​Kembara Xtra - Medicine - Hepatitis C

​Kembara Xtra - Medicine - Hepatitis C
infection with a systemic virus that affects the liver

Geriatric Considerations for Epidemiology
Patients over 60 years old respond to therapy less readily.


pregnant women's issues
Vertical transmission rate is 6/100 babies; risk doubles with co-infection with HIV. Routine prenatal HCV testing.

If there are no fractures or cracks, breastfeeding is secure.

Child Safety Considerations
Incidence: 0.3%
20% of newborns with HCV are HCV-negative, whereas 30% have chronic active HCV. Children with HCV-positive moms are free to participate in typical childhood activities.
Treatment begins around age 3.

Incidence
The age range with the highest occurrence is 20 to 39 years old.
Predominantly affects men and non-Hispanic whites.
60 to 70 percent of new cases are related to IV drug usage.

Prevalence
HCV-related deaths are more frequent than HIV-related deaths, and it is the most frequent cause of chronic liver disease and liver transplantation in the US.
Eight genotypes (GT) with 86 subtypes are known. GT 1 is the most common kind (75% in the US and 46% globally). GT forecasts a patient's response to care.

Pathophysiology and Etiology 

Genetics of a single-stranded RNA virus from the Flaviviridae family

There are no recognized hereditary risk factors.

The main method of transmission is parenteral exposure to contaminated blood.


Risk elements Exposure dangers
Chronic hemodialysis - Transfusion of blood or blood products or organ transplantation prior to July 1992
- Exposure from a household or a healthcare setting
- Infants born to mothers who have the HCV virus
● Other dangers
- A history of injecting drugs, past or present
- High-risk sexual practices and illicit drug usage intravenously
- Hepatitis B and HIV diseases, as well as a criminal record
- Tattooing in unsupervised areas
- Sharing nail clippers, razors, and other personal hygiene tools
- A needle stick injury occurring in a medical environment


Prevention 

Primary prevention: Don't trade personal care items.
- Use sterile needles and properly dispose of used needles.
- Cover cuts and sores; do not share needles.
Use condoms for safe sexual activity.
Secondary prevention options include using barrier contraception in the absence of a vaccine or postexposure prophylaxis.
- Determine the extent of liver fibrosis or cirrhosis.


Accompanying Conditions 

Extrahepatic symptoms and associated disorders include: Hepatitis B and HIV coinfection; mixed cryoglobulinemia; membranoproliferative glomerulonephritis, the most prevalent kidney disease associated with HCV; and diabetes mellitus and insulin resistance.
Dermatologic signs include erythema multiforme, erythema nodosum, mixed cryoglobulinemia, porphyria cutanea tarda, necrotizing vasculitis, and lichen planus.
Autoimmune diseases

Depression, drug use/recovery, and lymphoma—most usually non-Hodgkin

Introducing History 

Detailed social history, including IV drug and alcohol use, comorbid psychiatric and medical conditions, and coinfections, can be used to assess the risk of exposure.
Chronic HCV: The majority of cases are asymptomatic (isolated rise in ALT, AST) or minimally symptomatic (nonspecific fatigue, depression).
Acute HCV symptoms might appear 2 to 12 weeks after exposure and can include fatigue, jaundice, dark urine, steatorrhea, nausea, stomach pain, low-grade fevers, myalgias, and arthralgias.

clinical assessment 

Signs of advanced fibrosis/cirrhosis include spider angioma, caput medusa, palmar erythema, jaundice, gynecomastia, and Terry nails. They may also have RUQ pain, hepatomegaly, and/or jaundice.
Physical examination symptoms that are related with HCV include arthralgias/myalgias, neuropathy (decreased sensation), sun-exposed skin blisters (PCT), livedo reticularis, lichen planus (palpable purpura), acanthosis nigricans, and swollen lymph node.

Multiple Diagnoses 

Hepatitis A or B, EBV, CMV, alcoholic hepatitis, nonalcoholic steatohepatitis (NASH), hemochromatosis, Wilson disease, 1-antitrypsin deficiency, ischemic, drug-induced, or autoimmune hepatitis, as well as ischemic, autoimmune, or drug-induced hepatitis.

Laboratory Results 

Initial Tests (Lab, Imaging) Screening One-time, routine HCV antibody (Ab) screening for all individuals ages 18 to 79; routine prenatal HCV testing; screen patients under the age of 18 or over 79 if at high risk:
- IV drug users who are currently or have previously tested positive for HIV - High-risk sexual behavior - Patients with consistently high ALT
- Chronic hemodialysis - Before July 1992, blood transfusions or organ transplants
- Children born to mothers who have the disease - Needle sticks or mucosal contact with HCV-positive blood

Tests in the Future & Special Considerations

 Anti-HCV Ab - If nonreactive, no further action is necessary unless exposure occurred within the last six months (HCV RNA test).
Test for HCV RNA if reactive. If none were found, there would be no current HCV infection and no need for further intervention.
Anti-HCV antibodies are found 4 to 10 weeks after infection; 97% of HCV patients will have antibodies by 6 months.
As early as 1–2 weeks after infection, HCV RNA was found.

Hepatic fibrosis can be detected via diagnostic procedures or other methods. These methods include AST to Platelet Ratio Index (APRI), Fibrosis-4 (FIB-4) score, FibroIndex, Forns index, HepaScore, and FibroSURE. The majority of recommendations urge FIB-4 score calculation before starting treatment.
Transient US elastography, MR elastography, CT scan, and ultrasound (US) are all options for imaging the liver.
Liver biopsy: Test Interpretation (gold standard)

 FIB-4 scoring: A score of >3.25 on the fib-4 test (found at https://www.hepatitisc.uw.edu/page/clinicalcalculators/fib-4) shows advanced fibrosis.

If a patient's FIB-4 score is greater than 3.25, cirrhosis is assumed to be present.

Child-Pugh grading is available at https://www.mdcalc.com/child-pughscore-cirrhosis-mortality
After 12 weeks, there is no detectable HCV RNA, which is known as a sustained virologic response (SVR) and is regarded as a virological cure for HCV infection.


Goals for management include reducing unfavorable events and all-cause mortality while achieving SVR.
Inform the state health department of acute HCV.
Treat everyone who has virologic proof of HCV.
Children under the age of three and pregnant women are exceptions.

First Line of Medicine
Pegylated interferon (PEG-IFN) and ribavirin, two common treatments for chronic HCV, are frequently not well tolerated, which eliminates them from consideration as first-line therapies.
Prior to dividing patients into groups with and without compensated cirrhosis, treatment strategies are simplified and non-simple for each group.



Referral If fulminant acute hepatitis, an issue with end-stage disease, or HCC, refer the patient to a liver transplant program if they are unable to achieve SVR with initial first-line treatment.

Alternative Therapies 

There isn't enough data or recommendations to back up effective complementary or alternative therapies for HCV, cirrhosis, or HCC.


admissions requirements for safety

Follow-up AASLD and IDSA now advise an abdominal US every 6 months, with or without serum -fetoprotein (AFP), to monitor for HCC. Only monitor serial viral load if on antiviral medication.

Patients who have cirrhosis require endoscopic varices screening.
- Endoscopic examination every two to three years for compensated cirrhosis in the absence of recognized varices
- Endoscopic surveillance every one to two years for cirrhosis with known varices (3)
Medications* Common Side Effects of Standard Dose; Contraindications
A: 50 mg/100 mg of Elbasvirgrazoprevir (Zepatier) every day. Fatigue, headaches, and nausea; do not combine with CYP3A inducers or OATPIB1/3 inhibitors.
B: 300 mg/120 mg a day of glecaprevirpibrentasvir (Mavyret). drowsiness, headaches, nausea, and diarrhea; avoid with rifampin or atazanavir; must take with food.
C: 90/400 mg Ledipasvirsofosbuvir (Harvoni) per day Dizziness, depression, nausea, diarrhea, myalgia, coughing, dyspnea, weakness, headaches, irritability, sleeplessness, dizziness, and nausea
D: Epclusa sofosbuvirvelpatasvir 400 mg/100 mg daily fatigue, headaches, agitation, depression, sleeplessness, rash, nausea, and weakness
Simple treatment plan for patients without cirrhosis: B for eight weeks OR D for twelve
Simplified regimen for people with compensated cirrhosis:
For GT 3—NS5A RAS testing results determine the therapy regimen: For GT 1 to 6: regimen B for 8 weeks OR for GT 1, 2, 4, 5, and 6: regimen D for 12 weeks
- If NO Y93H: can be treated for 12 weeks with regimen D. 
Nonsimplified and Genotype-Directed 

Genotype-Directed, Nonsimplified Treatment Regimens for Treatment-
Naive Patients: Genotype, Regimen, Duration, Evidence
1A—without cirrhosis: A for 12 weeks [A], B for 8 weeks [A], C for 12 weeks
[A], C for 8 weeks‡ [B], D for 12 weeks [A]
1A—with compensated cirrhosis: A for 12 weeks [A], B for 8 weeks [B], C for
12 weeks [A], D for 12 weeks [A]
1B—without cirrhosis: A for 12 weeks [A], B for 8 weeks [A], C for 12 weeks
[A], C for 8 weeks‡ [B], D for 12 weeks [A]
1B—with compensated cirrhosis: A for 12 weeks [A], B for 8 weeks** [B], C
for 12 weeks [A], D for 12 weeks [A]
2—without cirrhosis: B for 8 weeks [A], D for 12 weeks [A]
2—with compensated cirrhosis: B for 12 weeks** [B], D for 12 weeks [A]
3—with compensated cirrhosis: B for 8 weeks** [A], D for 12 weeks*** [A]
4—without cirrhosis: B for 8 weeks [A], D for 12 weeks [A], A for 12 weeks [B],
C for 12 weeks [B]
4—with compensated cirrhosis: A for 12 weeks [B], B for 8 weeks** [A], C for
12 weeks [B], D for 12 weeks [A]
5 or 6—without cirrhosis: B for 8 weeks [A], C for 12 weeks [B], D for 12
weeks [B]
5 or 6—with compensated cirrhosis: B for 8 weeks [B], C for 12 weeks [B], D
for 12 weeks [B]
*Other medications still in use, although recommended for specific
circumstances include ombitasvir, paritaprevir, ritonavir, and dasabuvir,
ribavirin, simeprevir, daclatasvir, and voxilaprevir.
**If HIV/HCV-coinfected, duration recommendation is 12 weeks.
***Only without baseline NS5A RAS Y93H.
‡If HIV noninfected and HCV RNA <6 m IU/mL.

patient observation

Serial ALT/AST, CBCs, and renal function
12-week therapy period including follow-ups four weeks into and twelve weeks following the end of the program.
- 4-week HCV RNA: Recheck at week 6 if detectable. Stop therapy if RNA has multiplied by more than 10.
- SVR12: HCV RNA not detectable Long-term cure (the therapy's end goal) is often achieved 12 weeks after therapy ends.
– Once SVR is attained, there is no recommendation for further observation if there is no sign of cirrhosis. The patient should currently be treated as if they have never had HCV, according to the AASLD and IDSA recommendations.

SVR lowers the risk of HCC, hepatic decompensation, and portal hypertension. Keep an eye out for signs of decompensation, such as low albumin, ascites, encephalopathy, GI bleeding, etc.
 Keep an eye out for HBV reactivation.


Nutrition 
Exercise and a low-fat, high-fiber diet to treat obesity and fatty liver

 Additional fluids and protein while receiving IFN therapy
Beware of alcohol.
Refrain from using alcohol, tobacco, and illegal substances (including marijuana); instead, follow a 12-step program for rehabilitation and keep an eye out for relapses as needed.
Information about the dangers of sharing personal hygiene products and the possibility of transmission to sexual partners
Use caution when taking herbal remedies and dietary supplements because they may include hepatotoxins.


Only 50% of people with chronic HCV are diagnosed, which is the prognosis.
Medical care is associated with 43%. 15% receive a therapy recommendation, and 9% see SVR.

In most cases, modern treatment plans have SVRs of >95%.
Risk of hepatic decompensation is 3-6% per year.
HCC is an annual risk of 1-4% for HCV patients and an annual risk of 2-8% for cirrhosis patients.
Following a successful HCV SVR, the risk of HCC is reduced by about 70%.

Complications 

If left untreated, fibrosis and cirrhosis often appear during the first 5 to 10 years after infection.
Age, white race, hypertension, alcohol consumption, and anemia are risk factors for cirrhosis; diabetes, hypertension, and anemia are risk factors for decompensation.