San Diego’s huge outbreak of hepatitis A ― a preventable but deadly virus that is spread through contact with human feces ― captured national media attention in September. The city began washing streets it believed were contributing to the problem with bleach and initiated a local vaccination campaign among the communities most affected. Soon, it was out of the national conversation.
But similar outbreaks have continued throughout the country, still largely among the homeless and illicit drug-using populations who are most vulnerable to the disease, with few national headlines in sight. Meanwhile, the Morbidity and Mortality Weekly Report out of the Centers for Disease Control and Prevention ― which the agency itself calls the “voice of the CDC” ― has not provided accurate year-end numbers for hepatitis A, making the disease appear less widespread than it truly is.
A HuffPost analysis of CDC and California Department of Health data has found that from 2016 to 2017, hepatitis A cases shot up 48.7 percent nationwide ― an unprecedented spread of the sometimes deadly virus. That contrasts with what the CDC has reported in the MMWR: a mere 5.4 percent increase.
The CDC declined to publicly comment on the 48.7 percent figure.
But public health experts across the country point to a combination of forces that are driving the nationwide outbreak ― the vulnerable homeless population, whose numbers rose last year for the first time since 2010; rising illegal drug users, who often don’t seek or are unable to access medical care; and a lack of alternative sanitary services for those who don’t have housing.
“We’re continuing to have an affordable housing crunch, which means you have more homeless people. And oftentimes communities close the public bathrooms because of the opioid epidemic and people overdosing,” said Laura Hanen, interim executive director and chief of public affairs of the National Association of County and City Health Officials. “Some of that is likely contributing to what we’re seeing.”
What results are outbreaks like San Diego’s, which numbered over 580 cases from late 2016 through this March, including 20 deaths. Responding to the disaster has cost San Diego County’s health department more than $9.5 million. Michigan has seen its own outbreak spread across the state, culminating in 777 illnesses and 25 deaths since it began in a southeastern pocket of the state in August 2016. Louisville, Kentucky, which is the latest city to face an outbreak, has 128 sick and one dead since declaring that outbreak in November 2017, health officials told HuffPost.
“My guess is that we’re closer to the beginning than the end” of fighting the outbreak in Kentucky, said Dave Langdon, a public information officer for the Louisville Metro Department of Health and Wellness.
A new study shows that a government program for managing chronic care cuts costs while also improving care for the chronically ill.
A federal program for chronic care management (CCM) slows the increase in Medicare costs, helps keep people out of the hospital, and connects them with community-based resources, according to a recent report from the Center for Medicare and Medicaid Innovation (CMMI).
The program results could be replicated by private health plans.
The Centers for Medicare and Medicaid Services (CMS) established CMMI in 2015 to help provide support for patients with multiple chronic conditions in-between their provider visits and episodes of care, creating a new Medicare benefit. The program helps beneficiaries with two or more chronic conditions by providing new “in-between visit” payments to participating providers.
That revenue encourages healthcare providers to focus more on goal-directed, person-centered care planning, and to provide "aging-in-place" resources such as proactive care management, the report explains.
Over 684,000 beneficiaries received CCM services during the first two years of the new payment policy, the report says. They were generally concentrated in the South and had poorer health status than the general Medicare fee-for-service (FFS) population.
Narrator: You are listening to ReachMD. Welcome to this Medical Industry Feature, sponsored by Quest Diagnostics. The following program is intended for healthcare professionals only. Your host is Mario Nacinovich.
Host: On today’s program, we will be discussing IBS and the importance of testing to help your patients understand their gut problems.
I’m your host Mario Nacinovich and joining me today is Dr. Christine Frissora, Gastroenterologist and leading IBS expert.
Dr. Frissora, welcome to the program. We’re looking forward to hearing your perspectives today.
Guest: Thank you so much Mario. I’m glad to be here to discuss something that affects millions of Americans and causes a lot of suffering in my patients.
Host: Dr. Frissora, let’s start with some foundational updates on irritable bowel syndrome. How do we define the disease, who does it affect, and what do we think may cause it?
A neurokinin 3 receptor (NK3R) antagonist was effective at improving vasomotor symptoms without the need for estrogen exposure, both in the short and long-term, researchers reported.
The oral NK3R antagonist MLE4901 was able to reduce the frequency of hot flashes by 72% by day 3 of treatment versus baseline symptoms (95% CI -81.3% to -63.5%) and a 51% improvement in frequency with the oral treatment compared with those on placebo, according to Julia K. Prague, MBBS, of Imperial College London, and colleagues.
Without tapering off, this effect was maintained throughout the 4-week study, they wrote in Menopause: The Journal of The North American Menopause Society.
"We conducted this study because menopausal flushing is a major problem, which affects the lives of millions of women worldwide and current treatments have side effects or are not effective," co-author Waljit S Dhillo, MBBS, PhD, also of Imperial College London, explained to MedPage Today. "We expected the neurokinin 3 receptor antagonist to reduce hot flushes based on previous data in animals, which suggested this approach should work to relieve menopausal flushing. However we were surprised at how effective the drug worked -- almost a miracle drug for this condition."
Neurokinin B/NK3R signaling is critical in menopausal flushing, and may be attenuated by administration of an oral NK3R antagonist, but without the addition of estrogen, according to the authors.
Patients with untreated or uncontrolled hypertension reached blood pressure goals after treatment with a low-dose "triple pill," researchers reported here.
In a study conducted in Sri Lanka and among 647 patients with data at 6 months, the triple-pill was associated with greater achievement of blood pressure target levels compared with usual care (70% versus 55%, RR 1.23, [95% CI 1.09, 1.39, P=0.0007), according to Ruth Webster, PhD, MBBS, of the George Institute for Global Health at the University of New South Wales in Sydney, and colleagues.
The triple pill was a fixed-dose combination of telmisartan (20 mg), amlodipine (2.5 mg), and chlorthalidone (12.5 mg). An option for a a double dose version at or after 6 weeks was allowed.
The maximum difference in treatment arms was observed at 6 weeks (68% versus 44%, RR 1.53, 95% CI 1.33, 1.76, the authors reported in a presentation at the American College of Cardiology annual meeting.
"Based on our findings, we conclude that this new method of using blood pressure-lowering drugs was more effective and just as safe as current approaches," Webster said.
Just for context, the first half dozen expeditions into pre-revolutionary war Michigan resulted in a high death rate from malaria.
A one-time gene mutation in a West African human millennia ago gave them immunity to malaria and doomed some of their descendants to sickle cell anaemia, according to new research.
Today, about 300,000 children are born with sickle cell anaemia every year, with that number expected to rise to 400,000 in the next 30 years. The majority of these cases occur in Nigeria, the Democratic Republic of Congo, and India, and many of these babies are likely to die from the disease in which their red blood cells break apart, leaving their bodies starved of oxygen. It is caused by two copies of a gene mutation in their DNA. One copy is harmless; two copies can be deadly. Millions of people worldwide, frequently those with African heritage, are carriers of this mutant gene, but there are large gaps in our knowledge of the disease and its characteristic mutations.
Sickle cell anaemia contributes the equivalent of 5% of deaths of under-five-year-old children on the African continent, according to the W.H.O, more than 9% of such deaths in west Africa, and up to 16% of under-five deaths in individual west African countries.
The new research, published in scientific journal Cell, has found that this disease began with a single ancestor who developed the mutation to fend of malaria.
After we eat, our blood sugar levels increase. To counteract this, the pancreas releases a hormone called insulin. Part of insulin’s effect is to promote the uptake of sugar from the blood into muscle and fat tissue for storage. Under certain conditions, such as obesity, this process can become defective, leading to a condition known as insulin resistance. This condition makes a number of human diseases more likely to develop, including type 2 diabetes. Working out how insulin resistance develops could therefore unveil new treatment strategies for these diseases.
Mitochondria — structures that produce most of a cell’s energy supply — appear to play a role in the development of insulin resistance. Mitochondria convert nutrients such as fats and sugars into molecules called ATP that fuel the many processes required for life. However, ATP production can also generate potentially harmful intermediates often referred to as ‘reactive oxygen species’ or ‘oxidants’. Previous studies have suggested that an increase in the amount of oxidants produced in mitochondria can cause insulin resistance.
Fazakerley et al. therefore set out to identify the reason for increased oxidants in mitochondria, and did so by analysing the levels of proteins and oxidants found in cells grown in the laboratory, and mouse and human tissue samples. This led them to find that concentrations of a molecule called coenzyme Q (CoQ), an essential component of mitochondria that helps to produce ATP, were lower in mitochondria from insulin-resistant fat and muscle tissue. Further experiments suggested a link between the lower levels of CoQ and the higher levels of oxidants in the mitochondria. Replenishing the mitochondria of the lab-grown cells and insulin-resistant mice with CoQ restored ‘normal’ oxidant levels and prevented the development of insulin resistance.
Strategies that aim to increase mitochondria CoQ levels may therefore prevent or reverse insulin resistance. Although CoQ supplements are readily available, swallowing CoQ does not efficiently deliver CoQ to mitochondria in humans, so alternative treatment methods must be found. It is also of interest that statins, common drugs taken by millions of people around the world to lower cholesterol, also lower CoQ and have been reported to increase the risk of developing type 2 diabetes. Further research is therefore needed to investigate whether CoQ might provide the link between statins and type 2 diabetes.
New research from the University of British Columbia suggests that following a strict eating schedule can help clear away the protein responsible for Huntington disease in mice.
Huntington disease (HD) is an inherited, progressive disorder that causes involuntary movements and psychiatric problems. Symptoms appear in adulthood and worsen over time. Children born to a parent with HD have a one in two chance of inheriting the disease, which is caused by a buildup of mutant huntingtin protein (mHTT).
In research published today, scientists stimulated autophagy–a process in which the cell cleans out debris and recycles cellular material such as proteins–by restricting access to food in mice with HD to a six-hour window each day. This led to significantly lower levels of mHTT in the brain.
“We know that specific aspects of autophagy don’t work properly in patients with Huntington disease,” said study lead author Dagmar Ehrnhoefer, who conducted the study while she was a researcher with the UBC Centre for Molecular Medicine and Therapeutics. “Our findings suggest that, at least in mice, when you fast, or eat at certain very regulated times without snacking in between meals, your body starts to increase an alternative, still functional, autophagy mechanism, which could help lower levels of the mutant huntingtin protein in the brain.”