RESUMO
El escorbuto es una enfermedad ocasionada por el déficit de vitamina C. La vitamina C, también llamada ácido ascórbico, actúa como cofactor de la propil-lisil hidroxilasa, enzima que interviene en la biosíntesis de colágeno; por ello es de vital importancia en la integridad estructural de piel, mucosas, anexos, vasos sanguíneos, huesos y dientes. Las manifestaciones clínicas incluyen síntomas constitucionales severos como debilidad y fatiga. Los hallazgos cutáneos iniciales son pápulas hiperqueratósicas foliculares y púrpura palpable perifolicular. Con el tiempo aparecen áreas extensas de equimosis, edema en miembros inferiores, hemorragias en astillas en uñas y alopecia difusa. Por lo general se describe esta enfermedad como asociada a tiempos pasados y extremadamente infrecuente en países desarrollados. Sin embargo, actualmente se ha detectado un aumento en el número de casos, asociados con malnutrición severa. Desórdenes psiquiátricos como la anorexia nerviosa, alcoholismo y deficiencias nutricionales por dietas excesivas y mal balanceadas o escasez de recursos económicos constituyen los principales factores de riesgo hoy en día. El tratamiento consiste en la corrección del déficit mediante la mediante suplementación con vitamina C vía oral. Presentamos una mujer de 24 años con escorbuto asociado a anorexia nerviosa y a dieta pobre en vegetales y fruta.
Scurvy is a disease caused by a deficit of vitamin C. Vitamin C, also called ascorbic acid, acts as a cofactor for propyl-lysyl hydroxylase, an enzyme that is involved in collagen biosynthesis, vitally important in the structural integrity of skin, mucous membranes, annexes, blood vessels, bones and teeth. Clinical manifestations include severe constitutional symptoms such as weakness and fatigue. The initial cutaneous findings are follicular hyperkeratotic papules and perifollicular palpable purpura. Over time, large areas of ecchymosis, edema of the lower limbs, splinter hemorrhages in nails and diffuse alopecia appear. Usually this disease is described as associated with past times and extremely uncommon in developed countries. However, the number of cases have been increasing, especially those associated with severe malnutrition. Psychiatric disorders such as anorexia nervosa, alcoholism and nutritional deficiencies due to excessive and poorly balanced diets or shortage of economic resources are the main risk factors nowadays. Correcting the deficit with oral vitamin C supplementation is the treatment of the disease. We present a 24-year-old woman with scurvy associated with anorexia nervosa and a diet low in vegetables and fruit.
Assuntos
Humanos , Feminino , Adulto , Púrpura , Ácido Ascórbico/uso terapêutico , Deficiência de Ácido Ascórbico/terapia , Escorbuto/diagnóstico , Deficiências Nutricionais/terapia , Desnutrição/complicações , Diagnóstico PrecoceRESUMO
Iron is the most common micronutrient deficiency in the world and it is most prevalent in young children, exposing their developing brain to inadequate iron levels. The damage related to neuroanatomical parameters is not reversed after iron treatment. However, evidence suggest that tactile stimulation (TS) may offer great therapeutic efficacy in cases of nutritional disorders postnatally, since the brain is remarkably responsive to its interaction with the environment. Recently, we shown that neonatal iron deficient rats achieved some remedial effect by exposing them to TS treatment early in life, reinforcing the fact that the TS approach is a positive enriching experience, therefore, here we ask whether exposure to TS treatment, could also be employed to prevent fine structural changes in the fibers from optic nerve of rats maintained on an iron-deficient diet during brain development. To elucidate the protective effect of tactile stimulation, our methods resulted in 10,859 analyzed fibers, divided into small and large fibers. We found that iron deficiency led to a decreased axon, fiber and myelin size of small fibers, however, TS completely reversed the iron-decifiency-induced alteration on those fiber measurements. Large fibers were disproportionately affected by iron deficiency and there was no remediating effect due to tactile stimulation treatment. The present study adds new information regarding different alterations between small and large fibers due to diet and TS, which suggest a size-based selectivity. These results emphasize the concept that compromised brain development can be mitigated at an early age by environmental factors, such as tactile stimulation.
Assuntos
Axônios/patologia , Deficiências Nutricionais/patologia , Deficiências Nutricionais/terapia , Manobra Psicológica , Deficiências de Ferro , Fibras Nervosas Mielinizadas/patologia , Nervo Óptico/patologia , Tato/fisiologia , Animais , Animais Recém-Nascidos , Modelos Animais de Doenças , Masculino , Estimulação Física , Ratos , Ratos WistarRESUMO
No hiperparatireoidismo nutricional secundário ocorre uma secreção excessiva de paratormônio em resposta à deficiência dietética do cálcio, podendo ser estabelecido o diagnóstico através da história clínica do animal e exames complementares. A deficiência mineral é compensada parcialmente pelo aumento da absorção intestinal de cálcio, diminuição da excreção urinária de cálcio e reabsorção de cálcio nos ossos, podendo fazer com que o animal apresente graus variados de problemas locomotores, dor à palpação dos ossos, resistência ao apoiar uma extremidade, fraturas e até mesmo incapacidade para se manter em pé. O tratamento do HNS requer correção da deficiência dietética e reparo de qualquer anormalidade óssea que estiver presente.(AU)
In the secondary hyperparathyroidism nutrition occurs an excessive secretion of parathyroid hormone in response to dietary deficiency of calcium, which can be set by the diagnosis through the medical history of the animal and laboratory tests. The mineral deficiency is partially offset by increased intestinal calcium absorption, reduction of urinary excretion of calcium, and calcium resorption in bone, which can cause to the animal varying degrees of locomotor problems, pain on palpation of the bones, resistance to support an extremity, fractures and even inability to stand. Treatment of HNS requires correction of the dietary deficiency and repair of any bone abnormalities that are present.(AU)
En hiperparatiroidismo nutricional secundario ocurre una secreción excesiva de la hormona paratiroidea en respuesta a la deficiencia dietética de calcio, que se puede establecer el diagnóstico a través de la historia clínica de los animales y con pruebas adicionales. La deficiencia de minerales se ve parcialmente compensada por el aumento de la absorción intestinal de calcio, la reducción de la excreción urinaria de calcio y la reabsorción de calcio en los huesos, haciendo con que los animales tengan diferentes grados de problemas del aparato locomotor, dolor a la palpación de los huesos, resistencia para apoyar un extremo del cuerpo, trácturas e incluso incapacidad para ponerse de pie. El tratamiento de la HNS requiere la corrección de la deficiência en la dieta y reparar anomalías óseas que están presentes.(AU)
Assuntos
Animais , Cães , Hiperparatireoidismo Secundário/terapia , Hiperparatireoidismo Secundário/veterinária , Hormônio Paratireóideo/biossíntese , Hormônio Paratireóideo , Deficiências Nutricionais/terapia , Deficiências Nutricionais/veterinária , Desmineralização Patológica Óssea/terapia , Desmineralização Patológica Óssea/veterinária , Deficiência de Cálcio , Movimento , Cálcio da DietaRESUMO
No hiperparatireoidismo nutricional secundário ocorre uma secreção excessiva de paratormônio em resposta à deficiência dietética do cálcio, podendo ser estabelecido o diagnóstico através da história clínica do animal e exames complementares. A deficiência mineral é compensada parcialmente pelo aumento da absorção intestinal de cálcio, diminuição da excreção urinária de cálcio e reabsorção de cálcio nos ossos, podendo fazer com que o animal apresente graus variados de problemas locomotores, dor à palpação dos ossos, resistência ao apoiar uma extremidade, fraturas e até mesmo incapacidade para se manter em pé. O tratamento do HNS requer correção da deficiência dietética e reparo de qualquer anormalidade óssea que estiver presente.
In the secondary hyperparathyroidism nutrition occurs an excessive secretion of parathyroid hormone in response to dietary deficiency of calcium, which can be set by the diagnosis through the medical history of the animal and laboratory tests. The mineral deficiency is partially offset by increased intestinal calcium absorption, reduction of urinary excretion of calcium, and calcium resorption in bone, which can cause to the animal varying degrees of locomotor problems, pain on palpation of the bones, resistance to support an extremity, fractures and even inability to stand. Treatment of HNS requires correction of the dietary deficiency and repair of any bone abnormalities that are present.
En hiperparatiroidismo nutricional secundario ocurre una secreción excesiva de la hormona paratiroidea en respuesta a la deficiencia dietética de calcio, que se puede establecer el diagnóstico a través de la historia clínica de los animales y con pruebas adicionales. La deficiencia de minerales se ve parcialmente compensada por el aumento de la absorción intestinal de calcio, la reducción de la excreción urinaria de calcio y la reabsorción de calcio en los huesos, haciendo con que los animales tengan diferentes grados de problemas del aparato locomotor, dolor a la palpación de los huesos, resistencia para apoyar un extremo del cuerpo, trácturas e incluso incapacidad para ponerse de pie. El tratamiento de la HNS requiere la corrección de la deficiência en la dieta y reparar anomalías óseas que están presentes.
Assuntos
Animais , Cães , Deficiências Nutricionais/terapia , Deficiências Nutricionais/veterinária , Desmineralização Patológica Óssea/terapia , Desmineralização Patológica Óssea/veterinária , Hiperparatireoidismo Secundário/terapia , Hiperparatireoidismo Secundário/veterinária , Hormônio Paratireóideo , Hormônio Paratireóideo/biossíntese , Cálcio da Dieta , Deficiência de Cálcio , MovimentoRESUMO
Of the many evils that were inflicted upon the army of the West India Company in its years of activity in Brazil, few could be compared to diseases. However, there is little quantitative data in the field of historiography regarding the impact of disease on these troops. Apart from the limited amount of information about the diseases that affected many soldiers, little is known about the medical treatments that were available, the main diseases that affected the troops, and what were the causes. This article provides information to understand aspects that have been little studied in quantitative and systematic terms in the field of historiography, and demonstrates how the diseases afflicted the Company and affected its actions in the territory.
Assuntos
Doenças Transmissíveis/história , Deficiências Nutricionais/história , Militares/história , Brasil/epidemiologia , Doenças Transmissíveis/mortalidade , Doenças Transmissíveis/terapia , Deficiências Nutricionais/mortalidade , Deficiências Nutricionais/terapia , História do Século XVII , Humanos , Medicina Militar/história , Países BaixosRESUMO
Dos diversos males que infligiram o exército da Companhia das Índias Ocidentais em seus anos de atividade no Brasil, poucos podem ser comparados às doenças. São escassos, todavia, os dados quantitativos apresentados na historiografia para mostrar seu impacto nas tropas. Além dos índices de baixas por doença que ceifavam muitos militares, sabe-se pouco sobre os tratamentos médicos oferecidos, as principais doenças que atingiam a tropa e suas causas. Este artigo traz elementos que ajudam a compreender aspectos pouco trabalhados em termos quantitativos e sistemáticos pela historiografia e demonstra como as doenças afligiam a companhia e embaraçavam suas ações no território.
Of the many evils that were inflicted upon the army of the West India Company in its years of activity in Brazil, few could be compared to diseases. However, there is little quantitative data in the field of historiography regarding the impact of disease on these troops. Apart from the limited amount of information about the diseases that affected many soldiers, little is known about the medical treatments that were available, the main diseases that affected the troops, and what were the causes. This article provides information to understand aspects that have been little studied in quantitative and systematic terms in the field of historiography, and demonstrates how the diseases afflicted the Company and affected its actions in the territory.
Assuntos
Humanos , História do Século XVII , Doenças Transmissíveis/história , Deficiências Nutricionais/história , Militares/história , Brasil/epidemiologia , Doenças Transmissíveis/mortalidade , Doenças Transmissíveis/terapia , Deficiências Nutricionais/mortalidade , Deficiências Nutricionais/terapia , Medicina Militar/história , Países BaixosRESUMO
OBJECTIVES: To evaluate surfactant content and function through the lamellar body count (LBC) and stable microbubble test (SMT) in mechanically ventilated infants with severe acute viral bronchiolitis. STUDY DESIGN: Controlled cross-sectional study of 32 infants receiving mechanical ventilation: 16 with a diagnosis of acute viral bronchiolitis and 16 with normal lungs. Tracheal fluid was collected and LBC was performed in an automated cell counter. Samples were kept frozen and thawed for testing. At the time of analysis, samples were diluted in a dithiothreitol solution, vortexed for 10 seconds, and aspirated by the cell counter. SMT was performed using the Pattle technique. RESULTS: In the bronchiolitis group, the median (IQR) LBC was significantly lower than in the control group: 130,000 (61,250-362,250) vs. 518,000 (180,250-896,000) lamellar bodies/µL; P = .003. Median (IQR) SMT values were also significantly lower in the bronchiolitis group: 10 (2-13) vs. 400 (261-615) microbubbles/mm2; P < .001. CONCLUSIONS: Infants with acute viral bronchiolitis have reduced surfactant content and function. We speculate that these simple tests may be useful to identify infants with bronchiolitis who would benefit from surfactant replacement therapy.
Assuntos
Bronquiolite Viral/diagnóstico , Bronquiolite Viral/terapia , Deficiências Nutricionais/diagnóstico , Surfactantes Pulmonares/análise , Tensoativos/uso terapêutico , Doença Aguda , Líquido da Lavagem Broncoalveolar/química , Estudos de Casos e Controles , Terapia Combinada , Cuidados Críticos/métodos , Estudos Transversais , Deficiências Nutricionais/terapia , Feminino , Seguimentos , Humanos , Recém-Nascido , Unidades de Terapia Intensiva Neonatal , Masculino , Microbolhas , Valores de Referência , Respiração Artificial/métodos , Medição de Risco , Índice de Gravidade de Doença , Estatísticas não Paramétricas , Taxa de Sobrevida , Fatores de Tempo , Resultado do TratamentoRESUMO
Adenosine Desaminase (ADA) deficiency, is a purine metabolic disorder that cause severe combined immunodeficiency (SCID) due to the accumulation of toxic metabolites that primarily affects development, differentiation and function of T and B lymphocytes. In addition, some patients show neurological, renal and liver abnormalities, delayed in development, deafness and seizures. If the immune response is not restored, children with this disorder rarely survive; therefore, ADA deficiency must be suspected when difficulty gaining weight, recurrent infections and skeletal abnormalities are present. The ADA deficiency has clinical and immunological characteristics not seen in other immunodeficiencies, data that helps to guide the diagnosis and therapy. This review summarizes clinical, pathological, molecular and treatment findings described in this disease.