#8 Possible Causes of Nose Bleeding

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8 Possible Causes of Bleeding When You Blow Nose

Traveling outside home can be strenuous. Even for those who do it on a regular basis and have the routine so set that they can accomplish it on auto-pilot, a change in routine can be disconcerting and throw off the whole morning. When seasons change and your body reacts, issues can result. For example, imagine you are standing on the train, awaiting your stop, when a sudden sneeze leads to nose blowing, and you look down to see that there was blood. This can be a slight abnormality that is no cause for concern if you are generally in good health. However, it can be a precursor for the discovery of serious issues.

Why Is There Blood When Blowing Nose?

1. Chronic Congestion

For those who deal with congestion on a regular basis, the tissue lining the passages of the nose can become inflamed. When this occurs, blowing the nose can lead to some minor damage to the tissue and result in a tiny amount of blood being excreted. This is what leads to blood in the tissue after you blow your nose. This tends to not repeat or cause increasing amounts of blood. Therefore, this issue is not cause for serious concern.

2. Broken Capillaries

The capillaries are small blood vessels in the nose that provide oxygen to the organ. Capillaries are needed to keep the internal surface of the nose alive, and therefore are close to the surface. This means they can break easily. For individuals on blood-thinners like Plavix or Coumadin, this occurs even more regularly and the severity of the nosebleed is increased. Therefore, individuals on these medications are advised to avoid blowing their nose whenever possible.Cold and dry weather increases the issues with capillaries and their tendency to burst.

3. Infection

If blood when blowing nose appears in conjunction with crusting on the inside of the nose, a slight infection may be present in the lower nostrils. These blood vessels can become inflamed and bleed, sometimes extensively, when one blows their nose. It can require cauterization to deal with the problem. This will require a visit to the doctor and a discussion of how often the bleeding occurs.

4. Allergies

Congestion in the morning typically points toward an allergic reaction to something in the air. The inflammation associated with this can be called vasomotor rhinitis. This issue can occur during specific seasons of the year, when pollen is more prevalent, or it can be the result of a change in the bedroom environment, i.e. a new pillow or blanket. Identifying the cause can help resolve this particular issue, with no trip to the doctor necessary.

5. Weather

Dry air and sudden drastic changes of temperature can lead to issues with blood when blowing nose. Therefore, while these are not preventable, you can influence the humidity levels in the house and keep them at a level where your nasal tissues do not dry out and crack. If the weather changes quickly, investing in nasal drops and saline sprays can help resolve the damage to your nasal tissue.

6. Acute Bronchitis

While rare, the appearance of blood while blowing nose can indicate a case of acute bronchitis, where the airways that branch out from the trachea are inflamed. This can be caused by a bacterial infection or a viral infection. It can also present with a case of fever. An upper respiratory tract infection or a nasopharyngeal infection can also occur when someone is dealing with acute bronchitis, and these conditions can lead to bleeding when blowing nose as well.

7. Tuberculosis

A bacterial disease that requires aggressive antibiotics for treatment, tuberculosis can show up as blood in the mucus when blowing one’s nose. Even if not infected, a person may have the bacteria that cause tuberculosis, and that can lead to blood in the mucus. If this occurs at the same time as night sweats or fever, weakness and weight loss, it may be wise to consult a doctor.

8. Pulmonary Embolism

This possibility holds the most danger for the individual, if it is the cause of blood in the mucus. In this case, a blood clot develops somewhere in the body and travels until it becomes stuck in one of the arteries in the area of the lungs. Chest pain and shortness of breath that does not resolve with a period of rest are indications this condition is present. If not addressed immediately, a pulmonary embolism can be fatal. Therefore, consult a doctor if there is any possibility this is the reason for the bleeding when blowing nose.

What Can Be Done?

There are some things you can do to prevent or at least minimize the chance of blood when blowing nose. In order to avoid this condition, consider the following options:

  • Taking 25 micrograms of vitamin K twice each day can help blood clot more efficiently. This can help quickly resolve extensive and/or recurring nosebleeds. The vitamin K should be taken for a period of a month before expecting to see results.
  • Avoid blood thinners. Likewise, the use of vitamin E, aspirin and ginseng can thin the blood and increase the chance of bleeding when blowing nose. Therefore, avoid these if prudently possible. If you are prescribed blood thinners, let your doctor know you are having issues with nosebleeds.
  • Low humidity in the home can lead to more nosebleeds and mucus when blowing one’s nose. Therefore, consider increasing the humidity to between 60 and 64 degrees. This should be done especially for the bedroom. Keeping the home dry or too warm leads to drying up the mucous membranes in the nose.
  • Citrus can also be helpful when dealing with repetitive episodes of blood in nasal mucus. Eating more citrus means you get more bioflavonoid, which helps prevent mucus appearing when blowing your nose.

When to Worry

For those who deal with blood in the mucus on a regular basis after blowing their nose, consulting a doctor is a surefire way to help address the issue quickly and efficiently. While the cause is typically allergy or sinus congestion, consulting the doctor can rule out the more serious possibilities and give you peace of mind while addressing the actual cause.

Another definite warning that you should see the doctor is if you continually have issues getting the bleeding to stop. Seeing a doctor can determine the reason for this and help you get back to better health and life without frequent and long-lasting nosebleeds.

Remember to see the doctor immediately if:

  • A nosebleed continues for 20 minutes or more
  • A head injury occurs and the nosebleed is a result of that injury. X-rays can eliminate the possibility that a skull fracture is the cause of the nosebleed.
  • Frequent recurrence of a nosebleed is experienced, i.e. more than once a week.
  • For children with repetitive nosebleeds, a visit to the doctor is recommended in order to ensure no serious medical conditions are being experienced.

#Universidade da Flórida descobre cura para o Lúpus

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Universidade da Flórida descobre cura para o Lúpus


O lúpus é uma doença auto-imune crônica, que pode danificar qualquer parte do corpo, desde a pele até aos órgãos através das articulações.
É uma doença que age por brotamento e, em seguida, parece desaparecer antes de voltar novamente.
Mas os pesquisadores dizem que descobriram que, usando uma combinação de duas drogas já existentes, é possível reverter os efeitos do lúpus em ratinhos.
Em um novo estudo publicado na revista Sciense Translational Medicine, pesquisadores da Universidade da Flórida, Gainesville, descobriram que inibindo determinadas vias metabólicas em células do sistema imunológico que podem combater o lúpus em ratinhos. UF investigadores de saúde podem ter encontrado uma maneira de controlar o lúpus mudando a forma como as células do sistema imunológico utilizam energia.
“O resultado mais surpreendente deste estudo foi que a combinação dos dois inibidores metabólicos foram necessária para inverter a doença. diz a ” Dra. Laurence Morel, da Universidade da Flórida College of Medicine.

dra laurence morel

LES ou lúpus, é uma doença auto-imune em que o sistema imunitário é suposto proteger o organismo contra os invasores externos – ataca os tecidos do próprio corpo, causando inflamação. O lúpus pode, por vezes, têm sintomas semelhantes à artrite.
Um marcadores lúpus são células T CD4 + (células brancas do sangue que activam outras células do sistema imunológico). Para as pessoas com lúpus, o metabolismo das células T é hiperativa. As células T activadas aumentou-hiper envolvem inflamação, e isto significa que mais dano físico. Quando investigadores bloquearam o metabolismo da glicose usando inibidor da glicose, metformina (comum no tratamento da diabetes tipo 2), as células T CD4 voltar à atividade normal (metabolismo fica mais lento CD4 T) e lúpus sintomas foram revertidos. “Se a célula T é normal, a doença fica melhor”, disse Morel.
A equipa de investigação, inicialmente, teve a idéia de usar um ataque em duas frentes sobre lúpus depois de ver uma abordagem semelhante na pesquisa em câncer, disse a Dra. Laurence Morel, diretora de patologia experimental e professor de patologia, imunologia e medicina laboratório na faculdade do F da medicina.

“Se ele funciona para limitar o metabolismo das células cancerosas, deve funcionar para limitar o metabolismo das células T,” disse Dra.Morel.

A eficácia de metformina em restaurar a função normal das células T, quando estudados no laboratório é também um bom sinal para aplicação futura potencial no tratamento de pacientes com lúpus.


“Isto sugere que os inibidores metabólicos também podem ser utilizados para tratar pacientes”, disse Morel. “É a primeira vez que foi demonstrado que pode ter um efeito sobre os sintomas e manifestações de lúpus por normalização do metabolismo celular.”
Os dois utilizados em investigação neste medicamentos do estudo foram mostrados para inibir as vias metabólicas antes, mas a combinação parece ser a chave para o sucesso.

“O resultado mais surpreendente do estudo foi que a combinação dos dois inibidores metabólicos foram necessários para reverter a doença, como poderia ter sido previsto com base em modelos publicados por outras pessoas que se iria funcionar”, disse o co-autor , Dra.Laurence Morel, diretor de patologia experimental e professor de patologia, imunologia e medicina de laboratório na Universidade da Florida College of Medicine.

Outros pesquisadores que trabalharam no projeto são: Dr. Eric S. Sobel, professor de reumatologia e professor imunologia clínica; Dr. Byron P. Croker, professor de patologia renal e cirúrgico; e Dr. Todd Brusko, professor associado do Instituto de Diabetes UF, departamento de patologia, imunologia e para laboratórios médicos.
Sua pesquisa foi financiada por doações dos Institutos Nacionais de Saúde e da Aliança para Lupus Research.


#Support for Upfront Immunotherapy in Advanced Renal Cell Cancer

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Resultado de imagem para immunotherapy

Megan Brooks

In a phase 3 study of patients with previously untreated metastatic renal cell cancer (mRCC), use of the anti-PD-L1 immune checkpoint inhibitor atezolizumab (Tecentriq, Roche) in combination with bevacizumab (Avastin, Roche) delayed disease progression by about 3 months longer than standard treatment with sunitinib (Sutent, Pfizer), with fewer side effects.

The benefit of atezolizumab plus bevacizumab was greater for patients with programmed cell death ligand 1 (PD-L1)–positive tumors.

Results of the study “support the consideration of atezolizumab plus bevacizumab as a first-line treatment option” in patients with PD-L1–positive mRCC, said lead author, Robert J. Motzer, MD, a medical oncologist at Memorial Sloan Kettering Cancer Center, New York City.

He discussed the results at a presscast February 5 ahead of the Genitourinary Cancers Symposium (GUCS) 2018, which will be held later this week in San Francisco, California.

The study, known as IMmotion151, is the first randomized, phase 3 trial of a PD-L1/programmed cell death 1 pathway inhibitor (atezolizumab) combined with an anti–vascular endothelial growth factor agent (bevacizumab) as first-line therapy in patients with previously untreated mRCC.

A total of 915 patients were randomly assigned to receive atezolizumab (1200 mg) plus bevacizumab (15 mg/kg) intravenously every 3 weeks or oral sunitinib (50 mg/day for 4 weeks, followed by 2 weeks off treatment).  Patients were stratified by PD-L1 status (<1% vs ≥1% PD-L1 expression on tumor-infiltrating immune cells). A total of 362 patients were PD-L1 positive.

At a median follow-up of 15 months, PD-L1–positive patients treated with atezolizumab plus bevacizumab had a 26% lower chance of disease progression than those treated with sunitinib. The median time to progression was 3.5 months longer with the combined treatment than with sunitinib. The overall response rate (ORR) was also better with atezolizumab plus bevacizumab.

Table 1. Results in PD-L1–Positive Patients

Outcome Atezolizumab + Bevacizumab (n = 178) Sunitinib (n = 184) Hazard Ratio
Median PFS 11.2 mo (8.9 – 15.0 mo) 7.7 mo (6.8 – 9.7 mo) 0.74 (0.57 – 0.96)
ORR (%) 43 (35 – 50) 35 (28 – 42)
Values in parentheses are 95% confidence intervals. ORR, objective response rate; PFS, progression-free survival.

The benefits of atezolizumab plus bevacizumab were also observed, though more modest, in the entire study population (intention-to-treat [ITT] population), Dr Motzer reported. Patients who received atezolizumab and bevacizumab had a 17% lower chance of progression, with a median time of 2.4 months longer until the cancer worsened.


Table 2. Results in ITT Population

Outcome Atezolizumab + Bevacizumab (n = 454) Sunitinib (n = 461) Hazard Ratio
Median PFS 11.2 mo (9.6 – 13.3 mo) 8.4 mo (7.5 – 9.7 mo) 0.83 (0.70 – 0.97)
ORR (%) 37 (32 – 41) 33 (29 – 38)
Values in parentheses are 95% confidence intervals. ORR, objective response rate; PFS, progression-free survival.


“The results of the overall survival in the group of patients expressing PD-L1 and in the ITT group are immature. They await further follow-up but certainly the trend that we are seeing, or the path that is being taken here, is in favor of atezolizumab plus bevacizumab over sunitinib,” said Dr Motzer.

“One of the main benefits of the atezolizumab plus bevacizumab is its safety profile,” Dr Motzer said. “It is very well tolerated” and compared with sunitinib, was associated with fewer high-grade treatment-related adverse events (40% vs 54%), low steroid use, and delayed symptom interference with daily life, he noted.

[This study represents an] important breakthrough in kidney cancer therapy.Dr Sumanta Pal

Briefing moderator and American Society of Clinical Oncology expert Sumanta Pal, MD, said this study represents an “important breakthrough in kidney cancer therapy.”

“For several years now, we’ve had debates on which treatment strategy is best for this disease — targeted therapy or immune therapy.  This study, which is really the first of its kind, points to a combination of both as being highly effective in delaying cancer growth, and there is also an early trend toward improving survival. Another important piece of this data is the tolerability of combining targeted therapy with immune therapy,” said Dr Pal, a medical oncologist at the City of Hope Cancer Center in Los Angeles, California.

Dr Pal also said he agrees with Dr Motzer that the data support consideration of bevacizumab and atezolizumab as a first-line option.

This study was funded by F. Hoffmann-La Roche Ltd. Dr Motzer and several study authors have financial ties to industry, including Pfizer, Bristol-Myers Squibb and Genentech/Roche. Dr Pal has financial ties to multiple pharmaceutical companies.

Genitourinary Cancers Symposium (GUCS) 2018. Abstract 578. To be presented February 8, 2018.

#Dolutegravir-Rilpivirine Effective for Maintaining HIV Suppression

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Resultado de imagem para hiv

By Will Boggs MD

NEW YORK (Reuters Health) – The recently approved combination of dolutegravir and rilpivirine is effective for maintaining virological suppression in adults with HIV-1, according to results from the SWORD-1 and SWORD-2 noninferiority studies.

“The most interesting and significant finding in SWORD was that the dolutegravir and rilpivirine regimen achieved noninferior viral suppression (viral load <50 copies/mL) at 48 weeks compared with a three- or four-drug regimen,” Dr. Lesley P. Kahl from ViiV Healthcare, Brentford, UK, told Reuters Health by email. “This happened in both the pooled and individual analyses of SWORD 1 and SWORD 2.”

Current treatment guidelines support a three-drug antiretroviral therapy (ART) regimen, but there has been growing support for two-drug regimens to minimize cumulative drug exposure and reduce risks for long-term drug-related toxicities. The primary concern has been whether two-drug regimens lead to treatment-emergent resistance and subsequent virological failure.

Dr. Kahl and colleagues evaluated the efficacy and safety of dolutegravir-rilpivirine compared with continuation of current ART for 48 weeks in 1,028 adults infected with HIV-1.

At the week 48 primary-endpoint analysis, 95% of patients in SWORD-1 and 94% of patients in SWORD-2 maintained viral suppression after switching to dolutegravir-rilpivirine, compared with 96% and 94%, respectively, who remained on their current ART, the researchers report in The Lancet, online January 5.

In the pooled analysis, 95% of participants in both treatment groups maintained viral loads lower than 50 copies/mL, thereby confirming the noninferiority of dolutegravir-rilpivirine.

Adverse events considered to be drug related and those leading to withdrawal from the study were more common among patients switching to dolutegravir-rilpivirine than among those continuing their current ART.

Switching to dolutegravir-rilpivirine had no effect on lipid levels or inflammatory or cardiovascular biomarkers.

“The results from these studies change our understanding of how HIV can be managed,” Dr. Kahl said. “For more than 20 years we thought that three or more drugs were required to maintain virologic suppression, but the SWORD studies provide compelling data that suppression can be maintained with a two-drug regimen of dolutegravir and rilpivirine.”

“This was reflected in updates made to clinical guidelines during 2017, which saw both the U.S. Department for Health and Human Services (DHHS, October 2017) and the European AIDS Society (EACS, October 2017) guidelines recommend a dolutegravir and rilpivirine regimen as a switch option for virologically suppressed patients,” she said.

#A Way to Stop Allergic Reactions Before They Happen?

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A Way to Stop Allergic Reactions Before They Happen?

A Way to Stop Allergic Reactions Before They Happen?

If you’re one of the unlucky millions of people burdened by allergies, you know that sometimes there’s only so much antihistamines can do to help.

Researchers have been working to find more effective allergy treatments, and now they’ve discovered how a particular antibody can stop an allergic reaction from happening altogether.

An allergic reaction is the immune system’s way of completely overreacting to a normally benign substance, from proteins in cat saliva to surprisingly deadly peanuts.

When the body is exposed to an allergen, the immune system goes into overdrive producing ridiculous amounts of a specific type of antibody called immunoglobulin E (IgE). It’s a large, Y-shaped molecule that attaches itself to the immune cells tasked with releasing invader-attacking chemicals.

These compounds – especially histamine – go on to produce the varied and miserable symptoms of an allergy, whether it’s a runny nose and eyes, or the more serious anaphylactic reaction that accompanies severe food allergies or insect bites.

Allergy tablets typically target these immune system compounds or their receptors, therefore preventing or at least easing the allergy symptoms. But if we target IgE itself, there’s a chance to prevent the allergic reaction from even taking place.

A team led by scientists at Aarhus University in Denmark has now discovered a mechanism through which a particular anti-IgE antibody can make this miracle happen.

This new antibody, called 026 sdab, was first derived from llamas and is akin to a range of such molecules discovered in camelid species and cartilaginous fishes.

The way 026 sdab works in the human body is by preventing IgE from getting to two specific types of immune receptors – CD23 and FceRI – and thus stopping the allergic reaction before it even starts.

“Once the IgE on immune cells can be eliminated, it doesn’t matter that the body produces millions of allergen-specific IgE molecules,” says the senior author of the study, Edzard Spillner from Aarhus University.

“When we can remove the trigger, the allergic reaction and symptoms will not occur.”

While the antibody hasn’t yet been tested in actual people, the team used blood samples from people with diagnosed allergies to birch pollen and insect venom and watched how the antibody performed.

Within just 15 minutes, treatment with 026 sdab reduced IgE levels down to 30 percent from the starting amount, and even further down when the test lasted longer.

“We can now precisely map how the antibody prevents binding of IgE to its receptors,” says one of the team, molecular biologist Nick Laursen from Aarhus University.

“This allows us to envision completely new strategies for engineering medicine of the future.”

There’s already one anti-IgE therapy on the market, called omalizumab – it’s approved in over 90 countries for the treatment of stubborn cases of allergic asthma, but isn’t always effective.

According to the team, 026 sdab is a much smaller antibody than what’s currently available or in development. It’s also easier to produce and is “extremely stable”, which means it doesn’t have to be injected like omalizumab does.

“This provides new opportunities for how the antibody can be administered to patients,” says Spillner.

There’s still a while to go before this amazing-sounding treatment makes its way to humans – it still needs to undergo extensive testing, including safety research.

But the team’s findings could also open up avenues for discovering more similar antibodies, thus speeding up the process – and we’re really excited.

“Our description of the 026 sdab mode of action is likely to accelerate the development of anti-allergy and asthma drugs in the future,” the team writes in the paper.

The study has been published in Nature Communications.


#Antibody-Drug Conjugates in Glioblastoma Multiforme: Finding Ways Forward

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Antibody-Drug Conjugates in Glioblastoma Multiforme: Finding Ways Forward

Antibody-Drug Conjugates in Glioblastoma Multiforme: Finding Ways Forward
This interview focuses on the role of EGFR and other molecular pathways in GBM pathophysiology, and will review latest clinical trial data.
  • Overview

    Glioblastoma Multiforme (GBM) is the most common and most malignant of all glial tumors. These tumors present a challenge to the team managing the patient, as there is no curative treatment; the goal is to find the best approach and optimal role for each team member. There are a variety of treatment options, which include surgery (resection), radiotherapy, and chemotherapy. The prognosis for these patients is measured in years with respect to median survival; with one study reporting nearly 10% of patients live five years or longer.

    The current clinical research environment includes a variety of new approaches to treating patients with GBM, and antibody-drug conjugates (ADCs) are one type of treatment currently being investigated.

#Descoberta molécula contra a esclerose múltipla

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Descoberta molécula contra a esclerose múltipla

É a primeira vez o tratamento da doença é associado com sucesso à testosterona, um avanço que “poderá conduzir a um nível inteiramente novo de terapia”, diz investigadora.

Foto: André Kosters/Lusa
Foto: André Kosters/Lusa

Investigadores da Universidade de Northwestern, em Chicago, identificaram uma molécula ligada à testosterona, hormona masculina, que parece proteger contra a esclerose múltipla.

Nas experiências efectuadas com ratos do sexo feminino, manipulados geneticamente, o tratamento com esta molécula protectora levou ao desaparecimento dos sintomas.

A esclerose múltipla é uma doença inflamatória que ataca o sistema nervoso central e destrói a mielina, substância que envolve e protege as fibras nervosas no cérebro e na espinal medula.

A molécula agora descoberta desencadeia diversas reações químicas que impedem que a mielina seja atacada por outro tipo de célula.

“Este avanço poderá conduzir a um nível inteiramente novo de terapia contra a esclerose múltipla”, explica Melissa Brown, a principal autora do trabalho e professora de Imunologia da Faculdade de Medicina da Universidade de Northwestern.

A investigação permitiu compreender como a testosterona fornece protecção contra a esclerose múltipla, o que até ao momento não era possível.

A doença afecta sobretudo as mulheres, numa proporção de três a quatro vezes mais do que os homens.


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