Uterine Fibroid Treatment Shows Promise

A noninvasive method of destroying uterine fibroids greatly eases women's symptoms up to a year after the procedure, U.S. researchers report.

Previous papers had shown symptom relief up to six months for the technique, known as magnetic resonance-guided, focused ultrasound surgery or "MRgFUS."

"This is basically continuing out the data," said Dr. Fiona M. Fennessy, an instructor of radiology at Harvard Medical School and a staff radiologist at Brigham and Women's Hospital, both in Boston. "Symptom reduction extends out to 12 months and probably longer."

Fennessy was lead author of a paper to be presented Friday at the Radiological Society of North America annual meeting, in Chicago.

Others say the latest findings should pave the way for more widespread use of the technology.

"It's very promising," said Dr. Kenneth Levey, director of the New York University Center for Pelvic Pain and Minimally Invasive Gynecologic Surgery. "It's fantastic therapy and a wonderful start."

Uterine fibroids are benign tumors of muscle and connective tissue inside the uterus. About a quarter of women aged 25 to 50 have such fibroids, and as many as 50 percent of black women have the growths.

Although some women will report no symptoms, fibroids can cause pain, heavy menstrual bleeding, frequent urination as a result of pressure on the bladder and even infertility and miscarriages.

"The gold standard for treating fibroids is a hysterectomy, but that is very invasive," Fennessy said.

In fact, fibroids are one of the most common reasons for having a hysterectomy, which involves the removal of the entire uterus.

Researchers have been trying to develop both minimally invasive and noninvasive methods to treat fibroids.

MRgFUS, which has been approved by the U.S. Food and Drug Administration and available at several centers in the United States, uses ultrasound to deliver heat to the fibroid tissue. The heat kills the fibroid tissue, while the MRI component of the procedure lets clinicians monitor the location of the ultrasound beam and track temperature changes.

"It's totally noninvasive. There's no incision, no blood. The patient just lies belly down on the scanner, the ultrasound probe is underneath the belly where the fibroid is, and the beam shoots right through from the skin or underneath the skin or right through," Fennessy explained.

Previous studies had shown symptom relief up to six months. The current trial studied followed 160 women with symptomatic fibroids who received MRgFUS out to a year. The women received slightly different treatments. One group received 120 minutes of directed treatment covering a volume of up to 33 percent of total fibroid volume. The other received 180 minutes on a volume of 33 percent of total volume in fibroids on the outer wall of the uterus and 50 percent of volume in other fibroids.

Women who had more fibroid tissue destroyed reported more symptom improvement.

"You create this big hole of dead tissue," Fennessy said. 'The bigger the amount of dead tissue, the greater relief in symptoms. The pressure effect of the fibroid is less."

Will this eventually become the gold standard for fibroid treatment?

That's debatable, Fennessy said.

"It will be a treatment for some women," she said. "For the woman who is not looking for invasive therapy, who wants to go into the hospital for three hours, go home, then go back to work the next day, she will have her symptoms reduced by at least half."

More information

For more on uterine fibroids, head to the National Women's Health Information Center.

Alzheimer's Could Be Diabetes-like Illness, Study Suggests

Could Alzheimer's be a form of diabetes?

That's the tantalizing suggestion from a new study that finds insulin production in the brain declines as Alzheimer's disease advances.

"Insulin disappears early and dramatically in Alzheimer's disease," senior researcher Suzanne M. de la Monte, a neuropathologist at Rhode Island Hospital and a professor of pathology at Brown University Medical School, said in a prepared statement.

"And many of the unexplained features of Alzheimer's, such as cell death and tangles in the brain, appear to be linked to abnormalities in insulin signaling. This demonstrates that the disease is most likely a neuroendocrine disorder, or another type of diabetes," she added.

The discovery that the brain produces insulin at all is a recent one, and de la Monte's group also found that brain insulin produced by patients with Alzheimer's disease tends to fall below normal levels.

Now her group has discovered that brain levels of insulin and its related cellular receptors fall precipitously during the early stages of Alzheimer's. Insulin levels continue to drop progressively as the disease becomes more severe -- adding to evidence that Alzheimer's might be a new form of diabetes, she said.

In addition, the Brown University team found that low levels of acetylcholine -- a hallmark of Alzheimer's -- are directly linked to this loss of insulin and insulin-like growth factor function in the brain.

The report appears in the November issue of the Journal of Alzheimer's Disease.

In its study, de la Monte's team autopsied the brain tissue of 45 patients diagnosed with different degrees of Alzheimer's called "Braak Stages." They compared those tissues to samples taken from individuals with no history of the disease.

The team analyzed insulin and insulin receptor function in the frontal cortex of the brain, a major area affected by Alzheimer's. They found that as the severity of Alzheimer's increased, the levels of insulin receptors and the brain's ability to respond to insulin decreased.

"In the most advanced stage of Alzheimer's, insulin receptors were nearly 80 percent lower than in a normal brain," de la Monte said.

In addition, the researchers found two abnormalities related to insulin in Alzheimer's. First, levels of insulin dropped as the disease progressed. Second, insulin and its related protein -- insulin-related growth factor-I -- lose the ability to bind to cell receptors. This creates a resistance to the insulin growth factors, causing the cells to malfunction and die.

"We're able to show that insulin impairment happens early in the disease," de la Monte said. "We're able to show it's linked to major neurotransmitters responsible for cognition. We're able to show it's linked to poor energy metabolism, and it's linked to abnormalities that contribute to the tangles characteristic of advanced Alzheimer's disease. This work ties several concepts together and demonstrates that Alzheimer's disease is quite possibly a Type 3 diabetes," she said.

One expert believes declining insulin levels may be an important feature of Alzheimer's, but not the whole story.

"There is now increasing evidence primarily from observational studies that diabetes, its predecessor metabolic syndrome, and insulin resistance are implicated in increasing risk for Alzheimer's disease," said Dr. Hugh C. Hendrie. He is a professor of psychiatry and co-director of the Center for Alzheimer's Disease and Related Neuropsychiatric Disorders at Indiana University Center for Aging Research, in Indianapolis.

This study adds support to these biological hypotheses and has perhaps treatment implications for the use of certain types of anti-diabetes drugs that influence insulin resistance, Hendrie said.

"There are many other factors also implicated in Alzheimer's disease, such as hypertension and inflammation, so I think it's a bit of a stretch at the moment to describe Alzheimer's disease as an endocrinological disorder like diabetes," he said.

Another expert thinks that insulin and insulin-like growth factors may be the key to slowing the progression of Alzheimer's.

"We have shown that insulin-like growth factors regulate learning and memory," said Douglas N. Ishii, a professor in the Department of Biomedical Sciences at Colorado State University in Fort Collins. "We had shown that by blocking insulin-like growth factors in the brain you block learning and memory."

When Ishii's group treated rats with insulin-like growth factors, the researchers found that the intervention prevented the loss of both learning and memory. "In addition, we showed that insulin normally regulates brain weight in adults," he said.

"The clinical potential is that by injecting insulin-like growth factors into patients, one might be able to prevent the loss of learning and memory," Ishii said. "In particular, we have a paper coming out showing that insulin-like growth factors can not only prevent the loss of learning and memory, but prevent the loss of a protein in the brain. This may lead to the slowing down of the progression of Alzheimer's."

More information

For more on Alzheimer's disease, visit the Alzheimer's Association.