Information of Hepatitis C

  • Hepatitis C
    • Epidemiology. Hepatitis C virus (HCV), identified in 1988, is an RNA virus that appears to be responsible for most instances of parenterally transmitted non-A, non-B hepatitis. The virus seems to mutate frequently and appear in many subtypes. HCV is associated with transfusions of contaminated blood and blood products such as plasma, factor VIII, factor IX, fibrinogen, cryoprecipitate, and immune globulin.
      HCV is also transmitted by IV drug abuse, hemodialysis, and organ transplantation. It appears to be transmitted rarely by familial, sexual, or maternal-infant exposure. Heterosexual transmission seems to be much less frequent than homosexual transmission of the virus.
      Health-care workers exposed to a patient or the blood of a patient infected with HCV may acquire hepatitis C either from an accidental needle stick or without such an incident; however, the risk in such cases seems to be less than 10%. This occurrence has been documented in dialysis and oncology units and in plasmapheresis centers. Sporadic instances of hepatitis C occur and may account for 6% to 36% of the sporadic cases of hepatitis seen in urban areas. There may be unnoted percutaneous exposure among such patients. However, hepatitis C may also be transmitted by nonpercutaneous mechanisms. The epidemiology of hepatitis C has not been completely defined.


      The disease is found worldwide and appears to be almost as common in economically developed countries as it is in underdeveloped countries.
    • Clinical presentation
      • Acute hepatitis
        • The mean incubation period for transfusion-associated hepatitis C is 7 to 8 weeks with a range of 2 to 26 weeks. Shorter incubation periods of 1 to 2 weeks have also been recorded.
        • The acute illness associated with hepatitis C usually cannot be distinguished from hepatitis caused by other heterotropic viruses. However, it tends to be less severe. Usually patients complain of flulike symptoms, easy fatigability, malaise, and anorexia with occasional nausea and vomiting; fever, arthralgia, and skin rash are rare.
        • Approximately 25% of patients with hepatitis C are icteric. Jaundice usually lasts less than a month. The serum transaminase (ALT, AST) levels are only moderately elevated (<800 IU/L).
        • Transient agranulocytosis and aplastic anemia have been observed in patients with hepatitis C.
        • A clinical feature characteristic of hepatitis C is its episodic, fluctuating pattern of serum transaminase (ALT, AST) activity. Periods of elevation of these enzyme levels are interrupted by months of normal or near-normal levels of liver enzyme activity 
      • Chronic disease
        • Long-term follow-up studies in patients with hepatitis C have revealed that at least 90% of patients infected with HCV have chronic disease. The disease may continue to appear to resolve both biochemically and histologically, followed by intermittent or constant elevation of serum transaminases. Persistent viremia can prevail in the presence or absence of elevated ALT activity. In fact, spontaneous total resolution of the disease may occur in only a small proportion of infected individuals.
              • The progression to chronic hepatitis cannot be predicted from the clinical or biochemical severity of the acute illness. Anicteric as well as icteric disease may become chronic.
              • In most studies, the frequency of development of chronic liver disease from transfusion- associated hepatitis C is 85% to 90%. When biopsied, approximately 70% to 80% of these patients have chronic active hepatitis, and 10% to 20% have cirrhosis. The chronic active hepatitis in these patients is progressive and progresses to cirrhosis in most cases over 10 to 30 years.
              • Cofactors such as concomitant alcoholism, chronic hepatitis B or hemochromatosis are important contributors to progressive liver disease and cirrhosis in patients with chronic hepatitis.
              • Several studies have linked essential mixed cryoglobulinemia (EMC) (an immune complex vasculitis associated with joint, skin and sometimes kidney involvement) and porphyria cutanea tarda (PCT) with HCV infection.
            • Hepatitis C and hepatocellular carcinoma. There is convincingevidence that HCV infection is associated with the development ofhepatocellular carcinoma. Several patients have been reported to develop hepatocellular carcinoma 9 to 18 years after the onset of transfusion-associated hepatitis C.
          • Diagnosis
            • Serologic tests for HCV infection have been developed and continue to be in a stage of rapid evolution. Currently, second-generation enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA) tests for anti-HCV (or HCAb) are commercially available.
              Using the ELISA, anti-HCV is detected late during the course of acute hepatitis C, generally between 4 and 24 weeks after the onset of symptoms. In patients in whom chronic hepatitis C develops, anti-HCV appears to persist indefinitely; in patients in whom the infection resolves, anti-HCV reactivity disappears over the next few years. In acute hepatitis C, the antibody titers often rise slowly and may be detectable after many weeks; thus both acute and convalescence-phase samples must be tested.
              A high rate of false-positive anti-HCV reactions was reported in patients with alcoholic liver disease and autoimmune chronic active hepatitis when the first-generation ELISA test was being used. In these patients, anti-HCV positivity was correlated with the degree of hypergammaglobulinemia. In such cases, the RIBA test improves the accuracy of the diagnosis. A positive test for anti-HCV by RIBA provides confirmation of an ELISA result, but a negative, indeterminant reaction cannot be interpreted as proof of a false-positive ELISA reaction. The second-generation ELISA test uses recombinant proteins from various regions of the HCV genome as antigens, and RIBA uses four such proteins. By broadening the spectrum of antibodies detected, these assays have proved to be more sensitive and specific than the first-generation anti-HCV assays.
            • HCV RNA. HCV RNA cannot be detected in serum by the standard techniques such as northern blot analysis because the virus circulates in low levels. However, it can be detected by PCR in both serum and liver. Studies indicate that most patients with acute hepatitis C circulate HCV RNA during the incubation period and the symptomatic phase of the disease. Forty to seventy percent of patients with chronic hepatitis C have HCV RNA in their serum. Direct PCR for HCV RNA in serum may be the best means to confirm the presence of HCV infection and to quantify levels of HCV RNA in serum and the liver and thus become an important means of assessing the effectiveness of antiviral therapy.


            • Genotyping of HCV has been possible and has revealed few major genotypes: I (A and B), II, III, IV. Genotypes IV and I are most prevalent in the United States, comprising about 70% of infections. Genotypes V and I are also more resistant to the treatment modalities currently available.

Homeopathy has proven treatment for various viral infections. Based on this established fact, Suyog Gastro Liver Homeopathy team has been working on the treatment of Hepatitis C since last seven years. The treatment has shown promising results.

Homeopathic treatment works in the following manner:

  • Reduces the tendency of Hepatocellular carcinoma after hepatitis C infection
  • Reducing the viral count and activity by stimulating the immune system.
  • Treating the after effects of tissue changes due to Hepatitis C virus. 

 

At our center we have treated more than 450 cases of HEPATITIS c with homeopathic medicine with brilliant result.