#Acute and Chronic Leukemia: What Are the Differences?

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Acute and Chronic Leukemia: What Are the Differences?

Resultado de imagem para leukemia


Leukemia is a cancer of the blood. It forms when blood cells in the bone marrow malfunction and form cancerous cells. The cancerous blood cells then overrun the normal blood cells. This interferes with the body’s ability to fight infections, control bleeding, and deliver oxygen to normal cells. The cancerous cells can also invade the spleen, liver, and other organs.

Chronic leukemia is a slow-growing leukemia. Acute leukemia is a fast-growing leukemia that progresses quickly without treatment.

Signs and symptoms

Signs and symptoms of chronic leukemia

Chronic leukemia develops slowly, and the early symptoms may be mild and go unnoticed. Acute leukemia develops quickly. This is because the cancerous cells multiply fast.

Chronic leukemia is most commonly diagnosed after a routine blood test. You may have low-level symptoms for years before it’s diagnosed. The symptoms may be vague and could occur due to many other medical conditions. The signs and symptoms may include:

general feelings of malaise, such as tiredness, bone and joint pain, or shortness of breath
weight loss
a loss of appetite
a fever
night sweats
bruising or bleeding, such as nosebleeds
enlarged lymph nodes that aren’t painful
pain or a full feeling in the upper-left abdomen, which is where the spleen is located
Signs and symptoms of acute leukemia

The common signs and symptoms of acute leukemia are:

low white blood cell counts
tiredness that doesn’t go away with rest
shortness of breath
pale skin
sweating at night
a slight fever
bruising easily
bone and joint aches
slow healing of cuts
tiny red dots under the skin

No one knows the cause of leukemia or why some people have chronic leukemia and others have an acute form of the condition. Both environmental and genetic factors are thought to be involved.

Leukemia may occur due to changes in the DNA of your cells. Chronic myeloid leukemia (CML) may also be associated with a gene mutation called the Philadelphia chromosome. This gene mutation isn’t inherited.

Some studies show that a combination of genetic and environmental factors are involved in childhood leukemia. Some children may not have inherited the particular version of genes that can get rid of harmful chemicals. Exposure to those chemicals might increase their risk for leukemia.

Risk factors

Possible risk factors for the different types of leukemia exist, but it’s possible to get leukemia even if you don’t have any of the known risk factors. Experts still don’t understand a lot about leukemia.

Some factors for developing chronic leukemia include:

being over age 60
being Caucasian
exposure to chemicals such as benzene or Agent Orange
exposure to high levels of radiation
Some risk factors for developing acute leukemia include:

smoking cigarettes
having chemotherapy and radiation therapy for other cancers
exposure to very high radiation levels
having genetic abnormalities, such as Down syndrome
having a sibling with acute lymphocytic leukemia (ALL)
Having one or more of these risk factors doesn’t mean that you’ll get leukemia.

How is leukemia diagnosed?

All types of leukemia are diagnosed by examining blood samples and bone marrow. A complete blood count will show the levels and types of:

white cells
leukemia cells
red cells
Bone marrow and other tests will give your doctor further information about your blood to confirm a diagnosis of leukemia. Your doctor may also look at a blood smear under a microscope to see the shape of the cells. Other tests may grow your blood cells to help your doctor identify changes to the chromosomes or genes.


Your treatment plan will depend on the type of leukemia you have and how advanced it is at the time of your diagnosis. You may want to get a second opinion before starting treatment. It’s important to understand what your treatment choices are and what you can expect.

Chronic leukemia

Chronic leukemia progresses slowly. You may not be diagnosed until symptoms, such as enlarged lymph nodes, appear. Chemotherapy, corticosteroids, and monoclonal antibodies may be used to control the cancer. Your doctor may use blood transfusions and platelet transfusions to treat the decrease in red blood cells and platelets. Radiation may help reduce the size of your lymph nodes.

If you have CML and also have the Philadelphia chromosome, your doctor may treat you with tyrosine kinase inhibitors (TKIs). TKIs block the protein produced by the Philadelphia chromosome. They may also use stem cell therapy to replace cancerous bone marrow with healthy bone marrow.

Acute leukemia

People with acute leukemia will generally begin treatment quickly following a diagnosis. This is because the cancer can progress quickly. Treatment may include chemotherapy, targeted therapy, or stem cell therapy, depending on the type of acute leukemia you have.

The treatment for acute leukemia is generally very intense in the beginning. The main goal of treatment is to kill the leukemia cells. Hospitalization is sometimes necessary. The treatment often causes side effects.

Your doctor will do regular blood and bone marrow tests to determine how well your treatment is killing the leukemia cells. They may try various mixtures of drugs to see what works best.

Once your blood has returned to normal, your leukemia will be in remission. Your doctor will continue to test you in case the cancerous cells return.

What is the outlook?

Each type of leukemia is different and will require different treatment. The outlook is also unique to the type of leukemia you have and how advanced it is when you begin treatment. Other factors that will affect your outlook are:

your age
your general health
how much the leukemia has spread in your body
how well you respond to treatment
Survival rates for leukemia have greatly improved in the last 50 years. New drugs and new types of treatments continue to be developed.

Your doctor will give you your outlook based on leukemia research findings from the past years. These statistics are based on people who had your type of leukemia, but each person is different. Try not to focus too much on these types of statistics if you receive a diagnosis of leukemia. Your outlook will depend on your age, your overall health, and the stage of your leukemia. The following were the five-year survival rates for people with different types of leukemia in the United States from 2005 to 2011:

CML: 63.2 percent
CLL: 84.8 percent
ALL: 70.1 percent overall and 91.2 percent for those under 15
AML, or acute myeloid leukemia: 26 percent overall and 66.5 percent for those under 15
The outlook for people with any type of leukemia will continue to improve as the research advances. Researchers in many ongoing clinical trials are testing new treatments for each type of leukemia.


No early screening tests for leukemia are available. If you have risk factors and symptoms, ask your doctor about blood tests.

It’s important to keep copies of your treatments, the dates, and the drugs that were used. These will help you and your future doctors if your cancer comes back.

Experts haven’t found ways to prevent leukemia. Being proactive and telling your doctor if you notice any symptoms of leukemia may improve your chances of recovery.



#Antibiótico nanotecnológico desenvolvido pelo CNPEM pode eliminar superbactérias

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Antibiótico nanotecnológico desenvolvido pelo CNPEM pode eliminar superbactérias

por ASCOM – publicado 23/11/2017

Antibiótico nanotecnológico desenvolvido pelo CNPEM pode eliminar superbactérias
Nanotecnologia também é importante para a produção de fármacos. Foto: Ascom/MCTIC

A nanotecnologia foi o caminho usado por cientistas do Centro Nacional de Pesquisa em Energia e Materiais (CNPEM) para desenvolver um antibiótico capaz de eliminar superbactérias de forma seletiva, ou seja, sem comprometer as células humanas. Em testes preliminares, o nanoantibiótico demonstrou eficiência ao enfrentar formas resistentes da bactéria Escherichia coli, levando uma grande dose do princípio ativo ao alvo, ou seja, à superbactéria, preservando as células sadias. Era esse um dos gargalos no desenvolvimento de nanopartículas aplicadas à saúde. Não é mais.

“Nanomateriais têm sido utilizados como agentes antimicrobianos devido às suas propriedades físicas e químicas únicas. A grande vantagem das nanopartículas é a capacidade de serem seletivas às bactérias sem afetar as células humanas”, explica o pesquisador Mateus Borba Cardoso, um dos responsáveis pelo desenvolvimento do nanoantibiótico no CNPEM, vinculado ao Ministério da Ciência, Tecnologia, Inovações e Comunicações.

O estudo, cujos resultados foram publicados na revista Scientific Reports, revela como a tecnologia pode ajudar a enfrentar formas resistentes da Escherichia coli, comumente encontrada em hospitais. Em grandes quantidades no organismo, esta superbactéria pode causar infecção intestinal e urinária.

“Usamos o antibiótico como uma espécie de isca e, assim, conseguimos levar a nanopartícula até a bactéria com uma grande quantidade do fármaco. A ação combinada da droga com os íons de prata foi capaz de matar até mesmo microrganismos resistentes”, afirma Borba.

Para chegar a esse resultado, os pesquisadores criaram um método que combina minúsculas partículas de prata, recobertas com sílica e com moléculas de antibiótico, para tentar vencer a crescente resistência das bactérias aos medicamentos convencionais. “Há medicamentos comerciais que contêm nanopartículas que, de modo geral, servem para recobrir o princípio ativo e aumentar o tempo de vida dentro do organismo. Nossa estratégia é diferente. Decoramos a superfície da nanopartícula com determinados grupos químicos que servem para direcioná-la até o local onde deve agir, de modo seletivo.”

As soluções adotadas pelos pesquisadores do CNPEM para produzir essa nanopartícula com função antibiótica e com baixa toxidade podem ser estratégicas para o desenvolvimento de novas terapias, não só contra bactérias, mas também contra vírus e tumores. “Por meio de modelagem molecular, conseguimos determinar qual parte da molécula de ampicilina interage melhor com a membrana bacteriana. Deixamos então todas as moléculas do fármaco com essa parte-chave voltada para o lado externo da nanopartícula, aumentando as possibilidades de interação com o patógeno”, diz o pesquisador.

O estudo recebeu financiamento do Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) e da Fundação de Amparo à Pesquisa do Estado de São Paulo (Fapesp).

##In a First, CRISPR Gene Editing Used in an Adult

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In a First, CRISPR Gene Editing Used in an Adult
WRITTEN BY: Carmen Leitch

For the first time, CRISPR gene editing is being attempted in an adult; the patient has a disease called Hunter Syndrome. In California, 44-year-old Brian Madeux received an infusion of billions of copies of the correct version of a gene mutated in his disorder and the molecular tools to cut his DNA. While there are potential drawbacks, Madeux is “nervous and excited,” he said. “I’ve been waiting for this my whole life, something that can potentially cure me.”

Cures are rare in medicine, and CRISPR has opened up incredible new possibilities. While it has been used before to correct genes in cells that have been taken from patients, and then returned to the patient’s body, this is the first time the molecular reagents will be used directly in a person. Only one percent of his liver cells will need to be corrected, his doctors suggested, for his illness to be relieved.

Hunter syndrome is a devastating disease; few are afflicted and those that tend to die at a young age. They are unable to metabolize a type of carbohydrate because of a genetic mutation affecting a critical metabolic enzyme. The carbohydrates that aren’t broken down instead accumulate, wreaking havoc on the body.

It causes a host of problems; patients often get colds and ear infections, they may experience hearing loss, and have enlarged internal organs, joint stiffness, skeletal irregularities, and display aggressive behavior, among other symptoms. While patients can receive the missing enzyme by IV, easing some symptoms, it costs from $100,000 to $400,000 a year, and it does not stop brain damage.

CRISPR gene editing shows great potential. / Image credit: Pixabay

“Many are in wheelchairs … dependent on their parents until they die,” commented Dr. Chester Whitley, a University of Minnesota genetics expert. He wants to enroll patients in studies by Sangamo Therapeutics, a California company testing gene therapy for two metabolic diseases and hemophilia.

The changes that happen to the patient’s genome will be permanent, and it is possible that unintended changes will occur. That has been a risk the scientists, and the patient are willing to take. Dr. Howard Kaufman, a Boston scientist on the National Institutes of Health panel that approved the studies said that the promise of gene editing is too high to ignore. “So far there’s been no evidence that this is going to be dangerous,” he said. “Now is not the time to get scared.”

Indeed, scientists, doctors, and patients will be following this and other studies to see where the technology can take us. Learn more about how CRISPR works from the video.


Sources: AP, Mayo Clinic

In Labroots

#Understanding why Diet Restriction Aids Longevity

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Understanding why Diet Restriction Aids Longevity
WRITTEN BY: Carmen Leitch
Mitochondria are known as the powerhouses of the cell; they act in concert to generate energy according to demand. These coordinated mitochondrial networks in cells tend to have less capacity as we age. New research has shown that alteration of mitochondrial networks, whether by restricting diet or by manipulating genes, may promote good health and lead to an increase in lifespan. The work, published in Cell Reports by scientists at the Harvard T.H. Chan School of Public Health, indicates how periods of fasting are likely to encourage healthy aging.

Confocal image (cLSM) of living HeLa cells. Mitochondria are stained in red (Mitotracker red), the nucleus is seen in blue (DAPI). Mitochondria form dense and dynamic networks. /Credit: Wikimedia Commons/8x57is

Changes in the how mitochondrial networks are shaped have been found have a causal linked to longevity. Nematode worms are often used to study aging; their lifespan is only a few weeks. Restricting diet in these worms kept the mitochondrial networks in a youthful state. When the scientists genetically manipulated a protein that senses energy, AMP-activated protein kinase (AMPK), it had the same effect. These young mitochondrial networks were found to increase lifespan by signaling to other organelles, peroxisomes, which altered fat metabolism.

“Low-energy conditions such as dietary restriction and intermittent fasting have previously been shown to promote healthy aging. Understanding why this is the case is a crucial step towards being able to harness the benefits therapeutically,” explained the lead author of this work Heather Weir, who conducted the research while at Harvard Chan School and now works at Astex Pharmaceuticals. “Our findings open up new avenues in the search for therapeutic strategies that will reduce our likelihood of developing age-related diseases as we get older.”

The video features a lecture from Dr. Matt Piper, University College London, Institute of Healthy Ageing on aging and diet.

“Although previous work has shown how intermittent fasting can slow aging, we are only beginning to understand the underlying biology,” noted William Mair, senior study author and Associate Professor of Genetics and Complex Diseases at Harvard Chan School. “Our work shows how crucial the plasticity of mitochondria networks is for the benefits of fasting. If we lock mitochondria in one state, we completely block the effects of fasting or dietary restriction on longevity.”

The researchers now plan to investigate the role of the mitochondrial networks in fasting in mammals. They want to know whether mitochondrial flexibility defects may help explain why the risk of age-related diseases is heightened in the obese.


Sources: AAAS/Eurekalert! Via Harvard HSPH, Cell Metabolism

#Pruebas genéticas para #cáncer de mama y ovario: La demanda crece más que la respuesta sanitaria

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Matías A. Loewy

BUENOS AIRES, ARG. La disponibilidad de pruebas genéticas para identificar mutaciones en BRCA1 o BRCA2 es mayor; sin embargo, es necesaria una mejor respuesta sanitaria, informó la Dra. Luisina Bruno, especialista en asesoramiento genético en oncología del Instituto Alexander Fleming, en Buenos Aires, Argentina, durante el XXIII Congreso Argentino e Internacional de Oncología Clínica, que se celebró en esta ciudad entre el 31 de octubre y el 3 de noviembre.[1]

Dra. Luisina Bruno

Actualmente, visto en perspectiva, saber que se porta una mutación en los genes BRAC1 o BRAC2 quizá no sea tan mala noticia. Hoy día no solo se puede prevenir, evitar o mejorar el tratamiento de cánceres de mal pronóstico en pacientes que se realizan esas pruebas genéticas, sino que también es posible extender el beneficio a miembros de la familia. No obstante, el sistema sanitario no siempre está preparado para acompañar la decisión de aquellas mujeres que tienen resultados positivos de las pruebas, incluyendo el acceso a cirujanos para efectuar cirugías preventivas, o la disponibilidad de equipos de imágenes que permitan una vigilancia exhaustiva.

Desde que, en el año 2013 la actriz Angelina Jolie dio a conocer que se había sometido a una mastectomía bilateral, debido a que era portadora de una mutación en los genes BRCA, en el mundo aumentó la demanda por esas pruebas genéticas. Y en Argentina ese aumento sigue siendo “sostenido”, y se están creando nuevos consultorios de asesoramiento genético, afirmó la Dra. Bruno a Medscape en Español. La detección de cánceres hereditarios, que representan 5% – 10% de los carcinomas de mama, y 18% – 24% de los de ovario, “es la gran oportunidad de identificar pacientes que requieren estrategias de prevención diferentes, pero muy efectivas”.

La especialista puntualizó que cumplir las estrategias de prevención adecuadas “permite reducir el riesgo de enfermar, que implican las mutaciones (germinales) patogénicas de los genes de susceptibilidad BRCA de una forma tan efectiva, que el riesgo remanente puede ser similar, o inclusive inferior, al de la población general”. Aunque, para lograr ese objetivo, se requiere superar barreras y disparidades que subsisten, en mayor o menor grado, dentro de los países.

“Lo que me preocupa es el hecho de que si una mujer toma una decisión después de conocer que es portadora de una mutación de riesgo, encuentre una respuesta sanitaria adecuada”, destacó la Dra. Bruno.

Prevención primaria y secundaria

La causa más frecuente de síndromes hereditarios en cáncer de mama y ovario la constituyen las mutaciones en BRCA1 y BRCA2. La Dra. Bruno precisó que las portadoras tienen un riesgo de 50% – 85%, y de 15% – 45% de desarrollar tumores de mama y ovario, respectivamente, lo que implica que el riesgo aumenta hasta 30 veces respecto de la población general. Un estudio prospectivo reciente en JAMA precisó que el riesgo acumulado hasta los 80 años para cáncer de mama es de 72% y 69% en portadoras de mutaciones en BRCA1 y BRCA2, respectivamente. Mientras que el riesgo acumulado para cáncer de ovario es de 44% y 17%, respectivamente.

La detección de esas mutaciones presenta múltiples beneficios, tanto a nivel personal como familiar. Permite evitar o detectar de manera temprana cánceres de mama que, en países como Argentina, en 50% de los casos se detectan en etapas 3 y 4. “Permite evitar el cáncer de ovario, en el cual no existen métodos claramente efectivos de prevención por imágenes, y que en 75% de los casos, cuando se detectan, se encuentran en una etapa avanzada, y con altas probabilidades de recurrencia”. También sirve para aliviar a familiares no portadoras que pueden estar preocupadas, destacó la Dra. Bruno.

La identificación de esas mutaciones también tiene, o podría tener, implicaciones terapéuticas. Fármacos como olaparib ya están aprobados para tratar el cáncer de ovario avanzado con mutación en BRCA, y posiblemente también sean efectivos en tumores de mama (triple negativo y luminal metastásico) de pacientes con esa susceptibilidad genética. En la terapia neoadyuvante del cáncer de mama triple negativo, las pacientes con mutación en BRCA se beneficiarían de la adición de carboplatino al esquema de tratamiento.[2]

Sin embargo, lo que preocupa a la Dra. Bruno es el foco de prevención. Como estrategia de prevención primaria en mujeres con mutaciones BRCA positivas, sin olvidarse de los hábitos de vida saludables, de la quimioprevención (cuyos beneficios no se limitan solo a la población general), y hasta del uso de anticonceptivos orales, son dos medidas que han probado reducir el riesgo de padecer cáncer de mama o de ovario, de manera más significativa:

  • Mastectomía reductora de riesgo bilateral. Disminuye 90% a 98% el riesgo de desarrollar cáncer de mama. En un estudio prospectivo, ninguna de 257 mujeres con mutaciones en BRCA1 y BRCA2 que recibieron la intervención desarrolló el tumor, frente a 7% de quienes no lo hicieron.[3] Sin embargo, la Dra. Bruno señaló que no está probado que reduzca la mortalidad general. “Es una estrategia, pero no la única, y tendrá que evaluarse con cada paciente”. Las complicaciones del procedimiento alcanzan entre 16% – 21%, y la tasa de satisfacción, 80%.
  • Salpingooforectomía bilateral. La extirpación quirúrgica de ambos ovarios, y ambas trompas de Falopio, “es la terapéutica infalible”, subrayó la Dra. Bruno. Disminuye 95% el riesgo de presentar cáncer de ovario, 50% la incidencia de cáncer de mama, y 77% la mortalidad global.[4] Guías como las de la National Comprehensive Cancer Network (NCCN) la recomiendan después de los 35 a 40 años, cuando las mujeres completaron la paridad, aunque también plantean que es “razonable” retrasar el procedimiento hasta los 40 a 45 años, cuando se trata de una mutación en BRCA2 (el cáncer de ovario en esas pacientes aparece en promedio 8 a 10 años más tarde, que en quienes son portadoras de una mutación en BRCA1).[5]

Las alternativas a ambas cirugías podrían funcionar como estrategia de prevención secundaria, es decir, para facilitar el diagnóstico temprano. Pero el respaldo de la evidencia es diferente. Estas alternativas son las siguientes:

# Seu filho está acima do peso? Veja porque isso pode ser um problema

Postado em

Dra. Kelly Marques Oliveira



Posso provar para você que hoje temos mais crianças no mundo obesas e com sobrepeso do que crianças desnutridas, e mesmo que não estejam acima do peso, podem ter algum erro alimentar grave, ou hábitos ruins!

Aquela velha história do açúcar, porque faz mal introduzi-lo antes dos 2 anos de idade, ou mesmo que não introduza, como mesmo depois isso pode prejudicar o seu filho. Hábitos são difíceis de serem quebrados, e quando falamos em prevenção, é porque estamos contruindo hábitos ( e mudando também hábitos nossos) que levaremos para o resto da vida!

Vamos entender um pouco melhor sobre essa doença que acomete 6,5 milhões de crianças só no Brasil!

Para isso quem escreve hoje é a Dra. Ludmila Rachid, Endocrinopediatra que atende aqui no Espaço Médico Descomplicado


Por que falar de obesidade infantil?

“Pela primeira vez em anos, as crianças de hoje podem viver menos que seus pais devido às doenças consequentes do excesso de peso.” Organização Mundial da Saúde (OMS). No Brasil em torno de 6,5 milhões de crianças estão acima do peso, e em 2025 se nada for feito, teremos 11,3 milhões de crianças com sobrepeso e obesidade, com as seguintes consequências: 427 mil terão pré-diabetes, 150 mil terão diabetes tipo 2 e 1 milhão terão pressão alta!

Como saber se meu filho está acima do peso?

Para o diagnóstico de sobrepeso e obesidade nas crianças e adolescentes, o método mais utilizado são as curvas de Índice de Massa Corpórea (IMC). Essas curvas são de acordo com o sexo e a idade do paciente. O pediatra que acompanha seu filho deve preenchê-la a cada consulta, e avaliar se o peso esta adequado, e prosseguir com as orientações.

E o que é obesidade e por que ela ocorre?

A obesidade é o excesso de tecido adiposo/gorduroso decorrente de um desequilíbrio da oferta e do gasto de energia, que envolve diversos sistemas complexos no nosso organismo. Alguns casos raros de obesidade são causados por síndromes (Síndrome de Prader Willi) ou desregulação hormonal (deficiência do hormônio de crescimento, alterações da tireoide). Na maioria dos casos, ocorre pela interação de fatores genéticos e ambientais (sedentarismo e alimentação inadequada), e nesses casos chamamos de obesidade exógena.


Como ocorre o mecanismo da fome e da saciedade?

Diversos sistemas interligados funcionam para o controle do apetite. Basicamente, a curto prazo, temos no trato gastrointestinal, o estômago que produz a grelina e o intestino produz as incretinas. Esses hormônios vão atuar no hipotálamo, uma estrutura cerebral responsável pela ingesta/gasto energético. A longo prazo temos a insulina e leptina, que também atuam estimulando ou inibindo o hipotálamo. Na sensação de fome, a glicose, os nutrientes e a grelina no sangue estão baixas. Quando comemos, aumentamos gradativamente o nível desses elementos no sangue, além do alimento que ao chegar no estômago provoca estiramento da musculatura gástrica, que manda informação, via nervo vago ao hipotálamo: A comida chegou! Conforme a comida vai caminhando, os hormônios incretínicos vão sendo produzidos e liberados, como o GLP-1, GIP, e esses hormônios mandam o sinal de saciedade para o hipotálamo. Não é imediato como a informação que a comida chegou, por isso sempre orientamos comer devagar para saber a hora certa de parar!


Quais são as consequências da obesidade infantil?

A obesidade pode causar alterações do colesterol, alterações do açúcar (pré-diabetes e diabetes), pressão alta, dores no joelho, problemas no quadril, fígado gorduroso (esteatose hepática), roncos e cansaço durante o dia (Síndrome da Apneia Obstrutiva do Sono), além de problemas de relacionamento social e depressão. Hoje diversos estudos mostram que o sobrepeso, mesmo sem alterações nos exames laboratoriais, pode acarretar em alterações cardiovasculares no futuro.

Atualmente, além dos dados alarmantes, sabemos que 80% dos pacientinhos obesos se tornarão adultos obesos, portanto precisamos mudar esse cenário! A prevenção da obesidade é o melhor remédio sempre! Então o que podemos fazer para prevenir?

A prevenção começa na gestação: evitar o ganho de peso em excesso, assim como priorizar a alimentação saudável. Nos primeiros seis meses de vida: o aleitamento materno exclusivo tem fator protetor contra a obesidade e a síndrome metabólica no futuro. Após os 6 meses até dois anos: não utilizar açúcar refinado e produtos industrializados, dar preferência para alimentos saudáveis – comida de verdade! O paladar e a queda por doces ocorrem nessa época! Após essa idade, lembrar que pais, escolas e a mídia devem dar o exemplo, priorizar alimentação saudável, e estimular atividade física, e reduzindo o tempo de celular, televisão, tablets!

Vamos todos juntos combater a Obesidade! Visite seu pediatra regularmente e procure um endocrinologista infantil sempre que necessário! Até mais!

Dra. Ludmilla Rachid



#Women With Infertility Issues Have Higher Mortality Risk

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Women With Infertility Issues Have Higher Mortality Risk
Fran Lowry October 30, 2017

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For women with infertility issues, the risk for death is elevated, especially from breast cancer and diabetes, according to results from a new study.”Infertility might lead to disease because of long-term inflammation or other hormonal perturbations, but this remains to be seen with further research,” said Natalie Stentz, MD, from the University of Pennsylvania in Philadelphia.”An association between infertility and medical disease has been noted in the male population, but such an association in females is largely unknown,” Dr Stentz said at the American Society for Reproductive Medicine 2017 Scientific Congress in San Antonio.”We wanted to get a better understanding of the link between infertility and mortality in women,” she told Medscape Medical News.In their study, Dr Stentz and her colleagues assessed women 55 to 74 years of age who were prospectively enrolled in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial from 1992 to 2001.Of the 75,784 women for whom fertility history was available, 11,006 (14.5%) were infertile, defined as not having conceived despite a year of intercourse.After parity, socioeconomic risk factors, and underlying comorbidities were controlled for, risk for death during the 13-year follow-up period was 10% higher in women with infertility issues than without (hazard ratio [HR], 1.10; 95% confidence interval [CI], 1.03 – 1.17; P = .005).In addition, infertile women were almost 70% more likely to die from diabetes than fertile women (HR, 1.69; 95% CI, 1.15 – 2.49; P = .007), even though the prevalence of diabetes was similar in the two cohorts, and were 43% more likely to die from breast cancer (HR, 1.43; 95% CI, 1.06 – 1.94; P = .019).
There was no association between infertility and risk for ovarian cancer, risk for endometrial cancer, risk for death from cardiovascular disease risk, or for death from ovarian cancer. Mean age at death was 73 years in the two cohorts.We certainly do not want this research to be taken from an alarmist perspective.Dr Stentz was asked if infertile women should ask their doctors for special screening, especially for diabetes and breast cancer.It is premature at this point, she explained. “We are not recommending any change in the current standard of care for screening guidelines for cardiovascular disease, breast cancer, or any other disease.””We certainly do not want this research to be taken from an alarmist perspective. We simply want to raise awareness that infertility deserves to be acknowledged,” she added.The more we know about the genetic nature of infertility in both men and women, the more we realize that the condition may be related to general health.This “very interesting study” follows a previous study that found a relation between male infertility and mortality (Hum Reprod. 2014;29:1567-1574), said Alexander Pastuszak, MD, PhD, from the Baylor College of Medicine in Houston.”The actual increased risk of mortality is slightly higher than that observed in the male study, but it is still quite small,” he told Medscape Medical News.”The more we know about the genetic nature of infertility in both men and women, the more we realize that the condition may be related to general health,” he explained.”The PLCO database is an excellent data source and lends credibility to the work,” said Dr Pastuszak. However, he pointed out, it would have been interesting if the researchers had included “a third group of women with a common benign female condition not linked to mortality or fertility.””Women should realize that the risk of mortality is low,” he added, noting that these results “have not been confirmed by other studies, and we do not understand why this would be occurring on a physiological, genetic, or molecular level.”In addition, “fertile and infertile women lived to be the same average age. As such, we need to take this study in context and understand that it’s a first look,” he explained. More work is needed to confirm the association.Dr Stentz and Dr Pastuszak have disclosed no relevant financial relationships. The study authors acknowledge the National Cancer Institute for permission to access their database.

American Society for Reproductive Medicine (ASRM) 2017 Scientific Congress: Abstract O-6. Presented October 30, 2017.

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