Day: 04/11/2011

World is losing battle against drug resistance, warns WHO

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WHO poster on antimicrobial resistanceAntimicrobial resistance is a growing problem worldwide

 

A “post-antibiotic” era, in which many common infections no longer have a cure, is on the horizon, the WHO warned today — as scientists reported the discovery of superbugs resistant to almost all known antibiotics in water supplies in New Delhi, India.

“In the absence of urgent corrective and protective actions, the world is heading towards a post-antibiotic era, in which many common infections will … once again, kill unabated,” Margaret Chan, director-general of the WHO, said today, in an address to mark World Health Day, which this year is devoted to combating drug resistance.

“We are at a critical point where antibiotic resistance is reaching unprecedented levels and new antibiotics are not going to arrive quickly enough,” said Zsuzsanna Jakab, the WHO’s regional director for Europe.

“Until all countries tackle this, no country alone can be safe.”

Last year, at least 440,000 new cases of multidrug-resistant tuberculosis were detected, and the more serious, extensively drug-resistant tuberculosis has been reported in 69 countries to date, said the WHO.

Meanwhile, the malaria parasite is acquiring resistance to even the latest generation of medicines and resistance is also emerging to antiretroviral medicines for people with HIV/AIDS.

There are few antibiotics under development — only two new classes of antibiotic have been discovered in the last three decades compared with 11 in the 50 years before that.

The empty pipeline is partly the result of drug companies’ reluctance to spend millions developing a new antibiotic, only to be told by regulators to restrict its use in order to manage the spread of resistance.

“[Antibiotic] discovery needs to be underpinned by new financial mechanisms that allow companies to receive a return on their investment in new drugs, while limiting their use to situations of greatest need,” David Brennan, chief executive of AstraZeneca, told a World Health Day event.

“If leaders in government, science, economics, public policy, intellectual property and philanthropy can come together, we will maximise the opportunities to develop and implement the creative solutions that will truly make a difference to tackling anti-microbial resistance,” he said, according to the Dow Jones Newswires.

The dangers of rising drug resistance are underscored by the discovery, published today in The Lancet Infectious Diseases, that a gene that confers resistance to almost all known antibiotics is present in Indian water supplies.

Scientists from Cardiff University in the United Kingdom tested water samples within a 12-kilometre radius of New Delhi. They found the gene, known as New Delhi metallo-beta-lactamase (NDM-1), in a variety of bugs in two of 50 tap water samples and 50 of 171 community waste seepage samples, such as pools in streets.

Most worryingly, the study found the gene in cholera (Vibrio cholera) and dysentery (Shigella boydii).

The scientists said the discovery “has important implications for people living in the city who are reliant on public water and sanitation facilities”.

They added that “international surveillance of resistance, incorporating environmental sampling as well as examination of clinical isolates, needs to be established as a priority”.

Mohd Shahid, a researcher at the Jawaharlal Nehru Medical College and Hospital, Uttar Pradesh, India, wrote in an accompanying commentary: “Coordinated, concrete, and collective efforts are needed, initially, to limit … widespread dissemination, and finally to combat this emerging threatening resistance problem”.

The WHO today published a policy package that sets out the measures governments and their national partners need to take to combat drug resistance. It says they should develop and implement national plans; strengthen surveillance and laboratory capacity; ensure uninterrupted access to essential medicines of assured quality; regulate and promote rational use of medicines; enhance infection prevention and control; and foster innovation and research and development for new tools against drug resistance.

source: scivx/lancet

Vegetarians May Need to Boost Omega-3s, B12

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Researcher Says Deficiencies May Boost Heart Disease Risk, but Vegetarians’ Risk Still Lower Than Meat Eaters’ Risk
woman eating salad

Vegetarians have a reputation for being ”heart healthy.” However, a new report says some vegetarians may be increasing their risk of heart problems from nutritional deficiencies in their diets.

Overall, meat eaters are still at higher risk of heart attacks and strokes compared to vegetarians, says researcher Duo Li, a professor of nutrition at Zhejiang University in Hangzhou, China.

But in his review of published articles from medical journals, he found that vegetarian diets are often lacking in some key nutrients. These include vitamin B12 and omega-3 fatty acids. The deficiencies were especially evident, he says, in vegans. Vegans don’t eat meat, fish, or any kind of animal product, including eggs and milk.

The deficiencies in B12 and omega-3, in turn, are linked with higher blood levels of an amino acid called homocysteine. The deficiencies are also linked with decreased levels of HDL cholesterol, the so-called good cholesterol, he says. High homocysteine levels have been suggested as a risk factor for heart disease. Higher HDL levels are heart protective.

“This may be associated with an increased thrombotic [blood clot] and atherosclerotic [hardening of the arteries] risk,” he tells WebMD.

However, other nutrition experts say many vegetarians are already aware of the need to pay close attention to intake of vitamin B12 and omega-3s. They say the increased risk to heart health that Li suggests is only a hypothesis.

The study is published in the Journal of Agricultural and Food Chemistry.

Vegetarians, Vegans, and Heart Health

Li scanned the medical literature to study vegetarian diets and their effects.

On the plus side, he found benefits to vegetarian diets. They are typically rich in fiber, magnesium, folic acid, vitamins C and E, and antioxidants.

They are low in total fat and saturated fat, cholesterol, and sodium. But they are also often low in zinc, vitamins A, B12 and D, and omega-3 fatty acids.

His advice? “Vegans or vegetarians should try to healthfully increase their B12 intake by regularly eating seaweed [popular in China] or fortified cereals,” he says.

For a boost in omega-3s, he suggests plant oils such as flaxseed.

Vegetarians and Heart Health: Perspective

Two nutrition experts who reviewed the study put the findings in perspective.

The link between the deficiencies in vitamin B12 and omega-3 fatty acids and a higher heart disease risk is only a hypothesis at this point, says Lona Sandon, RD, a spokewoman for the American Dietetic Association and assistant professor of clinical nutrition at the University of Texas Southwestern Medical Center, Dallas.

“The majority of research on vegetarianism supports it as a heart health-promoting lifestyle,” she says. The author carefully chooses the word ‘may’ [to suggest risk linked with the deficiencies] as there is little evidence to support his hypothesis at this time.”

She does agree that vegetarians are often low in vitamin B12 and omega-3.

Her advice? ”If you choose to follow a vegetarian or vegan diet, plan wisely. Some thought needs to be put into planning balanced meals and a variety of foods as well as cooking methods to obtain all nutrients needed for optimal health.”

Most vegetarians are aware of the need to pay attention to B12 and omega-3 fatty acids, says Reed Mangels, PhD, RD, the nutrition advisor for the Vegetarian Resource Group.

She suggests for vitamin B12 that vegetarians consider taking a supplement or eat cereals fortified with the vitamin or drink soy, rice, or almond milk.

Vegetarians who eat eggs and drink cow’s milk, the so-called ovo-lacto vegetarians, can obtain their B12 from those foods, says Mangels, who has written a book for dietitians, The Dietitian’s Guide to Vegetarian Diets.

Omega-3 fatty acids are found in flaxseed, walnuts, and soy products.

According to the Institute of Medicine, adults should take in about 2.4 micrograms daily of vitamin B12. Men should eat 1.6 grams of omega-3s daily; women, 1.1 grams.

About 3% of the U.S. population is vegetarian, Mangels says. About one-third eat no meat but do eat eggs and dairy. Another one-third are vegans, who eat no dairy products. Another one-third eat no animal products, but do eat honey.

source: webMD

 

Study Offers First Look At Asian Americans’ Glaucoma Risk

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It’s generally known that African Americans have the highest risk for glaucoma (about 12 percent) among racial groups in the United States. They are more than twice as likely as non-Hispanic white Americans (5.6 percent) to develop this potentially blinding disease. But little was known about risks for Asian Americans until a National Eye Institute funded study published recently in the journal Ophthalmology. By reviewing insurance records of more than 44,000 Asian Americans older than 40, the researchers found their glaucoma risk to be 6.5 percent, which is about the same as U.S. Latinos.

Racial-ethnicity risk rates help people and doctors plan for eye care and take extra precautions if appropriate. Since Asian Americans are the second fastest growing population in the U.S.– a trend likely to continue for years to come– such risk information is urgently needed.

The study also detailed the Asian American ethnic groups most likely to develop the three main types of glaucoma: open-angle (OAG, the most common form), narrow-angle (NAG), and normal-tension (NTG).

The rate of NAG was higher in Asian Americans than in any other racial group in the study and highest of all among Chinese and Vietnamese Americans. With NAG, the part of the eye that drains excess fluid becomes blocked and pressure builds up in the eye; the patient usually feels severe, rapid-onset pain and needs immediate treatment to prevent vision damage. The risk of NTG was three to 10 times higher in Japanese Americans than other Asian ethnicities studied, and nearly all of the Asian sub-groups were at higher risk than non-Asian Americans. With NTG, the optic nerve and vision sustain damage even though the pressure within the eye remains within “normal” levels. Among Asian Americans, OAG rates were highest among Japanese Americans (about 9.5 percent), followed by Indian and Pakistani Americans (about 7.7 percent).

The study was led by Joshua D. Stein, MD, Kellogg Eye Center, University of Michigan, who said the results have implications for patient care.

“For example, the inner eye angle anatomy of patients of Chinese or Vietnamese ancestry should be carefully examined,” Dr. Stein said. “And since NTG won’t be detected by simply measuring intraocular pressure (IOP), eye doctors need to assess the status of the optic nerve in patients whose ethnicity makes them more susceptible to this type of glaucoma,” he added. He and his coauthors recommend that future studies explore potential genetic and environmental reasons for some of the observed differences in glaucoma rates among the different races and Asian ethnicities.

source: American Academy of Ophthalmology

Improving verbal communication in critical care medicinestar, open

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Human errors are the most common reason for planes to crash, and of all human errors, suboptimal communication is the number 1 issue. Mounting evidence suggests the same for errors during short-term medical care. Strong verbal communication skills are key whether for establishing a shared mental model, coordinating tasks, centralizing the flow of information, or stabilizing emotions. However, in contrast to aerospace, most medical curricula rarely address communication norms during impending crises. Therefore, this article offers practical strategies borrowed from aviation and applied to critical care medicine. These crisis communication strategies include “flying by voice,” the need to combat “mitigating language,” the uses of “graded assertiveness” and “5-step advocacy,” and the potential role of Situation, Background, Assessment, and Recommendation communication. We also outline the “step-back method,” the concept of communication “below ten thousand feet,” the impetus behind “closed-loop communication,” and the closely related “repeat-back method.” The goal is for critical care practitioners to develop a “verbal dexterity” to match their procedural dexterity and factual expertise.

source: journal of critical care

Pandemic influenza A (H1N1) 2009 in a critical care and theatre setting: beliefs and attitudes towards staff vaccination

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West Midlands was particularly affected by the 2009 H1N1 influenza A (pH1N1) pandemic. Vaccination of frontline healthcare professionals (HCPs) aimed to prevent spread to vulnerable patients, minimise service disruption and protect staff. HCPs involved in upper airway management are particularly at risk of aerosol exposure. We assessed the attitudes of these HCPs towards pandemic influenza A (H1N1) 2009 vaccination uptake: primary reasons for acceptance, barriers to vaccination, and knowledge surrounding pH1N1 influenza. We performed a voluntary, anonymous questionnaire survey based in two West Midlands National Health Service Trusts, one month after introduction of the vaccine. In all, 187 useable responses were received (60.5% response rate); 43.8% (N = 82) had/intended to receive vaccination. Concern over long term side-effects was the main deterrent (37.4%, N = 70). Primary reasons for potentially accepting vaccination were: to protect themselves (36.9%, N = 69), to protect family (35.3%, N = 66), and to protect patients (10.2%, N = 19). Of responders, 76.5% were unsure that the vaccines had undergone suitably rigorous clinical trials to ensure safety; 20.9% correctly identified reported vaccine efficacy. We conclude that pH1N1 vaccination uptake among high risk HCPs remained low, although twice that of peak seasonal influenza vaccination rates. HCPs’ knowledge of vaccine efficacy is poor. Barriers to vaccination include concerns over safety profile given the short chronological time-span between the pandemic being declared and vaccine introduction. Side-effects, both acute and chronic, are a significant barrier to vaccination. Further reassurance/education surrounding vaccine safety/efficacy at the time of any future pandemic may improve uptake rates.

source: Journal of hospital infection

Plasma gelsolin levels and 1-year mortality after first-ever ischemic stroke

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Plasma gelsolin depletion has been associated with poor outcome of critically ill patients. We sought to investigate change in plasma gelsolin level after ischemic stroke and to evaluate its relation with disease outcome.

Materials and Methods

Fifty healthy controls and 172 patients with first-ever ischemic stroke were included. Plasma samples were obtained within 24 hours from stroke onset. Its concentration was measured by enzyme-linked immunosorbent assay.

Results

Plasma gelsolin level in stroke patients was significantly decreased compared with healthy controls. A multivariate analysis showed that plasma gelsolin level was an independent predictor for 1-year mortality (odds ratio, 0.945; 95% confidence interval [CI], 0.918-0.974; P = .0002) and negatively associated with National Institutes of Health Stroke Scale (NIHSS) score (t = −4.802, P < .001) and plasma C-reactive protein level (t = −4.197, P < .001). A receiver operating characteristic curve identified that a baseline plasma gelsolin level less than 52.0 mg/L predicted 1-year mortality of patients with 73.0% sensitivity and 65.2% specificity (area under curve [AUC], 0.738; 95% CI, 0.666-0.802). The predictive value of the gelsolin concentration was similar to that of NIHSS score (AUC, 0.742; 95% CI, 0.670-0.806; P = .940). Gelsolin improved the AUC of NIHSS score to 0.814 (95% CI, 0.747-0.869; P = .032).

Conclusions

Plasma gelsolin level is a useful, complementary tool to predict mortality after ischemic stroke.

source: Journal of critical care

Revlimid (lenalidomide): Ongoing Safety Review – increased risk of developing new malignancies

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FDA is informing the public that we are aware of results from clinical trials conducted inside and outside the United States that found that patients treated with Revlimid (lenalidomide) may be at an increased risk of developing new types of cancer compared to patients who did not  take the drug.FDA is currently reviewing all available information on this potential  risk and will communicate any new recommendations once it has completed its review.

BACKGROUND: Revlimid is used to treat a type of blood disorder known as myelodysplastic syndrome. Revlimid is also used along with other drugs to treat people with the cancer known as multiple myeloma.

RECOMMENDATION: At this time, there is no recommendation to delay, modify or restrict the use of Revlimid for patients being treated according to the FDA-approved indications. FDA is currently reviewing all available information. on this potential risks and will communicate any new recommendations once it has completed its review.

source: FDA

Benzocaine Topical Products: Sprays, Gels and Liquids: Risk of Methemoglobinemia

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FDA notified healthcare professionals and patients that FDA continues to receive reports of methemoglobinemia, a serious and potentially fatal adverse effect, associated with benzocaine products both as a spray, used during medical procedures to numb the mucous membranes of the mouth and throat, and benzocaine gels and liquids sold over-the-counter and used to relieve pain from a variety of conditions, such as teething, canker sores, and irritation of the mouth and gums.

BACKGROUND: Methemoglobinemia is a rare, but serious condition in which the amount of oxygen carried through the blood stream is greatly reduced. In the most severe cases, methemoglobinemia can result in death. Patients who develop methemoglobinemia may experience signs and symptoms such as pale, gray or blue colored skin, lips, and nail beds; headache; lightheadedness; shortness of breath; fatigue; and rapid heart rate. Methemoglobinemia has been reported with all strengths of benzocaine gels and liquids, and cases occurred mainly in children aged two years or younger who were treated with benzocaine gel for teething. The signs and symptoms usually appear within minutes to hours of applying benzocaine and may occur with the first application of benzocaine or after additional use. The development of methemoglobinemia after treatment with benzocaine sprays may not be related to the amount applied. In many cases, methemoglobinemia was reported following the administration of a single benzocaine spray.

RECOMMENDATIONS:

  • Benzocaine products should not be used on children less than two years of age, except under the advice and supervision of a healthcare professional.
  • Adult consumers who use benzocaine gels or liquids to relieve pain in the mouth should follow the recommendations in the product label. Consumers should store benzocaine products out of reach of children. FDA encourages consumers to talk to their healthcare professional about using benzocaine.
  • Read the two Drug Safety Communications below for other specific recommendations for Healthcare Professionals, for Consumers and Caregivers and the Data Summary which supports these recommendations.

FDA is continuing to evaluate the safety of benzocaine products and the Agency will update the public when it has additional information. FDA will take appropriate regulatory actions as warranted.

source: FDA

Incretin secretion, action in the natural history of type 2 diabetes

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Incretin hormones contribute a major portion to the insulin secretory responses after meals in healthy people. The incretin effect describes the phenomenon that oral glucose elicits approximately threefold greater insulin responses than the elevation in glucose (achieved with glucose administered intravenously) alone.

The incretin effect is the result of nutrient-stimulated secretion of the incretin hormones glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 and their insulinotropic effect (ie, the augmentation of insulin secretion at elevated plasma glucose concentrations). In patients with type 2 diabetes, this incretin effect is severely impaired or even absent.

It is the purpose of this commentary to highlight current knowledge in incretin research and to answer the question of whether and to which degree abnormalities in incretin hormone secretion and action accompany the development of type 2 diabetes or even contribute to this process.

Michael A. Nauck, MD, PhD
Michael A.
Nauck		 Irfan Vardarli, MD
Irfan Vardarli		 Juris J. Meier, MD
Juris J.
Meier

History of incretin

The reduced incretin effect in patients with type 2 diabetes was first noticed in 1967 and was clearly established in 1986.

Three types of questions arose from this finding. What is the mechanism behind the reduced incretin effect? Is the secretion or insulinotropic action of GIP and GLP-1 at fault? Are defects in the enteroinsular axis (the signaling system between the gut, from where incretin hormones are secreted, and the endocrine pancreas, the main target tissue that incretin hormones act on) important for the development and/or progression of type 2 diabetes? Can the pathophysiological characterization of the incretin system in type 2 diabetes provide clues for the development of new approaches for the treatment of this metabolic disease?

A severe impairment in the insulinotropic activity of GIP in type 2 diabetes explains the reduced incretin effect. A large cross-sectional study by Toft-Nielsen and colleagues comparing GLP-1 responses after meal stimulation suggested a reduced release of GLP-1 in patients with type 2 diabetes and, to a lesser extent, impaired glucose tolerance (“prediabetes”). This widely quoted study was sometimes interpreted to indicate a progressive loss in the capacity of GLP-1 secretion in the natural history of type 2 diabetes, starting from normal secretion as long as glucose tolerance was normal with slight impairments when IGT develops, with a further deterioration after the diagnosis of type 2 diabetes and little residual capacity for GLP-1 secretion when the condition has progressed.

The logical consequence was to replace a missing hormone by advocating incretin-based antidiabetic agents (GLP-1 receptor agonists or dipeptidyl peptidase-4 inhibitors). However, not all studies that have compared the secretion of GLP-1 in patients with type 2 diabetes and in matched healthy people come to the same conclusions. A recent meta-analysis suggested no uniform reduction in L-cell secretion between healthy and type 2 diabetic patients, but a large interindividual variation, in part determined by age, obesity and plasma levels of glucagon and free fatty acids. In nondiabetics, the amount of GIP and GLP-1 secreted is significantly correlated to the incretin effect in quantitative terms. Thus, a low secretion of GLP-1 may determine a reduced incretin effect on an individual level, but does not explain the reduced incretin effect in patients with type 2 diabetes by and large.

If secretion is not the culprit, is there any peculiarity regarding the action of incretin hormones in type 2 diabetes? As originally described using GIP of the porcine amino acid sequence, and later confirmed using synthetic human GIP, the endocrine pancreas shows very little secretory response, even if exposed to supraphysiological concentrations of GIP. This inability to respond to GIP appears to be acquired, since populations at high risk for developing type 2 diabetes do not display a similar defect. Basically, the response to GIP seems to be normal in any form of prediabetes (first-degree relatives, patients recovering from gestational diabetes, etc.), but after diagnosis (ie, with a fasting glucose ≥126 mg/dL), the incretin effect is reduced or lost, as is the ability to respond to exogenous GIP.

Most likely, the inability to elicit insulin secretory responses with GIP, even at hyperglycemia, is explained by a generalized impairment in beta-cell secretory capacity, as is typical for type 2 diabetes, no matter which stimulus is looked at (hyperglycemia, amino acids, sulfonylureas, etc).

Chart

Source: Michael A. Nauck, MD, PhD

Furthermore, rodent studies have suggested a down-regulation of the GIP receptor by chronic hyperglycemia. The fact that this defect becomes apparent when glucose concentrations rise above the normal level has raised the question of whether this phenomenon is reversible by glucose normalization. A recent study by Højberg and colleagues suggested that this may be the case. However, although the insulin secretory responses to GIP and GLP-1 were significantly improved, normalization was not achieved after improved glucose control.

Abnormalities in the incretin system accompany the development of type 2 diabetes and may contribute to the velocity of progression. Figure 1 depicts the natural history of developing type 2 diabetes and also the progression of the disease after the diagnosis has been made. Changes in insulin secretory capacity, based on homeostasis model assessment (HOMA) estimation of beta-cell function, and insulin sensitivity preceding the diagnosis were taken from a recent analysis by Tabak and colleagues. The development after the diagnosis of diabetes was based on analyses from the UKPDS and ADOPT study.

Regarding the secretion of GIP and GLP-1, we refer to our recent review indicating no general abnormalities in K-cell (GIP) and L-cell (GLP-1) secretion associated with a diagnosis of type 2 diabetes. The fact that in none of the studies examining prediabetic populations, insulinotropic GIP effectiveness was impaired, but after the diagnosis, uniformly, a severe inability to respond to GIP with secreting insulin was documented, is the basis for assuming a substantial drop in beta-cell responsiveness to GIP around the time of diagnosis, with no further changes afterward (Figure 1). In a recent review, we have explained reasons to assume that this inability to secrete insulin in response to GIP stimulation goes along with a general impairment of beta-cell function, which is demonstrable with most other secretagogues as well.

Whether this inability of the endocrine pancreas to respond to GIP contributes to the natural history of type 2 diabetes can only be evaluated by quantitative considerations. If a mechanism to stimulate insulin secretion after meals that normally contributes two-thirds of the overall secretory responses is at fault, this almost certainly has the effect to accelerate the progression of type 2 diabetes because without the additional incretin stimulus, overall insulin secretion should be further impaired.

In the case of GLP-1, the insulinotropic activity is somewhat reduced after the diagnosis of type 2 diabetes, and even worse under the condition of uncontrolled hyperglycemia compared with healthy controls. High pharmacological doses of GLP-1, nevertheless, have the potential to raise insulin concentrations and to suppress glucagon secretion, with the overall result of normalizing glucose concentrations in the fasting state and after meals over a wide range of patients with type 2 diabetes, ranging from those treatable with lifestyle modification (“diet and exercise”) to those requiring insulin treatments.

Thus, the “resistance” to GIP of the type 2 diabetic beta-cell can be overcome by a compensatory exposure to high concentrations of the incretin hormone, GLP-1. GLP-1 itself appears to be less important than GIP for postprandial glucose control in healthy people and does not seem to be involved in the pathogenesis of type 2 diabetes. However, because of its preserved efficacy in type 2 diabetes, GLP-1 is an effective agent to treat hyperglycemia in type 2 diabetic patients, with the added benefits of inducing weight loss and avoiding hypoglycemia.

source: endocrine today

Once-weekly, investigational GH replacement safe, effective

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Weekly growth hormone replacement with an investigational, sustained-release formulation significantly reduced fat mass after 6 months and was well tolerated by adults with growth hormone deficiency, researchers found.

A 6-month study was conducted to evaluate the safety and efficacy of LB03002, a recently developed recombinant human GH formulation. The long-acting GH was developed for once-weekly administration by subcutaneous injection.

The study included 152 adults with GH deficiency who were randomly assigned to LB03002 or placebo once a week for 26 weeks. The researchers assessed changes in body composition, insulin-like growth factor I, adverse events, glucose homeostasis and antibody development.

According to the results, adults assigned to the LB03002 formulation experienced a significant increase in IGF-I (P<.001), whereas those assigned placebo experienced no change.

Mean fat mass decreased by 1 kg in the LB03002 group (95% CI, –1.614 to –0.491) but increased by 0.5 kg in the placebo group (95% CI, –0.205 to 1.345); the treatment difference was 1.622 kg (95% CI, –2.527 to 0.717). The researchers said the change in fat mass with LB03002 was primarily related to decreased trunk fat. LB03002 was also associated with positive effects on lean body mass; it increased significantly in the GH group vs. placebo (least square mean difference, 1.393; 95% CI, 0.614-2.171).

The researchers found “no concerning safety issues” related to LB03002 during the 6-month study.

“This study has provided evidence that GH replacement in adult patients with GH [deficiency] can be successful with the once-weekly sustained-release formulation,” the researchers concluded.

Disclosure: The study was jointly funded by LG Life Sciences Ltd., Korea, and Biopartners GmbH, Switzerland.

 

 

GH has to be given daily by subcutaneous injection. Treatment periods are always for several years, both in childhood and in adulthood. Therefore, compliance is often poor, contributing to poor outcome.

LB03002 is a new, sustained-release formulation of GH consisting of microparticles containing GH incorporated into hyaluronate and dispersed in an oil base of medium-chain triglycerides. In a recently published double blind, placebo-controlled study of adults with GH deficiency, an international group of investigators showed comparable responses of subcutaneously injected sustained-release GH given once a week, in terms of body composition. Mean fat mass reduction was mainly due to decreased trunk fat and lean body mass was significantly increased vs. placebo, thereby fulfilling the primary endpoint of the study. Patients showed a 1-kg decrease in fat mass and a 2-kg increase in lean body mass. Lipid parameters were not statistically different. No concerning safety issues arose during the 6-month study.

These data show the clinical efficacy and utility of a sustained-release, once a week GH preparation in adults with GH deficiency.

source: endocrine today