March 11, 2011 07:00 AM Eastern Time
Conference Call Today at 9:00 a.m. EST
ATLANTA--(BUSINESS WIRE)--Inhibitex, Inc. (NASDAQ:INHX) today announced its financial results for the fourth quarter and year ended December 31, 2010, and provided an update on recent clinical and corporate developments.
“We are very pleased with the progress we have made over the past year in advancing our antiviral pipeline, which culminated in establishing clinical proof of concept for both FV-100, which we are developing to treat shingles, and more recently, INX-189, which we are developing to treat chronic infections caused by hepatitis C virus,” stated Russell H. Plumb, President and CEO of Inhibitex, Inc. “Looking ahead in 2011, we expect to complete our Phase 1b trial of INX-189 in the near-term and are developing plans to further evaluate its safety and antiviral activity in a Phase 2 program that we estimate could begin in the third quarter of 2011. Further, over the next several months we anticipate completing our evaluation of the potential clinical and regulatory pathways and commercial opportunities for FV-100, and look forward to determining the possible next steps in its development.”
Clinical Development Highlights
• INX-189: Earlier this quarter, the Company announced favorable interim results from a Phase 1b study of INX-189 in HCV genotype 1 patients where INX-189, its nucleotide polymerase inhibitor, demonstrated a clinically meaningful antiviral effect (>1 log10 IU/mL reduction in baseline viral load) in seven days of monotherapy at a relatively low (25mg) once-daily dose.
• FV-100: In December 2010, the Company successfully completed a first-in-patient, Phase 2 clinical trial in shingles patients where a once-daily dose of 400mg FV-100 demonstrated the potential to reduce both the sub-acute pain and the incidence of post herpetic neuralgia (PHN) associated with shingles infections.
Fourth Quarter 2010 Financial Results
As of December 31, 2010, the Company held $19.6 million in cash, cash equivalents and short-term investments.
The Company reported a net loss for the fourth quarter of 2010 of $7.0 million, as compared to a net loss of $4.7 million in the fourth quarter of 2009. The $2.3 million increase in net loss in the fourth quarter of 2010 was primarily the result of higher research and development expense, and to a lesser extent, higher general and administrative expense and lower net interest income, offset in part by an increase in other income. Basic and diluted net loss per share was $0.11 for the fourth quarter of 2010 compared to $0.08 for the fourth quarter of 2009. The increase in net loss per share in the fourth quarter of 2010, as compared to the fourth quarter of 2009, was due to the higher net loss, offset in part by an increase in the weighted average number of shares outstanding.
Research and development expense increased to $6.6 million in the fourth quarter of 2010 from $4.3 million in the fourth quarter of 2009. This $2.3 million increase was primarily due to a $1.7 million increase in direct costs incurred in connection with the initiation of a Phase 1b clinical trial of INX-189 in November of 2010 and to a lesser extent, the completion of a Phase 2 clinical trial of FV-100 in the December of 2010, as well as an increase of $0.6 million in non-direct expenses associated with higher consulting and professional fees and compensation and share-based compensation expense.
General and administrative expense increased to $1.2 million in the fourth quarter of 2010 from $0.7 million in the fourth quarter of 2009. The increase of $0.5 million was primarily the result of an increase in legal and professional fees and compensation and share-based compensation expense.
Other income increased to $0.5 million in the fourth quarter of 2010 from zero in the fourth quarter of 2009 due to the receipt of $0.5 million Therapeutic Tax Credit grant in the fourth quarter of 2010 that was not received in 2009.
Year End 2010 Financial Results
For the year ended December 31, 2010, the Company reported a net loss of $22.7 million, as compared to $17.6 million for 2009. Basic and diluted net loss per share for the year ended December 31, 2010, was $0.37, as compared to $0.38 for 2009. The $5.1 million increase in net loss in 2010 was primarily the result of higher research and development expense associated with a Phase 2 clinical trial of FV-100, the initiation of a Phase 1 clinical program for INX-189 in mid-2010 and an increase in other non-direct research and development costs, as well as higher general and administrative expense and lower net interest income, offset in part by higher revenues from a collaborative license and development agreement and net other income. The slight decrease in net loss per share in 2010 was due to an increase in the weighted average number of shares outstanding, offset by the higher net loss.
Revenue increased to $1.9 million in 2010 from $1.2 million in 2009 due to the receipt of a $0.7 million milestone payment in the first quarter of 2010 that did not occur in 2009.
Research and development expense increased to $21.0 million in 2010 from $15.4 million in 2009, primarily due to a $4.9 million increase in direct costs incurred in connection with a Phase 2 clinical trial of FV-100 that was conducted throughout 2010 and the initiation of a Phase 1 clinical program of INX-189 in mid-2010, as well as an increase of $0.7 million in non-direct expenses associated with higher consulting and professional fees and compensation and share-based compensation expense.
General and administrative expense increased to $4.1 million in 2010 from $3.6 million in 2009. The increase of $0.5 million was primarily the result of an increase in legal and professional fees and compensation and share-based compensation expense incurred in the fourth quarter of 2010.
Other income increased to $0.5 million in 2010 from zero in 2009 due to the receipt of $0.5 million Therapeutic Tax Credit grant in the fourth quarter of 2010 that was not received in 2009.
Recent Corporate Developments
INX-189 for Chronic Hepatitis C – In January 2011, the Company reported favorable preliminary interim safety and antiviral data from the first two monotherapy cohorts of its ongoing Phase 1b clinical trial of INX-189. The Company reported that INX-189, dosed once-daily at 9mg and 25mg for seven days, demonstrated potent antiviral activity with a mean HCV RNA reduction from baseline levels of -0.71 and -1.03 log10 IU/mL, respectively. In addition to the mean reductions in viral load, clinically meaningful decreases in alanine transaminase (ALT) levels were observed for patients receiving INX-189 at both dose levels, and no patients experienced viral breakthrough. There were no serious adverse events reported, no discontinuations due to an adverse event, and no adverse events related to changes in clinical laboratory evaluations. All reported adverse events were mild or moderate and were not dose dependent. In addition, the pharmacokinetics of the 9mg and 25mg doses in HCV-infected patients were comparable to those observed in healthy volunteers.
The Phase 1b trial, which is being conducted under an IND in the United States, is a double-blind, placebo-controlled, dose escalation study designed to evaluate the safety, tolerability, pharmacokinetics and antiviral activity of INX-189, administered orally once-daily for seven days in HCV genotype 1 treatment-naïve patients. Each treatment cohort in the trial is comprised of 10 patients, eight that receive INX-189 and two that receive placebo. In addition to the 9mg and 25mg dose cohorts, the Company will enroll three more INX-189 monotherapy cohorts in the trial, including a recently-added 100mg cohort, as well as two cohorts that will receive 9mg and 25mg of INX-189 once daily for seven days in combination with ribavirin. The Company anticipates completing this ongoing Phase 1b trial around the end of the first quarter of 2011.
In February 2011, the Company reported that the U.S. Food and Drug Administration (FDA) designated the investigation of INX-189 as a Fast Track development program. Fast Track programs are designed to facilitate the development and expedite the review of new drugs that are intended to treat serious or life threatening conditions and that demonstrate the potential to address unmet medical needs.
FV-100 for Shingles – In December 2010, the Company reported top-line safety and efficacy data from its Phase 2 clinical trial of FV-100, an oral antiviral compound being developed to treat shingles, including the reduction of shingles-associated pain and the incidence of PHN. The study included 350 shingles patients and compared two once-daily doses of FV-100 (200mg and 400mg) to valacyclovir, one of the most commonly-used antiviral drugs to treat shingles. Valacyclovir was administered three times per day at 1,000 mg per dose.
Numerically favorable treatment differences were observed for both doses of FV-100 as compared to valacyclovir for the primary endpoint of the study, defined as the reduction in the severity and duration of shingles-associated acute pain over the first 30 days, or the Burden of Illness (BOI30 AUC), although these treatment differences were not statistically significant. There were also numerically favorable treatment differences observed for key secondary pain endpoints, including a 14% relative reduction in the severity and duration of shingles-associated pain over 90 days (BOI90 AUC) and a 39% relative reduction in the incidence of PHN for the 400mg dose of FV-100. The trial was not powered to demonstrate statistically significant treatment differences between the arms with respect to these and other secondary endpoints. FV-100 was generally well tolerated at both dose levels, and demonstrated a similar adverse event profile as compared to valacyclovir. All three treatment arms showed a relatively low proportion of adverse and serious adverse events. The Company is currently performing various analyses of the full Phase 2 data set and an evaluation of various clinical, regulatory and commercial pathways for the potential future development of FV-100, which it anticipates concluding in the first half of 2011.
Conference Call and Webcast Information
Russell H. Plumb, President and Chief Executive Officer of Inhibitex, and other members of management will review the Company’s fourth quarter and year-end 2010 operating results and financial position, as well as provide a general update on the Company via a webcast and conference call today at 9:00 a.m. EST. To access the conference call, dial (877) 407-9210 (domestic) or (201) 689-8049 (international). A replay of the call will be available from 11:00 a.m. EST on March 11 until April 11, 2011, at midnight. To access the replay, please dial (877) 660-6853 (domestic) or (201) 612-7415 (international) and reference the account # 286 and the conference ID # 366809. A live audio webcast of the call and the archived webcast will be available under the News and Events category on the Inhibitex website at http://www.inhibitex.com/.
About HCV and INX-189
Chronic hepatitis C is a disease of the liver caused by HCV, which can result in cirrhosis and cancer, and is the leading reason for liver transplants in the United States. Inhibitex is developing a series of proprietary nucleotide inhibitors, referred to as protides, which target and inhibit the RNA-dependent RNA polymerase (NS5b) of HCV. The Company believes that, based on in vitro data, INX-189 is one of the most potent HCV nucleotide polymerase inhibitor currently in clinical development, and that results from preclinical studies and its Phase 1 trials of INX-189 to-date support its potential as a once-daily oral antiviral therapy amenable to fixed-dose combination with other antivirals for the treatment of patients with chronic hepatitis C infections.
About Shingles and FV-100
The Company is developing FV-100 to treat herpes zoster, also commonly referred to as shingles, which is an infection caused by the reactivation of varicella zoster virus (“VZV”), the same virus that causes chicken pox. Published in vitro studies have demonstrated that FV-100, an orally available bicyclic nucleoside analogue, is significantly more potent against VZV and can inhibit its replication substantially faster than any other antiviral agent currently approved for the treatment of shingles. Inhibitex believes these characteristics, a favorable pharmacokinetic profile, and the results of a recently-completed Phase 2 trial support the potential of FV-100 as a once-daily oral therapy to reduce the incidence, severity and duration of shingles-associated pain and PHN.
About Inhibitex
Inhibitex, Inc. is a biopharmaceutical company focused on developing products to treat and prevent serious infectious diseases. In addition to its two clinical-stage programs, INX-189 and FV-100, the Company’s pipeline includes other HCV nucleotide inhibitors in preclinical development. It has also licensed its proprietary MSCRAMM® protein platform to Pfizer for its use in the development of a staphylococcal vaccine, which is currently being evaluated in Phase 1 clinical trials.
For additional information about the Company, please visit http://www.inhibitex.com/
Safe Harbor Statement
This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties. All statements, other than historical facts included in this press release, including statements regarding: the anticipated time it will take the Company to conclude its assessment of the FV-100 Phase 2 data and the compound’s potential clinical, regulatory and commercial pathways; the potential for FV-100 to be dosed once daily and reduce the incidence, severity and duration of shingles-associated pain and PHN; the Company plans to enroll additional cohorts in the ongoing Phase 1b trial of INX-189; the time frame in which a Phase 2 clinical program of INX-189 can be initiated; the Company’s belief that INX-189 is one of the most potent HCV nucleotide polymerase inhibitor currently in clinical development; the results of preclinical studies and the Phase 1 trials of INX-189 to-date supporting its potential as a once-daily oral antiviral amenable to fixed dose combination with other antivirals; and the anticipated time when the ongoing Phase 1b trial of INX-189 will be completed, are forward looking statements. These intentions, expectations, or results may not be achieved in the future and various important factors could cause actual results or events to differ materially from the forward-looking statements that the Company makes, including the risk of: the Company, the FDA, a data safety monitoring board, or an institutional review board (IRB) delaying, suspending or terminating the clinical development of FV-100 or INX-189 at any time for a lack of safety, tolerability, antiviral activity, commercial viability, or any other reason; FV-100 not demonstrating sufficient activity or potential in reducing the incidence and severity of shingles-related pain and PHN, to be clinically relevant or commercially viable; the Company or its clinical investigators not being able to enroll additional HCV patients in the Phase 1b trial on a timely basis; obtaining, maintaining and protecting the intellectual property incorporated into and supporting the commercial viability of the Company’s product candidates; and other cautionary statements contained elsewhere herein and in its Annual Report on Form 10-K for the year ended December 31, 2009, as filed with the Securities and Exchange Commission, or SEC, on March 26, 2010, and its Quarterly Reports on Form 10-Q for the quarter ended March 31, 2010, June 30, 2010, and September 30, 2010, as filed with the SEC on May 13, 2010, August 12, 2010, and November 15, 2010, respectively. Given these uncertainties, you should not place undue reliance on these forward-looking statements, which apply only as of the date of this press release.
There may be events in the future that the Company is unable to predict accurately, or over which it has no control. The Company's business, financial condition, results of operations and prospects may change. The Company may not update these forward-looking statements, even though its situation may change in the future, unless it has obligations under the Federal securities laws to update and disclose material developments related to previously disclosed information. The Company qualifies all of the information contained in this press release, and particularly its forward-looking statements, by these cautionary statements.
Inhibitex® and MSCRAMM® are registered trademarks of Inhibitex, Inc.
Source
March 11, 2011
HIV Raises Risk of Broken Bones
Published: March 11, 2011
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
People with HIV are at higher risk of bone fractures than the general population, researchers reported.
And the increased risk appears to be driven mainly by fragility fractures at the wrist, vertebra, and femoral neck, according to Benjamin Young, MD, PhD, of the Rocky Mountain Center for AIDS Research, Education, and Services in Denver, and colleagues.
Factors such as older age, substance abuse, hepatitis C co-infection, and diabetes were associated with fracture risk, Young and colleagues reported online in Clinical Infectious Diseases.
One new finding, Young said in a statement, is that the state of the patient's immune system at its worst point -- that is, its lowest CD4 count -- is associated with an increased risk of fracture.
The findings may help improve clinical management of bone health in HIV-positive people, Young added, noting that the optimal care "is not well defined and remains controversial."
Low bone mineral density has been observed among HIV patients for many years, but there is limited data on the incidence of fractures, Young and colleagues noted.
An analysis of nearly 120,000 veterans, reported in 2010, suggested HIV was a risk factor for fragility fracture. And other studies have suggested the prevalence of fractures among those with HIV was increased, compared with other groups.
To look at fracture incidence, Young and colleagues turned to the long-running HIV Outpatient Study, an open, prospective observational cohort of HIV-positive people followed at 10 specialty clinics in eight U.S. cities.
The study has data on incident fractures from 2000 through 2008; Young and colleagues included all 5,826 participants who had at least two clinical visits during that time.
For comparison, they used data from the National Hospital Ambulatory Medical Care Survey of outpatient departments, which had fracture information through 2006.
The researchers found that the fracture rate rose over the first three years of the study -- from 57.7 per 10,000 population in 2000 to 84.8 in 2002. The change was significant at P=0.01, but the incidence rates stabilized in subsequent years.
On the other hand, rates of fracture in the outpatient survey did not change significantly from 2000 through 2006, the researchers reported.
But rates in the HIV cohort were always higher than those in the outpatient survey, they found:
• From 2000 through 2006, the incidence rates per 10,000 population in the HIV-positive cohort ranged from 57.5 to 83.2, with all but two (in 2000 and 2001) above 80.
• Over the same period, rates per 10,000 population in the outpatient survey ranged from 25.8 to 40.3.
• The differences were statistically significant in most years overall and for men, but not for women, who formed 21% of the HIV-positive cohort.
A multivariate analysis found that factors associated with fracture risk were age older than 47, nadir CD4-positive T-cell count below 200 cells per cubic millimeter, hepatitis C infection, diabetes, and substance abuse.
Men ages 25 through 54 in the HIV-positive cohort had significantly more fractures at the wrist and vertebra (at P<0.01 for each comparison) than did men of the same age in the outpatient survey.
Similarly, HIV-positive women ages 25 through 54 had more fractures at the vertebra and femoral neck sites, significant at P<0.01 and P=0.04, respectively.
But both men and women in the HIV-positive cohort had relatively fewer fractures at nonfragility sites, compared with those in the outpatient survey, Young and colleagues found.
Risk of a fragility fracture was associated in a multivariate analysis with:
• Increasing age, HR 1.43 per 10 years, 95% CI 1.03 to 1.98
• Hepatitis C, HR 1.99, 95% CI 1.01 to 3.90
• Body mass index less than 18.5, HR 3.72, compared with all other categories, 95% CI 1.14 to 12.09
The researchers cautioned that fracture incidence in the HIV-positive cohort was based on charts, and events were not confirmed by radiological findings or central adjudication.
They also noted that they did not have data for bone mineral density among those patients or use patterns for tobacco, alcohol, or other abused substances and so were unable to assess contribution of these to fracture rates.
The study was supported by the CDC.
Young reported financial links with Cerner, Gilead Sciences, Merck, GlaxoSmithKline, and Viiv Healthcare.
Primary source: Clinical Infectious Diseases
Source reference:
Young B, et al "Increased rates of bone fracture among HIV-infected persons in the HIV Outpatient Study (HOPS) compared with the U.S. general population, 2000-2006" Clin Infect Dis 2010; 52(8): 1061-1068.
Source
Hepatic Encephalopathy
From: The American Liver Foundation
Explore this section to learn more about Hepatic Encephalopathy, including a description of the disease and how it's diagnosed.
Why is the liver important?
The liver is the second largest organ in your body and is located under your rib cage on the right side. It weighs about three pounds and is shaped like a football that is flat on one side.
The liver performs many jobs in your body. It processes what you eat and drink into energy and nutrients your body can use. The liver also removes harmful substances from your blood.
What is hepatic encephalopathy?
Hepatic encephalopathy (HE) is a brain disorder that is caused by liver damage. HE can be an acute (short-term) or chronic (long-term) condition and can be mild, moderate, or severe.
What causes an episode of hepatic encephalopathy?
HE occurs when the liver is damaged and cannot remove toxic chemicals, such as ammonia, from the blood. These chemicals then enter the brain and cause it to not function well.
The following factors may trigger HE:
HE can cause mental and physical symptoms. They can vary person to person, and may progress slowly or occur suddenly.
Symptoms may include:
Complications of HE may include:
HE can be a medical emergency and hospitalization is usually required. It is important to see a doctor as soon as symptoms begin. At the hospital, doctors determine and treat what may have caused hepatic encephalopathy. Treatments aim to manage the disease and keep people out of the hospital.
Depending on the cause, treatments may include:
The best way to reduce the risk of HE is to prevent, treat, or manage liver disease. Talk to your doctor about risk factors and steps that can be taken to prevent chronic HE.
Facts-At-A-Glance
Explore this section to learn more about Hepatic Encephalopathy, including a description of the disease and how it's diagnosed.
Why is the liver important?
The liver is the second largest organ in your body and is located under your rib cage on the right side. It weighs about three pounds and is shaped like a football that is flat on one side.
The liver performs many jobs in your body. It processes what you eat and drink into energy and nutrients your body can use. The liver also removes harmful substances from your blood.
What is hepatic encephalopathy?
Hepatic encephalopathy (HE) is a brain disorder that is caused by liver damage. HE can be an acute (short-term) or chronic (long-term) condition and can be mild, moderate, or severe.
What causes an episode of hepatic encephalopathy?
HE occurs when the liver is damaged and cannot remove toxic chemicals, such as ammonia, from the blood. These chemicals then enter the brain and cause it to not function well.
The following factors may trigger HE:
- Dehydration (loss of water from the body)
- Low oxygen levels in the body
- Eating too much protein
- Constipation
- Medications that affect the nervous system, such as tranquilizers or sleep medications
- Infections
- Intestine, stomach, or esophagus bleeding
- Kidney problems
- Surgery
HE can cause mental and physical symptoms. They can vary person to person, and may progress slowly or occur suddenly.
Symptoms may include:
- Mild confusion
- Forgetfulness
- Personality or mood changes
- Poor concentration
- Poor judgment
- Stale or sweet odored breath
- Change in sleep patterns
- Worsening of handwriting or small hand movements
- Unusual movements or shaking of hands or arms (also known as “flapping”)
- Extreme anxiety
- Seizures
- Severe confusion
- Sleepiness or fatigue
- Severe personality changes
- Jumbled and slurred speech
- Slow movement
Complications of HE may include:
- Brain swelling
- Permanent nervous system damage
- Increased risk of heart failure, kidney failure, respiratory failure and sepsis (blood poisoning)
- Coma
HE can be a medical emergency and hospitalization is usually required. It is important to see a doctor as soon as symptoms begin. At the hospital, doctors determine and treat what may have caused hepatic encephalopathy. Treatments aim to manage the disease and keep people out of the hospital.
Depending on the cause, treatments may include:
- Stopping intestine, stomach, and esophagus bleeding
- Healing infections
- Addressing kidney failure
- Providing life support if the person is in a coma
- Diet changes such as avoiding too much or too little protein
- Rifaximin (Xifaxan) to reduce bacteria in the intestines that make toxins the liver cannot process
- Lactulose (type of sugar) to prevent the liver from absorbing toxins from the intestine
- Prevention and treatment of constipation
- Medicine to remove blood from the intestines or procedures to control active bleeding
- Medicine to treat infections
The best way to reduce the risk of HE is to prevent, treat, or manage liver disease. Talk to your doctor about risk factors and steps that can be taken to prevent chronic HE.
Facts-At-A-Glance
- Hepatic encephalopathy (HE) is a brain disorder caused by liver damage
- HE can be an acute (short-term) or chronic (long-term) condition and can be mild, moderate, or severe
- HE occurs when the liver cannot remove toxic chemicals in the blood and these chemicals enter the brain
- Symptoms of HE may progress slowly, or may occur suddenly
- Common symptoms of HE include confusion, forgetfulness, personality or mood changes, poor concentration and judgment, stale or sweet odored breath, change in sleep patterns, and worsening of handwriting or small hand movements
- People with HE can enter a coma or have brain damage
- HE can be a medical emergency and hospitalization is usually required
- Treatments aim to manage the disease and keep people out of the hospital
- The best way to reduce the risk of HE is to prevent, treat, or manage liver disease
Know Your ALT
The Serum Alt: Frequently Asked Questions
What is it?
The ALT is a protein manufactured in the liver which participates in metabolism. The term ALT refers to alanine-amino transferase. This protein is an enzyme which participates in modifying amino acids, the building blocks of proteins. The ALT is made predominately in the liver and therefore alterations in the serum ALT can be directly related to disturbances of liver structure and function.
Is the serum ALT hard to measure?
It is straightforward to have ones blood sample tested for a serum ALT, it only requires obtaining a blood sample. The serum ALT is easily measured in laboratories throughout the world. The methodology may vary from laboratory to laboratory, making direct comparisons of the absolute serum ALT value difficult, but all laboratories have a normal range for men and women.
What does an elevated serum ALT reflect?
The ALT is manufactured within liver cells. Elevations in the serum ALT reflect alterations in the structure and function of the liver. Damaged liver cells release ALT into the blood stream where it can then be measured. The serum ALT, therefore, reflects damage to liver cells, liver injury, and underlying liver disease.
Why should I know my serum ALT?
We should all be aware of our health. Unfortunately, unlike diseases affecting other organs, injury to the liver can be silent. Patients may not have any symptoms and the ALT can be elevated for years before one is aware of an underlying liver disease. When one develops symptoms from liver disease, it usually reflects advanced damage to the liver. Once significant damage to the liver has occurred, therapies other than liver transplantation, may not be very beneficial. Therefore, making the diagnosis of a liver disease early in its course can be very beneficial in regards to receiving specific therapies and modifying lifestyle.
My doctor also measures other blood tests. What are they and is the serum ALT the best test?
The liver is a complex organ with a variety of essential functions for the body. It participates in metabolism, produces bile, and generates proteins secreted into the blood, so your doctor may measure compounds associated with all of these liver functions. All of those tests are frequently measured in a battery of tests referred to as a “liver panel.” Depending upon the type and nature of the underlying liver injury and therefore the liver disease, changes in the magnitude of the various components of this panel provide meaningful information to your physician. However, if one simply wants to know whether one has liver wellness or may have an underlying liver disease, the ALT is likely the most sensitive test for the vast majority of liver illness.
Is there a direct correlation between the magnitude of the serum ALT elevation and the severity of the underlying liver disease?
Although there can be a relationship between the magnitude of elevation in the serum ALT and the severity of the abnormalities in liver structure and function, this relationship is not absolute. Patients with advanced scarring of the liver may have significant liver dysfunction despite only mild elevations of the serum ALT. Therefore, any elevation of the serum ALT should be taken seriously and one should seek appropriate medical care to determine the cause.
What are some common causes of an elevated serum ALT?
Perhaps the most common cause in the North American population is fat accumulation within liver cells. Fat can accumulate anywhere in the body, but its accumulation in the liver cells is toxic to the liver. In particular, patients who are above their ideal body weight, have diabetes, or elevations in their blood lipids, may be at risk for having fat within the liver. The serum ALT is a common approach to determine whether one may have fat in the liver and if it is injurious to this organ. Other common causes of an elevated serum ALT include excessive consumption of alcohol, infection by chronic hepatitis viruses such as hepatitis B and C, toxicity from pharmaceutical medications, a genetic liver disease associated with an excess accumulation of iron in the liver, and autoimmune liver diseases. The latter are a variety of liver diseases in which the body’s immune system inflicts damage on ones own organ.
I have an elevated ALT. What should I do?
If you have an elevated ALT, you should seek medical attention. The vast majority of primary care physicians and specialists in gastroenterology and hepatology, can perform the necessary testing to determine the cause of an elevated serum ALT.
How often should I have my serum ALT measured?
Like the serum cholesterol and blood glucose tests for elevated cholesterol and diabetes, respectively; one should have the serum ALT measured repeatedly and regularly over time. A conservative approach would be to have ones serum ALT measured on an annual basis during the annual physical examination.
Source
What is it?
The ALT is a protein manufactured in the liver which participates in metabolism. The term ALT refers to alanine-amino transferase. This protein is an enzyme which participates in modifying amino acids, the building blocks of proteins. The ALT is made predominately in the liver and therefore alterations in the serum ALT can be directly related to disturbances of liver structure and function.
Is the serum ALT hard to measure?
It is straightforward to have ones blood sample tested for a serum ALT, it only requires obtaining a blood sample. The serum ALT is easily measured in laboratories throughout the world. The methodology may vary from laboratory to laboratory, making direct comparisons of the absolute serum ALT value difficult, but all laboratories have a normal range for men and women.
What does an elevated serum ALT reflect?
The ALT is manufactured within liver cells. Elevations in the serum ALT reflect alterations in the structure and function of the liver. Damaged liver cells release ALT into the blood stream where it can then be measured. The serum ALT, therefore, reflects damage to liver cells, liver injury, and underlying liver disease.
Why should I know my serum ALT?
We should all be aware of our health. Unfortunately, unlike diseases affecting other organs, injury to the liver can be silent. Patients may not have any symptoms and the ALT can be elevated for years before one is aware of an underlying liver disease. When one develops symptoms from liver disease, it usually reflects advanced damage to the liver. Once significant damage to the liver has occurred, therapies other than liver transplantation, may not be very beneficial. Therefore, making the diagnosis of a liver disease early in its course can be very beneficial in regards to receiving specific therapies and modifying lifestyle.
My doctor also measures other blood tests. What are they and is the serum ALT the best test?
The liver is a complex organ with a variety of essential functions for the body. It participates in metabolism, produces bile, and generates proteins secreted into the blood, so your doctor may measure compounds associated with all of these liver functions. All of those tests are frequently measured in a battery of tests referred to as a “liver panel.” Depending upon the type and nature of the underlying liver injury and therefore the liver disease, changes in the magnitude of the various components of this panel provide meaningful information to your physician. However, if one simply wants to know whether one has liver wellness or may have an underlying liver disease, the ALT is likely the most sensitive test for the vast majority of liver illness.
Is there a direct correlation between the magnitude of the serum ALT elevation and the severity of the underlying liver disease?
Although there can be a relationship between the magnitude of elevation in the serum ALT and the severity of the abnormalities in liver structure and function, this relationship is not absolute. Patients with advanced scarring of the liver may have significant liver dysfunction despite only mild elevations of the serum ALT. Therefore, any elevation of the serum ALT should be taken seriously and one should seek appropriate medical care to determine the cause.
What are some common causes of an elevated serum ALT?
Perhaps the most common cause in the North American population is fat accumulation within liver cells. Fat can accumulate anywhere in the body, but its accumulation in the liver cells is toxic to the liver. In particular, patients who are above their ideal body weight, have diabetes, or elevations in their blood lipids, may be at risk for having fat within the liver. The serum ALT is a common approach to determine whether one may have fat in the liver and if it is injurious to this organ. Other common causes of an elevated serum ALT include excessive consumption of alcohol, infection by chronic hepatitis viruses such as hepatitis B and C, toxicity from pharmaceutical medications, a genetic liver disease associated with an excess accumulation of iron in the liver, and autoimmune liver diseases. The latter are a variety of liver diseases in which the body’s immune system inflicts damage on ones own organ.
I have an elevated ALT. What should I do?
If you have an elevated ALT, you should seek medical attention. The vast majority of primary care physicians and specialists in gastroenterology and hepatology, can perform the necessary testing to determine the cause of an elevated serum ALT.
How often should I have my serum ALT measured?
Like the serum cholesterol and blood glucose tests for elevated cholesterol and diabetes, respectively; one should have the serum ALT measured repeatedly and regularly over time. A conservative approach would be to have ones serum ALT measured on an annual basis during the annual physical examination.
Source
Conatus Pharmaceuticals Will Display HCV Clinical Trial Data at the International Liver Congress™ (EASL) in March
SAN DIEGO, March 11, 2011 /PRNewswire/ -- Conatus Pharmaceuticals Inc. today announced the acceptance of two poster presentations of Phase 2 clinical trial data of CTS-1027 for the treatment of hepatitis C virus-infected patients at the 46th annual meeting of the European Association for the Study of the Liver (EASL) to be held in Berlin, Germany, on March 30 to April 3, 2011.
Specifically, abstract 562 entitled: 24-WEEK TREATMENT WITH CTS-1027 IN COMBINATION WITH RIBAVIRIN REDUCES HCV-RNA IN TREATMENT NAIVE GENOTYPE-1 PATIENTS will be presented.
In addition, abstract 549 entitled: UNIQUE PATTERN OF VIROLOGIC RESPONSE IN PATIENTS WITH GENOTYPE-1 HCV: A PHASE II STUDY OF CTS-1027 IN COMBINATION WITH PEGINTEFERON/RIBAVIRIN (SOC) IN NULL RESPONDERS will also be presented.
"This will be the first public disclosure of these exciting clinical results and represents a significant step forward to raise awareness of CTS-1027 for the treatment of HCV," said Alfred P. Spada, Ph.D., Senior Vice President, Research and Development at Conatus.
"CTS-1027 is a first-in-class oral, small molecule inhibitor of host matrix metalloprotease (MMP) activity. There are no other drugs under development for HCV that operate by the same mechanism of action. Most other approaches to treat HCV infection are direct-acting anti-viral drugs whose activity is directed against virus proteins or enzymes with the objective of reducing the production of virus in infected cells. CTS-1027 by comparison is distinctly different in that its activity is hypothesized to facilitate the immune clearance of virus-infected cells and decrease the frequency of new infections, both of which are of key importance in curing HCV infections," said Steven J. Mento, Ph.D, President and CEO of Conatus.
Conatus Pharmaceuticals Inc. is a privately-held biopharmaceutical company engaged in the development of innovative human therapeutics to treat liver disease and oncology. Conatus' lead drug candidate, CTS-1027 is in multiple Phase 2 clinical trials for the treatment of hepatitis C virus (HCV). Conatus was founded by the executive management team of Idun Pharmaceuticals in July 2005 following the sale of Idun to Pfizer. For additional information, please visit http://www.conatuspharma.com/.
SOURCE Conatus Pharmaceuticals Inc.
RELATED LINKS
http://www.conatuspharma.com/
Source
Specifically, abstract 562 entitled: 24-WEEK TREATMENT WITH CTS-1027 IN COMBINATION WITH RIBAVIRIN REDUCES HCV-RNA IN TREATMENT NAIVE GENOTYPE-1 PATIENTS will be presented.
In addition, abstract 549 entitled: UNIQUE PATTERN OF VIROLOGIC RESPONSE IN PATIENTS WITH GENOTYPE-1 HCV: A PHASE II STUDY OF CTS-1027 IN COMBINATION WITH PEGINTEFERON/RIBAVIRIN (SOC) IN NULL RESPONDERS will also be presented.
"This will be the first public disclosure of these exciting clinical results and represents a significant step forward to raise awareness of CTS-1027 for the treatment of HCV," said Alfred P. Spada, Ph.D., Senior Vice President, Research and Development at Conatus.
"CTS-1027 is a first-in-class oral, small molecule inhibitor of host matrix metalloprotease (MMP) activity. There are no other drugs under development for HCV that operate by the same mechanism of action. Most other approaches to treat HCV infection are direct-acting anti-viral drugs whose activity is directed against virus proteins or enzymes with the objective of reducing the production of virus in infected cells. CTS-1027 by comparison is distinctly different in that its activity is hypothesized to facilitate the immune clearance of virus-infected cells and decrease the frequency of new infections, both of which are of key importance in curing HCV infections," said Steven J. Mento, Ph.D, President and CEO of Conatus.
Conatus Pharmaceuticals Inc. is a privately-held biopharmaceutical company engaged in the development of innovative human therapeutics to treat liver disease and oncology. Conatus' lead drug candidate, CTS-1027 is in multiple Phase 2 clinical trials for the treatment of hepatitis C virus (HCV). Conatus was founded by the executive management team of Idun Pharmaceuticals in July 2005 following the sale of Idun to Pfizer. For additional information, please visit http://www.conatuspharma.com/.
SOURCE Conatus Pharmaceuticals Inc.
RELATED LINKS
http://www.conatuspharma.com/
Source
Many Hepatitis C-Positive Patients Are Uninsured
Last Updated: March 11, 2011
U.S. patients infected with hepatitis C virus are more likely to be uninsured, and the rate of insurance coverage is even lower in those who are eligible for treatment, according to a study in the March issue of Hepatology.
FRIDAY, March 11 (HealthDay News) -- U.S. patients infected with hepatitis C virus (HCV) are more likely to be uninsured, and the rate of insurance coverage is even lower in those who are eligible for treatment, according to a study in the March issue of Hepatology.
Maria Stepanova, Ph.D., from the Inova Fairfax Hospital in Falls Church, Va., and colleagues examined the health insurance status and treatment candidacy of HCV-positive (HCV+) participants in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2008.
The investigators found that 1.16 percent of NHANES participants were defined as HCV+ with detectable HCV RNA. A significantly lower percentage (61.2 percent) of HCV+ individuals were insured compared to HCV-negative individuals (81.2 percent). HCV+ individuals were also less likely to have private insurance. There was no difference in terms of cover by Medicare/Medicaid or other government plans. HCV infection remained an independent predictor of not having insurance in multivariate analysis, even after adjusting the data for demographic disparity among the HCV+ cohort. In total, 66.7 percent of HCV+ patients were eligible for health treatment, 54.3 percent had insurance, and only 36.3 percent of HCV+ patients were eligible for treatment and had insurance coverage.
"A high proportion of HCV+ individuals in the United States are currently uninsured, and many have publicly funded health insurance," the authors write. "This issue of access to care for HCV patients is critical and must be considered by policy makers."
Abstract
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Source
U.S. patients infected with hepatitis C virus are more likely to be uninsured, and the rate of insurance coverage is even lower in those who are eligible for treatment, according to a study in the March issue of Hepatology.
FRIDAY, March 11 (HealthDay News) -- U.S. patients infected with hepatitis C virus (HCV) are more likely to be uninsured, and the rate of insurance coverage is even lower in those who are eligible for treatment, according to a study in the March issue of Hepatology.
Maria Stepanova, Ph.D., from the Inova Fairfax Hospital in Falls Church, Va., and colleagues examined the health insurance status and treatment candidacy of HCV-positive (HCV+) participants in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2008.
The investigators found that 1.16 percent of NHANES participants were defined as HCV+ with detectable HCV RNA. A significantly lower percentage (61.2 percent) of HCV+ individuals were insured compared to HCV-negative individuals (81.2 percent). HCV+ individuals were also less likely to have private insurance. There was no difference in terms of cover by Medicare/Medicaid or other government plans. HCV infection remained an independent predictor of not having insurance in multivariate analysis, even after adjusting the data for demographic disparity among the HCV+ cohort. In total, 66.7 percent of HCV+ patients were eligible for health treatment, 54.3 percent had insurance, and only 36.3 percent of HCV+ patients were eligible for treatment and had insurance coverage.
"A high proportion of HCV+ individuals in the United States are currently uninsured, and many have publicly funded health insurance," the authors write. "This issue of access to care for HCV patients is critical and must be considered by policy makers."
Abstract
Full Text (subscription or payment may be required)
Source
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