Emma Hitt, PhD

May 22, 2012

May 22, 2012 (Florence, Italy) — In patients with Prader-Willi syndrome (PWS), the use of growth hormone can increase the risk for insulin resistance, regardless of body mass index (BMI), according to a prospective 1-year study.

Anders Palmstrøm Jørgensen, MD, from the Department of Endocrinology at the Oslo University Hospital in Norway, and colleagues presented the findings here at the Joint 15th International Congress of Endocrinology and 14th European Congress of Endocrinology.

"There are only a few studies published on this topic, and our results add some new information — normal-weight PWS subjects, not only the obese, develop insulin resistance with growth hormone therapy," Dr. Jørgensen told Medscape Medical News.

According to the researchers, diabetes mellitus is prevalent in adults with PWS, and growth hormone therapy might deteriorate glucose balance.

To investigate this issue, the researchers evaluated the effects of growth hormone over the course of 12 months in 35 patients with PWS, assessing parameters such as body composition, insulin resistance, and BMI.

Average age of the patients was 28.5 years, and PWS was confirmed with genetic testing. Patients with diabetes at baseline were excluded from the study. Of the patients, 14 had a BMI below 25 kg/m², 10 had a BMI from 25 to 30 kg/m², and 11 had a BMI above 30 kg/m².

Growth hormone was associated with significant increases in insulin-like growth factor 1 (IGF1), lean mass, 2-hour postprandial glucose, and homeostasis model assessment of insulin resistance (HOMA-IR) (P < .05 for all), and a decrease in fat mass (P < .02).

Although baseline IGF1 was lower at baseline in patients with the lowest BMI, final mean growth hormone dose and IGF1 levels did not differ among the BMI groups.

"A reduction in fat mass was seen only with [a BMI of 25 to 30 kg/m²]...and HOMA-IR increased in the lowest BMI group only," the researchers note.

According to Dr. Jørgensen, the long-term effects of growth hormone therapy on the prevalence of diabetes in adults with PWS remain to be determined. "Clinicians should be aware of the risk of diabetes when treating adult Prader-Willi subjects," he said.

The biochemical/metabolic disturbance regulated by the genetic defect of PWS remains, regardless of the presence or absence of weight, so the findings are not surprising, said Merlin G. Butler, MD, PhD, clinical geneticist and director, the Division of Research Professor of psychiatry, behavioral sciences, and pediatrics at the Kansas University Medical Center in Kansas City, who was asked to comment on the study.

"In addition, even though the weight of a PWS adult may be normalized, the body composition may continue to be disturbed — that is, the fat/mass ratio is not normalized, compared with controls," he told Medscape Medical News.

However, he pointed out that the findings illustrate that at any particular time in the life of an individual with PWS, "they are at risk of complications or outcomes of treatment in spite of their weight."

"When managing and caring for our patients, we must not lose sight of the diagnosis of PWS, regardless of a patient's weight, and complications and health-related issues related to the diagnosis," he said.

The study was investigator initiated and commercially funded by Novo Nordisk. Dr. Jørgensen and Dr. Butler have disclosed no relevant financial relationships.

Joint 15th International Congress of Endocrinology (ICE) and 14th European Congress of Endocrinology (ECE): Abstract OC1.6. Presented May 7, 2012.


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