I was reading a post earlier today that sort of touched on what you are asking. A few of the names of members who posted are still active on the forum so one may come along and respond to your post. Until then, here is this:
This is an oldie but might provide some insight given SSDI is not easy to obtain with HCV alone. Don't know much about osteoarthritis tho.
One of Forseegood's posts has link to some guy's forum who explained his experience with it.
"Are there qualifying conditions to receive Soc. Sec. benefits?"
In a word, No.
As someone who receives SSDI I can tell you that chronic viral liver diease, (hepatitis C), with bridging fibrosis does not qualify anyone for SSDI or SSI.
As most people with these conditions are able to live normal, productive lives (meaning they are not "disabled") and these are not conditions that are fatal in the near term.
People with hepatitis C only qualify for social security disability benefits when they develop End-Stage Liver Disease (liver failure) and suffer with the complications of liver failure or have unresectable hepatocellular carcinoma (liver cancer) which is terminal without a transplant. A patient will be considered disable when they have a liver transplant for one year and will be reviewed after that.
You must prove using your medical records and test results that you meet all the requirements for liver failure mentioned in the Blue Book (see below). You must be unable to perform your old job with accommodations for your illness or any job in the US economy that you are qualified for due to your medical disability. In others words you must be totally disabled and your disability must last for at least one year or result in death to qualify as being disabled.
What does SSA define as a disability?
"The definition of disability under Social Security is different than other programs. Social Security pays only for total disability. No benefits are payable for partial disability or for short-term disability.
"Disability" under Social Security is based on your inability to work. We consider you disabled under Social Security rules if:
You cannot do work that you did before;
We decide that you cannot adjust to other work because of your medical condition(s); and
Your disability has lasted or is expected to last for at least one year or to result in death.
This is a strict definition of disability. Social Security program rules assume that working families have access to other resources to provide support during periods of short-term disabilities, including workers' compensation, insurance, savings and investments."
"In addition to meeting our definition of disability, you must have worked long enough--and recently enough--under Social Security to qualify for disability benefits.
Social Security work credits are based on your total yearly wages or self-employment income. You can earn up to four credits each year.
The amount needed for a credit changes from year to year. In 2012, for example, you earn one credit for each $1,130 of wages or self-employment income. When you've earned $4,520, you've earned your four credits for the year.
The number of work credits you need to qualify for disability benefits depends on your age when you become disabled. Generally, you need 40 credits, 20 of which were earned in the last 10 years ending with the year you become disabled. However, younger workers may qualify with fewer credits."
In order to qualify for disability due to Liver Disease a person must meet the following requirements which amounts to having End-Stage Liver Disease (decompensated cirrhosis).
"5.05 Chronic liver disease,with:
A. Hemorrhaging from esophageal, gastric, or ectopic varices or from portal hypertensive gastropathy, demonstrated by endoscopy, x-ray, or other appropriate medically acceptable imaging, resulting in hemodynamic instability as defined in 5.00D5, and requiring hospitalization for transfusion of at least 2 units of blood. Consider under disability for 1 year following the last documented transfusion; thereafter, evaluate the residual impairment(s).
B. Ascites or hydrothorax not attributable to other causes, despite continuing treatment as prescribed, present on at least 2 evaluations at least 60 days apart within a consecutive 6-month period. Each evaluation must be documented by:
1. Paracentesis or thoracentesis; or
2. Appropriate medically acceptable imaging or physical examination and one of the following:
a. Serum albumin of 3.0 g/dL or less; or
b. International Normalized Ratio (INR) of at least 1.5.
C. Spontaneous bacterial peritonitis with peritoneal fluid containing an absolute neutrophil count of at least 250 cells/mm3.
D. Hepatorenal syndrome as described in 5.00D8, with on of the following:
1. Serum creatinine elevation of at least 2 mg/dL; or
2. Oliguria with 24-hour urine output less than 500 mL; or
3. Sodium retention with urine sodium less than 10 mEq per liter.
E. Hepatopulmonary syndrome as described in 5.00D9, with:
1. Arterial oxygenation (PaO2) on room air of:
a. 60 mm Hg or less, at test sites less than 3000 feet above sea level, or
b. 55 mm Hg or less, at test sites from 3000 to 6000 feet, or
c. 50 mm Hg or less, at test sites above 6000 feet; or
2. Documentation of intrapulmonary arteriovenous shunting by contrast-enhanced echocardiography or macroaggregated albumin lung perfusion scan.
F. Hepatic encephalopathy as described in 5.00D10, with 1 and either 2 or 3:
1. Documentation of abnormal behavior, cognitive dysfunction, changes in mental status, or altered state of consciousness (for example, confusion, delirium, stupor, or coma), present on at least two evaluations at least 60 days apart within a consecutive 6-month period; and
2. History of transjugular intrahepatic portosystemic shunt (TIPS) or any surgical portosystemic shunt; or
3. One of the following occurring on at least two evaluations at least 60 days apart within the same consecutive 6-month period as in F1:
a. Asterixis or other fluctuating physical neurological abnormalities; or
b. Electroencephalogram (EEG) demonstrating triphasic slow wave activity; or
c. Serum albumin of 3.0 g/dL or less; or
d. International Normalized Ratio (INR) of 1.5 or greater.
G. End stage liver disease with SSA CLD scores of 22 or greater calculated as described in 5.00D11. Consider under a disability from at least the date of the first score."
"5.09 Liver transplantation. Consider under a disability for 1 year following the date of transplantation; thereafter, evaluate the residual impairment(s) (see 5.00D12 and 5.00H)."
"3.00 Malignant Neoplastic Diseases (Cancer)
13.19 Liver or Gallbladder-- tumors of the liver, gallbladder, or bile ducts."
For information about SSDI visit their web page at
what is bridging fibrosis
When I person has a biopsy of the liver the amount of fibrosis (scaring (septa) caused by injury done to the liver done by a chronic hep C virus infection) is graded on a scale using the METAVIR system.
METAVIR Fibrosis Stages:
• F0: no fibrosis
• F1: minimal fibrosis in one portal of the liver, with no septa
• F2: some fibrosis in one portal, with rare septa
• F3: bridging fibrosis (septa that extend over adjacent portals)
• F4: cirrhosis with loss of normal liver architecture
Septa - thick bands of fibrous tissue
Portals - The "classic" liver lobule (individual liver cell) is the sixsided polyhedral prism with portal triads (hepatic artery, portal vein, and bile duct) at each of the corners.
So bridging fibrosis is commonly know as "stage 3 liver disease".
Someone with stage 3 liver disease caused by hepatitis C, should seriously think about treating their hepatitis C before their liver disease progresses to stage 4 (cirrhosis) which will reduce their chances of SVR using current treatment drugs.
"Chronic infection with hepatitis C (HCV) can lead to long-term liver damage including fibrosis, cirrhosis, and hepatocellular carcinoma (liver cancer). It is estimated that about 20 percent of people with chronic hepatitis C will develop cirrhosis, a process that usually takes 20-30 years.
The Fibrosis Process
Liver fibrosis refers to the accumulation of fibrous scar tissue in the liver. The formation of scar tissue is a normal bodily response to injury, but in fibrosis this healing process goes awry. When hepatocytes (functional liver cells) are injured due to viral infection, alcohol consumption, toxins, trauma, or other factors the immune system is activated and the repair process swings into gear. The injury or death (necrosis) of hepatocytes stimulates inflammatory immune cells to release cytokines, growth factors, and other chemicals. These chemical messengers direct support cells in the liver called hepatic stellate cells to activate and produce collagen, glycoproteins (such as fibronectin), proteoglycans, and other substances. These substances are deposited in the liver, causing the buildup of extracellular matrix (nonfunctional connective tissue). At the same time, the process of breaking down or degrading collagen is impaired. In a healthy liver, the synthesis (fibrogenesis) and breakdown (fibrolysis) of matrix tissue are in balance. Fibrosis occurs when excessive scar tissue builds up faster than it can be broken down.
Fibrosis Risk Factors
Liver fibrosis does not occur at the same rate in all individuals, and in some people fibrosis remains stable or may even regress over time. Several factors influence fibrosis progression. Fibrosis occurs more rapidly in men than in women, and also in older people, particularly those over age 50. Progression does not seem to be linear; that is, the process appears to accelerate later in the course of disease. Immune system compromise for example, due to coinfection with HIV or use of immunosuppressive drugs after a liver transplant also has been shown to accelerate fibrosis. Heavy alcohol consumption is strongly associated with worsening fibrosis and cirrhosis. Finally, studies indicate that steatosis (fatty liver) and insulin resistance are associated with more rapid and severe fibrosis. In contrast, HCV or HBV viral load and HCV genotype do not appear to have much effect on fibrosis progression (although genotype 3 is associated with a higher risk of steatosis).
Advanced Fibrosis and Cirrhosis
Early in the course of fibrosis, a person usually will experience few or no symptoms. Over years or decades, however, the liver can become excessively scarred, developing nodules and thick bands of fibrous tissue (septa) that extend from one area or portal of the liver to another—a condition known as cirrhosis. As cirrhosis sets in, scar tissue replaces working hepatocytes and the basic architecture or structure of the liver changes, affecting the organ’s ability to function. One such change is the obstruction of the normal flow of blood through the liver. Early on, this can deprive hepatocytes of nutrients, causing increased cell death. In an attempt to restore circulation, new blood vessels form. But these new vessels do not drain efficiently and accumulating scar tissue may put pressure on other vessels, causing blood to back up in the portal vein (portal hypertension). One symptom is stretched and weakened blood vessels (varices) in the esophagus and stomach, which may burst and bleed. Compensated cirrhosis occurs when the liver is heavily scarred but can still function relatively normally. Decompensated cirrhosis occurs when the liver is so damaged that its vital functions are impaired. The organ loses its ability to filter toxins from the blood and to synthesize important proteins, leading to clinical symptoms such as cognitive dysfunction (hepatic encephalopathy), accumulation of fluid in the abdomen (ascites), and prolonged bleeding. In the most severe cases, cirrhosis may progress to hepato-cellular carcinoma or end-stage liver disease (liver failure), necessitating a transplant."