla 5 y figura 1 (AU)
Aetiology. Painful diabetic neuropathy affects approximately 25% of diabetic patients, those treated with insulin and/or glucose lowering drugs, and is characterised by presenting as a distal symmetric neuropathy associated with chronic pain. Pathophysiology. The cause is generally vascular, which produces a lesion of the primary sensory nerves due to neuronal hypoxia and lack of nutrients. Symptoms. The onset is usually bilateral in the toes and feet. In cases where it is asymmetric, it progresses to be bilateral. It can gradually progress to the calves and the knees, in which case the patient may experience symptoms of pain and/or paresthesia both in the hands and feet (glove-stocking pattern). Symptoms. They describe the pain using diverse terms: burning, electric, deep, etc. Allodynia and hyperalgesia are less common. The pain intensity is usually gets worse at night. Symptoms. Other symptoms: vascular claudication, dysautonomic signs (skin colour, abnormal temperature, sweating), depression and anxiety, sleep disorders. Physical findings. Sensory loss and the loss or decrease in Achilles tendon reflex is characteristic in glove-stocking, although some patients who only have small nerve fibres involvement may have normal reflexes and vibratory sensitivity. Diagnosis. It is clinical. There is no need for electro-physiological studies when the history and physical findings are consistent with the diagnosis of painful diabetic neuropathy. Natural history. The natural history of painful diabetic neuropathy varies and its clinical course unpredictable. In some patients, the pain may improve after months or years, while in others it persists and gets worse. Treatment. Due the great number of causal and contributing factors in the pathogenesis of diabetic neuropathy, there is no single satisfactory treatment. The maintenance of a glycosylated haemoglobin between 6.5 and 7.5% can slow down and even prevent the progression of neuropathy. Treatment. The current treatment recommendations for painful diabetic neuropathy can be seen in table 5 and figure 1 (AU)
Subject(s)
Humans , Male , Female , Diabetic Neuropathies/complications , Diabetic Neuropathies/diagnosis , Antidepressive Agents/therapeutic use , Pain/drug therapy , Anticonvulsants/therapeutic use , Electromyography/methods , Antidepressive Agents, Tricyclic/therapeutic use , Lidocaine/therapeutic use , Hyperalgesia/complications , Hyperalgesia/diagnosis , Hyperalgesia/drug therapy , Diabetes Complications/diagnosis , Diagnosis, Differential , Antipsychotic Agents/therapeutic useABSTRACT
Objetivos: 1-Determinar la prevalencia de obesidad y sobrepeso en niños que cursan 5° año de la EGB en establecimientos escolares de la ciudad de Venado Tuerto. 2-Determinar si existe relación entre el estado nutricional y la actividad física en los niños. Matriales y métodos: se encuestaron 444 niños de 5to. año EGB en 23 establecimientos escolares de la ciudad de Venado Tuerto. Las encuestas realizadas constaron de 14 preguntas y un registro de las comidas que el niño realizó durante un día. Las mismas fueron entregadas en mano y se las retiró después de 1 semana. Los niños fueron previamente evaluados según su índice de masa corporal en relación de su edad. Las categorías asignadas fueron: desnutridos (D), peso normal(PN), sobrepeso (S), obesidad (O). Como punto de corte se utilizó para S (entre los percentilos 85 y 95) y para los O (> percentilo 95) según las curvas del Instituto Nacional d Estadísticas en Salud (NCHS)...
Subject(s)
Nutritional Status , Obesity , Prevalence , School Health ServicesABSTRACT
Objetivos: 1-Determinar la prevalencia de obesidad y sobrepeso en niños que cursan 5º año de la EGB en establecimientos escolares de la ciudad de Venado Tuerto. 2-Determinar si existe relación entre el estado nutricional y la actividad física en los niños. Matriales y métodos: se encuestaron 444 niños de 5to. año EGB en 23 establecimiento
Subject(s)
Obesity , Prevalence , Nutritional StatusABSTRACT
OBJECTIVE: Maternal phenylketonuria (MPKU) is characterized by intrauterine growth retardation, microcephaly, congenital malformations (mainly cardiac defects), dysmorphic facial features and mental retardation. There are women of child-bearing age that do not know that they are affected by phenylketonuria (PKU) and their pregnancies could result in damage to the fetus expressed as different neurological and congenital abnormalities. PATIENTS AND METHODS: We report 8 patients from 4 families. The first family had two offspring with intrauterine growth retardation, microcephaly and psychomotor retardation. The second family consisted of a daughter with mental retardation (without further data), a second baby which died during the first day of life, and a third child which died at 7 months of age with cardiac defects, microcephaly and dysmorphic features. Another child had intrauterine growth retardation, microcephaly psychomotor retardation, dysmorphic features and cardiac defects (coarctation of the aorta and subaortic stenosis). The third family had a son with microcephaly and mental retardation. The fourth family had a boy that died at 3 weeks of age with microcephaly, dysmorphic facial features, congenital heart disease (mitral atresia and septal defects) and Meckel diverticulum and a girl 5 years of age with intrauterine growth retardation, microcephaly and mental retardation. In all cases the mothers were unaware that they were affected by PKU and had mild intellectual defects. Two of them had PKU phenotypes. CONCLUSIONS: The offspring of PKU mothers untreated during pregnancy are affected by characteristic embriopathies related to the level of phenylalanine during pregnancy. In Spain, massive routine newborn screening was introduced around 1980-1985 and at present there are women of child-bearing age and are unaware that they are affected by the disease and that their pregnancies may result in fetal damage, as we demonstrate in these 8 patients. When faced with women with mental handicap or with antecedents of offspring with mental retardation, cardiac defects, microcephaly or intrauterine growth retardation, the determination of maternal phenylalanine concentrations is recommended. These teratogenic pathologies tend to disappear, but for the moment it is necessary to prevent this teratogenicity. The diagnosis is easy, avoids complementary exams, may help family studies and allows the implementation of dietary restriction during the subsequent pregnancy that would prevent fetal damage.
Subject(s)
Fetal Diseases/diagnosis , Fetal Diseases/etiology , Intellectual Disability/diagnosis , Phenylketonuria, Maternal/complications , Phenylketonuria, Maternal/diagnosis , Child, Preschool , Diagnosis, Differential , Female , Humans , Infant , Male , PregnancyABSTRACT
A very sensitive kinetic spectrophotometric method for the determination of copper(II) concentrations as low as 0.07 ng ml(-1) is described. This method is based on the oxidation of salicylic acid by hydrogen peroxide in ammoniacal medium, catalysed by copper(II) ion. The figures of merit of the procedure and the results of a study of interferences are given. The method is applied to the assay of copper in human blood serum.
