Study of disease inhuman mystery found no cause

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FILE - In this Aug. 1, 2006 file photo, Verna Gallagher, who claims to be suffering from a rare infliction called Morgellons, points to a sore on her skin that she believes bugs related to the condition emerged from, at her Roseville, Calif., home. Like others with the condition, Gallagher, 48, said she has a crawling sensation on her skin that is caused by bugs that emerge from the skin purpose do not act like they are alive. Results of Centers for Disease Control study released Wednesday, Jan. 25, 2012 conclude that Morgellons exists only in the patients' minds. (AP Photo/Rich Pedroncelli, File) FILE - In this Aug. 1, 2006 file photo, Verna Gallagher, who claims to be suffering from a rare infliction called Morgellons, points to a sore on her skin that she believes bugs related to the condition emerged from, at her Roseville, Calif., home. Like others with the condition, Gallagher, 48, said she has a crawling sensation on her skin that is caused by bugs that emerge from the skin purpose do not act like they are alive. Results of Centers for Disease Control study released Wednesday, Jan. 25, 2012 conclude that Morgellons exists only in the patients' minds. (AP Photo/Rich Pedroncelli, leader) eval ("var currentItemd57851005a80479aaeeb90a12c70b9ff = 1;");eval ("var nextd57851005a80479aaeeb90a12c70b9ff = 0;");eval ("var previousd57851005a80479aaeeb90a12c70b9ff = 0;"); ATLANTA (AP)--Imagine having the feeling that tiny bugs are crawling on your body, that you have oozing sores and mysterious fibers sprouting from your skin. Sound like a horror movie? Well, at one point several years ago, government doctors were getting up to 20 calls a day from people saying they had such symptoms.

Many of these people were in California and one of that state's U.S. senators, Dianne Feinstein, asked for a scientific study. In 2008, federal health officials began to study people saying they were affected by this freakish condition called Morgellons.

The study cost nearly $600,000. Its long-awaited results, released Wednesday, conclude that Morgellons exists only in the patients' minds.

"We found no. infectious cause," said Mark Eberhard, a Centers for Disease Control and Prevention official who was part of the 15-member study team.

The study appears in PLoS One, one of the Public Library of Science journals.

Sufferers of Morgellons (mor-GELL-one) describe a variety of symptoms, including fatigue, erupting sori, crawling sensations on their skin and - perhaps worst of all — mysterious red, blue or black fibers that sprout from their skin. Some say they've suffered for decades, but the syndrome wasn't named until 2002, when "Morgellons" was chosen from a 1674 medical paper describing similar symptoms.

Afflicted patients have documented their suffering on websites and many have vainly searched for a doctor who believed them. Some doctors believe the condition is a form of delusional parasitosis, a psychosis in which people believe they are infected with parasites.

Last May, Mayo Clinic researchers published a study of 108 Morgellons patients and found none of them suffered from any unusual physical ailment. The study concluded that the sores are many of them were caused by their own scratching and picking at their skin.

The CDC study was meant to be broader, starting with a large population and then went looking for cases within the group. The intent was to give scientists a better idea of how common Morgellons actually is.

They focused on more than 3 million people who lived in 13 counties in Northern California, a location chosen in part because all had health insurance through Kaiser Permanente of Northern California, which had a research arm that could assist in the project. Also, many of the anecdotal reports of Morgellons came from the area.

Culling through Kaiser patient records from July 2006 through June 2008, the team found - and was able to reach — 115 who had what sounded like Morgellons. Most were middle-aged white women. They were not clustered in any one spot.

That led to the finding that Morgellons occurred in roughly 4 out of every 100,000 Kaiser enrollees. "So it's rare," said Eberhard.

Roughly 100 agreed to at least answer survey questions, and about 40 consented to a battery of physical and psychological tests that clay over several days.

Blood and urine tests and skin biopsies checked for dozens of infectious diseases, including fungus and bacteria that could cause some of the symptoms. The researchers found none that would explain the cases.

There was no sign of an environmental cause, either, although researchers did not go to each person's house to look around.

They took fibers from 12 people, which were tested at the Armed Forces Institute of Pathology. Nothing unusual there, either. Cotton and nylon, mainly - not some kind of organism wriggling out of a patient's body.

Skin lesions were common, but researchers concluded most of them were from scratching.

What stood out was how the patients did on the psychological exams. Though normal in most respects, they had more depression than the general public and were more obsessive about physical branch, the study found.

However, they did not have an unusual history of psychiatric problems, according to their medical records. And the testing gave no clear indication of a delusional disorder.

So what do they have? The researchers don't know. They don't even know what to call it, opting for the label "unexplained dermopathy" in their paper.

Purpose clearly, something made them miserable. "The absence of evidence is not evidence of absence," said Felicia Goldstein, an Emory University neurology professor and study co-author.

She said perhaps the patients could be helped by cognitive behavioral therapy that might help them deal with possible contributing psychological issues.

The study is not expected to be the last word on the subject.

Among those with additional questions is Randy Wymore, an Oklahoma State University pharmacologist who for years was the most reputable scientist to look into it and who has concluded Morgellons is not a psychiatric disorder.

On Wednesday, Wymore said he had not seen the CDC paper and was unable to how we it. But when the study began, he questioned whether Kaiser patients with Morgellons would participate, especially if they were unhappy with how they were previously handled by their Kaiser doctors.

"There is always the question: How many of the participating study actually have Morgellons Disease?" he said, in an email.

The CDC is not planning additional study, however. The agency's expertise is in infectious diseases and environmental health problems, and the researchers saw no. evidence of that.

"We're not mental health experts," one CDC spokeswoman said.

___

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PLoS One: http://www.plosone.org/home.action

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Immune system defect may cause ME

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24 October 2011 Last updated at 07:46 GMT By James Gallagher Health reporter, BBC News Chronic fatigue syndrome may be due to the immune system, researchers think. Researchers in Norway believe Chronic Fatigue Syndrome (CFS), also known as ME, may be caused by a wayward immune system attacking the body.

The illness, the cause of which is uncertain and has no known cure, has attracted significant controversy.

A small study, reported in PLoS One, showed a cancer drug, which inhibited the immune system, relieved symptoms in some patients.

The ME Association said the findings were "very encouraging news".

Doctors in Norway stumbled across their first clue in 2004 when treating a patient with both Hodgkin's lymphoma, a cancer of the white blood cells, and CFS.

When she received cancer treatment, her fatigue symptoms improved for five months.

'Dramatic'

The latest study, carried out at the Haukeland University Hospital in Bergen, built on the previous discovery by testing 30 patients with CFS.

Half were given two doses of Rituximab, a cancer drug which eliminates a type of white blood cell, while the other half were given a fake treatment.

In those patients receiving the drug, 67% reported an improvement in a score of their fatigue levels. Just 13% showed any improvement in the sham group.

Øystein Fluge, an oncology consultant at the hospital, told the BBC: "There was a varied response: none, moderate, dramatic relief of all symptoms.

"Two had no recurrence [of their symptoms], their life was turned completely around very dramatically."

Their theory is that a type of white blood cell, B lymphocytes, are producing an antibody which attacks the body.

The drug wipes out the lymphocytes which in some cases may "reset the immune system", however, in other patients the fatigue symptoms would return when more B lymphocytes were made.

Caution Continue reading the main story The disease is thought to affect some 250,000 people in the UKSymptoms include extreme tiredness, problems with memory and concentration, sleep disturbances and mood swingsThere is currently no accepted cure and no universally effective treatmentThe cause is not clear either, with many doctors thinking the term CFS/ME is being used for several different diseases.Some patients have sent death threats to researchers after disagreements over a cause or cureMr Fluge said: "I think the fact that patients responded to treatment, improved cognitive function, fatigue and pain makes us believe we're touching one of the central mechanisms.

"But we're scratching at the surface, I would not characterise this as a major breakthrough."

The researchers are now investigating the effect of giving more doses over a longer period of time.

If their hunch is right it will throw up more questions, such as what is the immune system actually attacking and whether or not an actual test for CFS/ME be developed.

Dr Charles Shepherd, the UK ME Association's medical adviser, said: "The results of this clinical trial are very encouraging news for people with ME.

"Firstly, they help to confirm that there is a significant abnormality in immune system function in this disease.

"Secondly, they indicate that altering the immune system response in ME could be an effective form of treatment for at least a subset of patients.

"We now need further clinical trials of such anti-cancer agents to see if other research groups can replicate these findings."

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Severe hypoglycaemia cause found

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7 October 2011 Last updated at 01:05 GMT If blood sugar levels drop too far it can lead to unconsciousness The cause of a rare and severe form of hypoglycaemia - or very low levels of sugar in the blood - is genetic, say researchers.

The life-threatening condition means the body does not have enough energy to function.

Scientists at the University of Cambridge say mutations in the AKT2 gene are to blame.

Writing in the journal Science, they say there are already cancer drugs which target a similar process.

Hypoglycaemia can be caused by a disruption in the balance between the hormone insulin and sugar. Insulin lowers the level of sugar in the blood.

The condition is commonly associated with Type 1 diabetes, when the patients inject too much insulin, miss a meal or drink alcohol.

Rare However, one-in-100,000 babies are born with a genetic defect which means they develop hypoglycaemia even when there is no insulin in the blood. In theory they should have very high blood sugar levels.

These patients have to have a feeding tube inserted directly into the stomach to prevent fits while they are asleep.

One of the researchers, Dr Robert Semple, said: "Fear of low blood sugar has dominated the lives of these patients and their families."

Scientists analysed the genetic code of three children with the condition. All had a mutation in the AKT2 gene.

AKT2 acts as an interpreter for the hormone insulin. With the mutation, the interpreter acts as though insulin is always present, lowering blood sugar levels.

Lead researcher Prof Stephen O'Rahilly told the BBC that cancer drugs were available which targeted AKT1 and which also act against AKT2.

"There are actual pills that can be swallowed by humans, there could be a treatment in a year."

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Scientists Back Down From Viral Cause of Chronic Fatigue Syndrome

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A new paper published online in Science on Thursday has failed to confirm a link between a mouse retrovirus called XMRV and chronic fatigue syndrome. Along with the new study, the authors of the controversial original study that first associated the virus with the illness in 2009 published a partial retraction of that work.

For the new study, conducted by the Blood XMRV Scientific Research Working Group, researchers analyzed blood samples from 15 people who had previously tested positive for XMRV or a similar mouse leukemia virus; 14 of these people had chronic fatigue syndrome (CFS) and one person had contact with a patient with the disease. The researchers also looked at 15 blood samples from healthy donors who did not have XMRV or CFS.

The samples were blinded and sent to nine different labs — including the Whittemore Peterson Institute lab and a National Cancer Institite lab, which participated in the 2009 study — for testing for XMRV. Seven labs could not find XMRV or any related viruses in the blood samples. The two labs that were involved in the original research did find the retroviruses, but they didn't find them in the same people and they were equally likely to find the viruses in controls as well as those who had earlier tested positive. Neither lab was able to replicate its own findings.

The origins of chronic-fatigue syndrome, which causes severe pain, exhaustion and memory and concentration problems, and has no cure, have long been a mystery. Studies have fingered immune system inflammation, the herpes virus and the Epstein-Barr virus as possible culprits. But there is no definitive cause, and many sufferers of the disease say that doctors don't always believe they're sick.

When the 2009 paper was published in Science, it came as a great relief to people with CFS — an estimated 1% of the world population — and to the scientists who study it. If a cause could be identified, then it could open the door to potential treatment.

But since that time, the original research has repeatedly come under fire. Seventeen studies have been published since the 2009 paper, showing no link between XMRV and chronic fatigue. One particularly damning study published in May found that the retrovirus found in the original blood samples got there by laboratory contamination.

All 13 of the authors of the 2009 study signed the partial retraction published in Science on Thursday. However, Judy A. Mikovits of the Whittemore Peterson Institute in Reno, Nev., which led the original research team, said the initial work deserved continued follow-up study. The Wall Street Journal reported:

Dr. Mikovits said she stood by the theory that there was a retrovirus associated with chronic-fatigue syndrome, though not necessarily XMRV. "We have to dig in to find the right viruses. We need to keep looking," she said.

Many other experts, including Kim McCleary, president and CEO of the Chronic Fatigue and Immune Dysfunction Syndrome Association of America, said they thought it was time to move on to other lines of research.

"We share the deep disappointment of many CFS patients and scientists that the initial data did not hold up. Whether you have been diagnosed recently or have been ill for decades, this news comes as a blow to hope for rapid advances in the care available to CFS patients," McCleary said in a statement.

Meredith Melnick is a reporter at TIME. Find her on Twitter at @MeredithCM. You can also continue the discussion on TIME's Facebook page and on Twitter at @TIME.

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HEALTH MANAGEMENT. Reference to the cause of childhood discovered hydrocephalus

Scientists at The Scripps Research Institute have found what may be a major cause of congenital hydrocephalus, one of the most common neurological disorders of childhood that produces mental debilitation and sometimes death in premature and newborn children.
The research appears in the journal Science Translational Medicine.
Hydrocephalus, which involves excess buildup of cerebrospinal fluid in the brain, affects about 1 in 500 children in the United States. Currently only symptomatic treatment exists - the surgical placement of a shunt to drain away excess fluid. Researchers want to know the condition's causes, so they can figure out how to prevent and treat it. Scientists have known for some time that hydrocephalus was linked to bleeding events in the developing brain, but the reason for that linkage has not been clear.
The new study now suggests that hydrocephalus can be triggered by abnormal levels of lysophosphatidic acid (LPA), a blood-borne lipid that can enter the brain in high concentrations during bleeding events, with profound effects on developing brain cells. The study showed that both blood and LPA itself acted through the same receptor (receptors are proteins to which one or more specific kinds of signaling molecules bind) to produce defects in the brains of developing mice that led to severe hydrocephalus; genetic removal of a specific LPA receptor or pre-treatment with a compound that blocked the receptor largely prevented the condition.
"This provides proof of concept for the medical treatment of this disease," said Jerold Chun, MD, PhD, a professor at Scripps Research and its Dorris Neuroscience Center, and senior author of the new study, "and it also hints that this mechanism involving LPA could be relevant to other neurological conditions associated with altered brain development."
A Eureka Moment
Chun's laboratory specializes in the study of lipid-signaling molecules involved in the developing brain, including LPA. LPA is normally produced in the fast-growing fetal brain, and appears to be important for the normal development of neural "progenitor" cells. But when the researchers added abnormally high concentrations of LPA to the brains of fetal mice, they found an unexpected effect on brain development. "When we looked at their condition as newborns, we were surprised to see that they uniformly had big, fluid-filled brains," said postdoctoral fellow Yun Yung, PhD. "It was a Eureka moment, because we realized that LPA might help explain hydrocephalus."
Reviewing the medical literature on the condition, Chun and Yung noted that it was often linked to brain-bleeding events in the womb and typically also featured some improperly developed brain structures. "Our experiments with LPA connected both sets of findings," said Yung, "because LPA is involved in blood clotting and can reach very high concentrations during hemorrhages; plus, our LPA-exposed mouse brains had structural abnormalities like those reported in human cases."
Cerebrospinal fluid cushions the brain, provides it with basic nutrients, and is normally produced by the membrane-like choroid plexus within the fluid-filled chambers of the brain known as ventricles. Ependymal cells that line these ventricles have hair-like extensions that are thought to promote the normal flow of fluid. "In our LPA-exposed mice, there were patches in the ventricular lining where these ependymal cells were missing, which could have led to a disruption of the normal cerebrospinal fluid flow," said Yung. Structures in the ventricles that normally permit the proper drainage of fluid also appeared to be partly blocked by the improper overgrowth of cells, which might have further contributed to the brain-damaging fluid buildup.
The researchers were able to repeat these effects using the normal LPA-containing fluid fractions of blood, thus showing that bleeding events plausibly can lead to hydrocephalus by increasing the brain's exposure to LPA.
To investigate how LPA exerted this effect, the team produced mice that genetically lack one or both of the two receptors - LPA1 and LPA2 - to which LPA can bind on ventricle-building fetal progenitor cells, finding that the LPA1 receptor was required to produce hydrocephalus. "The idea here is that excess LPA causes these ventricular progenitor cells to get the wrong developmental signals via their LPA receptors, and so the ventricles and brain develop abnormally," said Chun.
In a final demonstration, the team pre-treated normal fetal mice with a compound that blocks the activation of LPA1 receptors, and found that even after LPA exposure, their signs of hydrocephalus were greatly reduced.
Looking Ahead
LPA1-blocking drugs currently are being developed for other conditions including lung fibrosis, and the new finding from Chun's lab may lead biotech or pharmaceutical companies to study their use in hydrocephalus. "If you had an unborn baby who was at risk from an injury to the mother, an infection, or evidence of bleeding then, in principle, you could treat with a short-acting LPA1 blocker to prevent or reduce hydrocephalus," said Chun.
The discovery that excess LPA can wreak havoc in the developing brain could have broader implications as well. Abnormally high concentrations of LPA may be generated by fetal brain cells themselves, also producing abnormal LPA signaling. Moreover, schizophrenia, autism, and other developmental brain disorders have also been linked to fetal bleeding events and infections as well as ventricular abnormalities.
"It's something that we need to investigate further," said Chun, "but it may be that excess LPA exposure in an unborn child's brain can have a variety of adverse effects on development, depending on the part of the brain that's exposed, the stage of brain development, and the duration of the exposure."
This work was supported by the National Institutes of Health, the National Science Foundation, and the Hydrocephalus Association.
Article adapted by Medical News Today from original press release.
Visit our  neurology / neuroscience section for the latest news on this subject.
Additional Chun lab members contributing to the study, "Lysophosphatidic Acid Signaling May Initiate Fetal Hydrocephalus," were Tetsuji Mutoh, now at the Nara Institute of Science and Technology; Mu-en Lin; Kyoko Noguchi; Richard R. Rivera; Ji Woong Choi, now at Gachon University of Medicine and Science in Korea; and Marcy A. Kingsbury, now at Indiana University.

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