Primeiras cirurgias robóticas em crianças são feitas no Brasil

O paciente --uma criança de seis anos-- está deitado na mesa cirúrgica para ser operado. Enfermeira e auxiliares estão ao redor dele. Mas o cirurgião se afasta.

Assim que os braços do robô são colocados nos três furinhos feitos no abdome do menino (de 5 mm e 8,5 mm), o médico assume seu lugar no console, de onde controla os movimentos do aparelho, batizado de Da Vinci.

Ali, ele vê as imagens do interior do corpo do paciente em 3D, manuseia joysticks e aperta pedais. Para leigos, parece até um videogame.

O menino é uma das primeiras crianças a ser operada via robô no Brasil. Até agora, quatro pacientes, de um a 12 anos, foram submetidos à cirurgia robótica pediátrica. Os casos foram de retirada de tumores, desobstrução entre rim e ureter e refluxo da urina para o rim.

VANTAGENS

A cirurgia robótica em relação à cirurgia aberta proporciona menos dor no pós-operatório, cicatrizes menores e recuperação mais rápida, segundo o urologista Carlo Passerotti, do Instituto da Próstata e Doenças Urinárias do Hospital Alemão Oswaldo Cruz, em São Paulo.

É lá que as cirurgias robóticas pediátricas estão sendo feitas, há seis meses. O Da Vinci também está no Albert Einstein e no Sírio-Libanês.

De acordo com ele, a cirurgia robótica é pouco invasiva, da mesma forma como a que é feita por laparoscopia.

Mas, com o robô, é possível fazer movimentos precisos das mãos com a mesma habilidade de uma cirurgia aberta e ver imagens ampliadas do interior do corpo. "Conseguimos dar ponto mais rapidamente e diminuir o tempo da cirurgia e da anestesia", diz Passerotti.

No caso das crianças, o trabalho é mais delicado porque o espaço é menor e a cirurgia não pode ser muito longa, já que ela tem menor reserva respiratória. Isso requer mais treinamento e habilidade.

"ROBÔ DO BEN 10"

Na semana passada, Gian Lucca, de seis anos, de São Paulo, foi a quarta criança a passar pelas "mãos" do robô Da Vinci. Ele tinha refluxo vesico-ureteral, um retorno da urina da bexiga para o rim.

Na operação, o ureter é reposicionado na bexiga, para refazer o mecanismo de válvula que está deficiente.

A mãe de Gian Lucca, Maria Margarita Quintáns, diz que a recuperação foi tranquila. "Ele saiu do hospital no dia seguinte e não sentiu quase nada depois", conta. Ao preparar o filho para a operação, Margarita disse ao filho que um robô do desenho Ben 10 iria operá-lo.

Para Passerotti, muitos pacientes acham que a cirurgia robótica é "mais perfeita".

Mas os riscos, segundo o urologista Sidney Glina, professor da Faculdade de Medicina do ABC, são os mesmos das outras técnicas. "Deve-se entender que a robótica é só uma maneira de se fazer a operação", afirma.

Combinação de remédios para idosos a maior risco de morte

Mistura perigosa

Um estudo revelou que a combinação de medicamentos usados para combater problemas cardíacos, depressão e alergias pode aumentar o risco de morte e de deterioração de funções cerebrais entre idosos.

Cientistas estimam que metade das pessoas com 65 anos ou mais consomem regularmente tais medicamentos.

A pesquisa foi realizada entre 13 mil pessoas de 65 anos ou mais, pela Universidade de Anglia, na Grã-Bretanha, a partir de dados envolvendo medicamentos vendidos mediante a apresentação de receita médica ou outros que dispensavam a apresentação de receita.

Efeitos colaterais

O estudo centrou-se nos efeitos colaterais desses remédios sobre uma substância química chamada acetilcolina, produzida no cérebro.

A aceliticolina é um neurotransmissor que exerce um papel vital no sistema nervoso, o de passar mensagens de célula nervosa para célula nervosa.

Mas muitos remédios, quando tomados simultaneamente, afetam o funcionamento da acetilcolina.

Anticolinérgicos

A pesquisa classificou 80 medicamentos de acordo com sua suposta capacidade "anticolinérgica". Anticolinérgicos são substâncias extraídas de plantas ou sinteticamente produzidas que inibem a produção de acetilcolina.

Elas foram classificadas em um placar que ia de 1 a 5.

Remédios considerados amenos foram avaliados como sendo de categoria 1. Os de efeitos considerados moderados foram listados como sendo 2. E os avaliados como tendo efeitos severos foram listados na categoria 3.

Pacientes que tomavam uma droga considerada severa, juntamente com outras duas consideradas amenas eram enquadrados na categoria 5.

Entre os considerados moderados figuram o analgésico codeína e o anticoagulante warfarin. Os que foram classificados como severos estão o ditropan, tomado para prevenir incontinência, e o antidepressivo seroxat.

Associação

Entre 1991 e 1993, 20% dos pacientes que marcaram 4 pontos ou mais morreram. Entre aqueles que não tomaram medicamentos anticolinérgicos, apenas 7% morreram.

Pacientes que marcaram 4 pontos ou mais tiveram um aumento de 4% na degeneração de suas funções cerebrais.

O estudo não pode, no entanto, concluir que necessariamente os medicamentos causaram morte ou reduziram as funções cerebrais, apenas indica uma associação.

Genetic Study Shows That Low Body Fat May Not Lower Risk for Heart Disease and Diabetes

ScienceDaily (June 26, 2011) — Having a lower percentage of body fat may not always lower your risk for heart disease and diabetes, according to a study by an international consortium of investigators, including two scientists from the Institute for Aging Research of Hebrew SeniorLife, an affiliate of Harvard Medical School (HMS).

The Institute researchers, Douglas P. Kiel, M.D., M.P.H., and David Karasik, Ph.D., who are working with the Framingham Heart Study, identified a gene that is linked with having less body fat, but also with an increased risk of type 2 diabetes and heart disease, examples of so-called "metabolic diseases."

"We've uncovered a truly fascinating genetic story and, when we found the effect of this gene, we were very intrigued by the unexpected finding," says Dr. Kiel, a senior scientist at the Institute for Aging Research and a professor of medicine at HMS. "People, particularly men, with a specific form of the gene are both more likely to have lower percent body fat, but also to develop heart disease and type 2 diabetes. In simple terms, it is not only overweight individuals who can be predisposed for these metabolic diseases."

Reported online in the journal Nature Genetics on June 26, 2011, the investigators examined the genomes of more than 75,000 people to look for the genes that determine body fat percentage. They found strong evidence for a gene, called IRS1, to be linked with having less body fat. On further study, they found that this gene also leads to having unhealthy levels of cholesterol and blood glucose.

To understand why a gene that lowers body fat can be harmful, the scientists in the international consortium found that the gene lowers only the "subcutaneous" fat under the skin, but not the more harmful "visceral" fat that surrounds organs. The study authors speculate that people with this gene variant are less able to store fat safely under the skin and may, therefore, store fat elsewhere in the body, where it may interfere with normal organ function. All observations were more pronounced in men than in women and, indeed, many apparently lean men still carry too much abdominal fat.

"Genetic variants may not only determine the amount of total fat in your body," says Dr. Kiel, "but also what kind of fat you have. Some collections of fat, such as the kind located just under the skin, may actually be less harmful than the type located in the abdominal cavity, which may increase the risk of developing metabolic disease."

The effect, the researchers add, may be more pronounced in men due to the different body fat distributions between the sexes. Men store less fat than women, so they are more sensitive to changes in its distribution.

Premature Aging Caused by Some HIV Drugs, Study Shows

ScienceDaily (June 26, 2011) — A class of anti-retroviral drugs commonly used to treat HIV, particularly in Africa and low income countries, can cause premature aging, according to research published June 26 in the journal Nature Genetics. The study shows that the drugs damage DNA in the patient's mitochondria -- the 'batteries' which power their cells.

Image: Three mitochondria (blue), fractured to reveal the internal structure. DNA in mitochondria can be damaged by a class of antiretroviral drugs. 

The findings may explain why HIV-infected people treated with antiretroviral drugs sometimes show advanced signs of frailty and age-associated diseases such as cardiovascular disease and dementia at an early age.

Nucleoside analogue reverse-transcriptase inhibitors (NRTIs) -- of which the most well known is Zidovudine, also known as AZT -- were the first class of drug developed to treat HIV. They were a major breakthrough in the treatment of the disease, greatly extending lifespan and leading the condition to be seen as a chronic, rather than terminal, condition.

In high income countries, such as Europe and North America, the older NRTIs are used less commonly now due to concerns over toxicity and side-effects when taken over a long period of time. However, as they are now off-licence and hence relatively cheap, the drugs have proved to be an important lifeline for people infected with HIV in Africa and low income countries.

Professor Patrick Chinnery, a Wellcome Senior Fellow in Clinical Science from the Institute of Genetic Medicine at Newcastle University, says: "HIV clinics were seeing patients who had otherwise been successfully treated but who showed signs of being much older than their years. This was a real mystery. But colleagues recognised many similarities with patients affected by mitochondrial diseases -- conditions that affect energy production in our cells -- and referred them to our clinic."

Mitochondria are the 'batteries' in our cells which provide them with the energy to carry out their functions. During natural human aging, these mitochondria acquire mutations, though it is unclear whether these mutations are a cause of aging or a consequence.

In an attempt to understand what was happening at a cellular level, Professor Chinnery and colleagues studied muscle cells from HIV-infected adults, some of whom had previously been given NRTIs.

The researchers found that patients who had been treated with NRTIs -- even as long ago as a decade previously -- had damaged mitochondria which resembled that of a healthy aged person.

"The DNA in our mitochondria gets copied throughout our lifetimes and, as we age, naturally accumulates errors," explains Professor Chinnery. "We believe that these HIV drugs accelerate the rate at which these errors build up. So over the space of, say, ten years, a person's mitochondrial DNA may have accumulated the same amount of errors as a person who has naturally aged twenty or thirty years. What is surprising, though, is that patients who came off the medication many years ago may still be vulnerable to these changes."

Co-author and HIV specialist, Dr Brendan Payne, a Medical Research Council fellow from the Department of Infection and Tropical Medicine at the Royal Victoria Infirmary, Newcastle, believes that despite the side effects caused by NRTIs, they are still important drugs and the risks are relative.

"These drugs may not be perfect, but we must remember that when they were introduced they gave people an extra ten or twenty years when they would otherwise have died," he says. "In Africa, where the HIV epidemic has hit hardest and where more expensive medications are not an option, they are an absolute necessity."

Professor Chinnery and colleagues are now looking at ways to repair or stall some of the damage caused by the medication and believe that focusing on exercise -- which appears to have a beneficial effect on patients with mitochondrial diseases -- may help.

The study was funded by the Medical Research Council, the British Infection Society, the Newcastle Healthcare Charity, the UK NIHR Biomedical Research Centre for Aging and Age-related Disease and the Wellcome Trust.

Barrett’s Esophagus, Often a Precursor to Esophageal Cancer, Results from Residual, Embryonic Cells

ScienceDaily (June 26, 2011) — Researchers have discovered a new mechanism for the origin of Barrett's esophagus, an intestine-like growth in the esophagus that is triggered by chronic acid reflux and often progresses to esophageal cancer. Studying mice, the researchers found that Barrett's esophagus arises not from mutant cells in the esophagus but rather a small group of previously overlooked cells present in all adults that can rapidly expand to cancer precursors when the normal esophagus is damaged by acid.

Embryonic cell precursors (green) of Barrett’s esophagus at the junction between the stomach and esophagus (red).

This research will be published online in the June 24th issue of Cell.

Decades of cancer research tells us that most of the common cancers begin with genetic changes that occur over a period of 15 to 20 years, in some cases leading to aggressive cancers. However, for a subset of cancers that appear to be linked to chronic inflammation, this model might not hold.

Barrett's esophagus, which was first described by the Australian surgeon Norman Barrett in 1950, affects two to four million Americans. In this condition, tissue forms in the esophagus that resembles the intestinal tissue normally located much farther down the digestive tract. As a result, a person's chances of developing a deadly esophageal adenocarcinoma increase by 50- to 150-fold. Late stage treatment is largely palliative, so it is important to understand how acid reflux triggers it in the first place.

Research from the laboratory of Frank McKeon, Harvard Medical School professor of cell biology, together with Wa Xian, a postdoctoral researcher at Brigham and Women's Hospital and the Institute of Medical Biology, Singapore, along with an international consortium including Christopher Crum, director of Women's and Perinatal Pathology at Brigham and Women's Hospital, has shown that Barrett's esophagus originates from a minor population of non-esophageal cells left over from early development.

For the past decade, McKeon and his laboratory have been using mouse models to investigate the role of p63, a gene involved in the self-renewal of epithelial stem cells including those of the esophagus. McKeon joined forces two years ago with Wa Xian, an expert in signal transduction in cancer cells, to tackle the vexing problem of the origin of Barrett's esophagus.

At that time, the dominant hypothesis for Barrett's was that acid reflux triggers the esophageal stem cells to make intestine cells rather than normal esophageal tissue. However, McKeon and Xian felt the support for this concept was weak. Taking a different track, they studied a mouse mutant lacking the p63 gene and mimicked the symptoms of acid reflux. As a result, the entire esophagus was covered with a Barrett's-like tissue that proved to be a near exact match with human Barrett's at the gene expression level.

The researchers were particularly surprised by the sheer speed with which this Barrett's esophagus appeared in the mice.

"From the speed alone we knew we were dealing with something different here," said Xia Wang, postdoctoral fellow at Harvard Medical School and co-first author of this work.

Yusuke Yamamoto, a postdoctoral fellow at the Genome Institute of Singapore and also co-first author, added that, "we just had to track the origins of the Barrett's cells back through embryogenesis using our markers from extensive bioinformatics."

In essence, the investigators tracked the precancerous growth to a discrete group of leftover embryonic cells wedged between the junction of the esophagus and the stomach--precisely where endoscopists have argued Barrett's esophagus begins. As predicted by the mouse studies, the researchers identified a group of embryonic cells exactly at the junction between the esophagus and the stomach in all normal humans.

"Barrett's arises from this discrete group of pre-existing, residual embryonic cells present in all adults that seemingly lie-in-wait for a chance to take over when the esophagus is damaged," said McKeon. Added Xian, "We know these embryonic cells have different gene expression patterns from all normal tissues and this makes them inviting targets for therapies to destroy Barrett's before it progresses to cancer."

The therapeutic opportunities of this work are potentially immense.

"We are directing monoclonal antibodies to cell surface markers that can identify these precursor cells, so we may have a new opportunity to intervene therapeutically and prevent Barrett's esophagus in at-risk patients," said Wa Xian.

"Additionally," noted McKeon, "we are cloning the stem cells for both these precursors and for Barrett's esophagus itself, and these should represent critical targets for both monoclonal antibodies and small molecule inhibitors."

Finally, there is reason to believe that this unusual mechanism might apply to a subset of other lethal cancers with unsure origins.

Crum noted that "some very aggressive cancers arise at junctions of two tissues and these deserve closer scrutiny to get at their origins if we are to surmount these diseases."

This work was supported by the National Institutes of Health.