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HIV and the use of herbs; St Johns Wort and Panax ginseng.

HIV and the use of herbs; St Johns Wort and Panax ginseng.

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HIV and herbal medicine

The introduction of highly active antiretrovital therapy (HAART) into clinical practice has dramatically changed the development of HIV-related diseases in industrialised countries (Vella 2000) but HIV infection still remains an incurable disease (Wei et al 1995). HAART alone cannot eradicate the virus in the human body (Finzi et al). Drug resistance is probably the most important factor contributing to the failure of treatment today (Richman D 1997). The antiretrovirals have an impact on reducing morbidity and mortality, prolonging lives, improving the quality of life of many people living with HIV (WHO 2002). Many people in developing countries cannot afford the high cost of HAART (Asres et al 2005), it has a limited response in some patients, it has a complicated dosage regimen leading to non-compliance, and is associated with drug toxicity and the emergence of drug resistance (Bonfanti et al 1999). The majority of people living with HIV are using complementary medicine (Ozsoy 1999). In Europe herbal treatments have been the most popular complementary medicine used by HIV infected individuals (Ozsoy 1999). Research has been carried out and is in progress to isolate the active constituents from plants for the prevention of transmission of HIV and treatment of AIDS (Asres et all 2005). Many plants are active against HIV replication at least in vitro, whose significance is not yet clear, and have not been followed up to see their actual clinical usefulness in combating HIV/AIDS(De Clercq 2000). Being a relatively new disease there is no tradition of herbs used for HIV/AIDS. So is there any clinical evidence for use of herbal medicine in HIV positive patients?
HIV and herbal medicine

The introduction of highly active antiretrovital therapy (HAART) into clinical practice has dramatically changed the development of HIV-related diseases in industrialised countries (Vella 2000) but HIV infection still remains an incurable disease (Wei et al 1995). HAART alone cannot eradicate the virus in the human body (Finzi et al). Drug resistance is probably the most important factor contributing to the failure of treatment today (Richman D 1997). The antiretrovirals have an impact on reducing morbidity and mortality, prolonging lives, improving the quality of life of many people living with HIV (WHO 2002). Many people in developing countries cannot afford the high cost of HAART (Asres et al 2005), it has a limited response in some patients, it has a complicated dosage regimen leading to non-compliance, and is associated with drug toxicity and the emergence of drug resistance (Bonfanti et al 1999). The majority of people living with HIV are using complementary medicine (Ozsoy 1999). In Europe herbal treatments have been the most popular complementary medicine used by HIV infected individuals (Ozsoy 1999). Research has been carried out and is in progress to isolate the active constituents from plants for the prevention of transmission of HIV and treatment of AIDS (Asres et all 2005). Many plants are active against HIV replication at least in vitro, whose significance is not yet clear, and have not been followed up to see their actual clinical usefulness in combating HIV/AIDS(De Clercq 2000). Being a relatively new disease there is no tradition of herbs used for HIV/AIDS. So is there any clinical evidence for use of herbal medicine in HIV positive patients?

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03/26/2013

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HIV and herbal medicine; the use of St Johns Wort and Panax ginseng.by Hananja Brice-Ytsma Medical Herbalist (MSc, MNIMH)http://creativecommons.org/licenses/by-nc-nd/2.0/uk/HIV and herbal medicineThe introduction of highly active antiretrovital therapy (HAART) into clinicalpractice has dramatically changed the development of HIV-related diseases inindustrialised countries (Vella 2000) but HIV infection still remains an incurabledisease (Wei et al 1995). HAART alone cannot eradicate the virus in the human body(Finzi et al). Drug resistance is probably the most important factor contributingto the failure of treatment today (Richman D 1997). The antiretrovirals have animpact on reducing morbidity and mortality, prolonging lives, improving thequality of life of many people living with HIV (WHO 2002). Many people indeveloping countries cannot afford the high cost of HAART (Asres et al 2005), ithas a limited response in some patients, it has a complicated dosage regimenleading to non-compliance, and is associated with drug toxicity and the emergenceof drug resistance (Bonfanti et al 1999). The majority of people living with HIVare using complementary medicine (Ozsoy 1999). In Europe herbal treatments havebeen the most popular complementary medicine used by HIV infected individuals(Ozsoy 1999). Research has been carried out and is in progress to isolate theactive constituents from plants for the prevention of transmission of HIV andtreatment of AIDS (Asres et all 2005). Many plants are active against HIVreplication at least in vitro, whose significance is not yet clear, and have notbeen followed up to see their actual clinical usefulness in combating HIV/AIDS(DeClercq 2000). Being a relatively new disease there is no tradition of herbs usedfor HIV/AIDS. So is there any clinical evidence for use of herbal medicine in HIVpositive patients?Panax ginseng (Korean Red Ginseng KRG)Panax ginseng is an herbal root that has been known in China for more than 2000years (Li et al 1973). A study in healthy human volunteers revealed that KRGsignificantly increases neutrophil, CD4 T cells and NK cell function (Scallione etal 1990). Ginseng was found to increase the cellular immune functions ofperipheral blood mononuclear (PBMC) from AIDS patients and normal individuals (Seeet al 1997). KRG was given for 6 months to HIV-1 infected individuals (5.4mgdaily), CD4T cell counts in HIV-1-infected patients treated with only KRG weremaintained or even increased for a prolonged period. The development of resistancemutations in RT to zidovudine (ZDV) was delayed by combined therapy with KRG andZDV (Cho et al 1993). Some of those patients have maintained CD4+ count for 8years with KRG-intake only (Cho et al 2001). It was suggested that the maintenanceof CD4T cell counts by ZDV and KRG intake for a prolonged period might beindirectly associated with delayed development of resistance to ZDV by KRG intake(Cho et al 2001). No details are given on the trial itself, the number of patientsinvolved, the stage of disease, no control, so we cannot draw any conclusion ofthe above but the initial observation led to the following study done by the sameauthors. A study investigated whether the maintenance of CD4+ T cell count in HIV-1-infected patients treated with ZDV and KRG is associated with the delay of thedevelopment of resistance to ZDV (Cho et al 2001). Nine of the 18 pt were in theKRG group, daily dose of 5.4g, and had been treated with KRG for 60 months and ZDV
 
for more than 18 months, nine were in the control group and been treated with ZDVonly. KRG intake was the only significant variable between the two groups. Therewas no significant difference in clinical stages and demographics between the KRGgroup and the control group. Maintenance or increase in CD4+ T cell counts inpatients treated with KRG was found. Mild but consistent decrease in p24 antigenduring KRG-intake was also detected as long as KRG was taken. In Combination withZDV, the beneficial effects associated with KRG-intake were a decrease in CD4+ Tcell count was not detected during at least a few years of therapy. Based on theseobservations, the authors concluded that KRG intake itself is likely to havebeneficial effects in HIV patients. Over the 24 months of treatment, the overallincidence of 6 resistance mutations to ZDV was significantly reduced in the KRGgroup. The authors conclude that the maintenance of CD4+ T cell counts by ZDV andKRG-intake for a prolonged period might be indirectly associated with delayeddevelopment of resistance to ZDV by KRG-intake. The authors recommend KRG intakeas early stage as possible to get good prognosis over a long term. The number inthis study is very small but well accounted for. There was a significant timescale used. Individuals respond different to the virus and cofactors could lead toearlier development of AIDS. Being such a small number it is difficult to say howvalid and reliable the measurements were. The patients and investigators were notblinded. No side effects were reported. The data suggests that the combination ofantiretroviral drugs with KRG could be a new therapeutic modality to treat HIV-1infected patients but larger trials are needed. KRG was tested with ZDV so wecannot draw a conclusion on the combination of other antiretroviral drugs with KRGand that would need to be investigated.Another original study was done to investigate whether this slow progression ormaintenance of CD4 T cell over 10 years was affected by KRG intake alone or incombination with HLA factor (Sung et al 2004). Many patients have maintained theirCD4 T cell counts for more than 10 years without antiretroviral drugs therapy andprognosis of HIV-1 infected patients has been found to be strongly associated withtheir HLA alleles. They determined HLA class I in 90 HIV-1 infected patientsdiagnosed from 1987 to 2001. They were randomly recruited nation-wide however, itis not stated how. At enrolment the patients were asked to return for an interviewand for clinical examination and a blood sample every 6 months. Estimating therate of progression of HIV-1 infection was accomplished by measuring the annualdecrease in CD4 T cells. The HLA results were compared with those of a controlgroup, which was comprised of 199 uninfected Korean people drawn for thepopulation. 22 patients were treated with antiretroviral drugs or were monitoredfor less than 60 months. Changes in the CD4 T cells and correlation among KRGintake, CD4-Tcells and HLA were finally analysed in the 68 out of 90 patients. Themedian follow up time in the 68 pt was 113.5 months (range 60-164 months. 61 outof the 68 pt were treated with KRG (5.4g per day). A strong correlation was foundbetween KRG intake and annual decrease in CD4 T cells, and between KRG intake andsCD8, together with a significant inverse correlation between HLA prognostic scoreand annual decrease in CD4 cells. In addition they found that KRG intake aloneslows the decrease in CD4 T cells irrespective of HLA prognostic score. Also, asignificant decrease in serum sCD8 was found which is an immune activation markerphysiologically secreted from CD8T cells. The significant and consistent decreasein serum sCD8 was maintained as long as KRG was taken continuously. Thus thedecrease in serum sCD8 may be indicative of a lower level of destruction of CD8 Tcells in patients ingesting KRG and suggests that KRG intake is associated withprolonged maintenance of enhanced CD8T lymphocyte activity. The authors concludedthat KRG intake independently has beneficial effects on the slow decrease in CD4 Tcells and on serum sCD8 levels in HIV- infected patients, although the HLA factorwas also significantly associated with the rate of CD4 T cell depletion in theKorean population.The population studied was small, and only seven were not taking KRG, but over asignificant amount of time, no side effects are mentioned, patients and
 
investigators were not blinded so open to systematic bias. To say if themeasurements were valid, reliable, and reproducible, one might need a largergroup. The paper could point to possible use of KRG, but is difficult to concludewithout more rigorous trials.Hypericum perforatum (HP); St John's WortHypericum perforatum (HP); St John’s WortHypericin or HP is taken commonly by HIV-infected persons (Kassler et al 1991).Hypericin has activity against many HIV in vitro Hudson et al 1991). In 1989researchers found that two extracts of HP had anti-HIV activity in lab experimentswith cells and viruses. Since hypericin is known to exhibit a similar inhibitoryproperty, it is likely to be one of the active constituents of St Johns wort(Taher et al 2002). Hypericin appears to inactivate free virions and interferewith steps in the replicative cycle (Hudson 1991). Hypericin and pseudohypericindisplay an extremely effective antiviral activity when administered to mice afterretroviral infection (Muerelo et al 1988). It was found that relatively smalldoses of hypericin or pseudohypericin 10-50ug per mouse can prolong survival ofHIV infected mice. When the compounds interact with the infection particlesshortly after in vivo administration, disease is completely prevented. Thecompounds can cross the blood-brain barrier (Meruela et al 1988). Initial studieslooked promising (James 1989).An uncontrolled study of 26 pt self-administering Hypericum containing herbalextract (Cooper and James 1990) concomitant, used AZT, and other treatment waspermitted. All patients were HIV positive, at various stages of the disease, andwere taking approximately 1 mg total hypericin per day. They received baseline and4 monthly checks, including physical examinations, T-cell subsets and p24 antigen.Toxicity was limited to mild reversible liver enzyme elevation in 5 patients, withlevels returning to baseline after 1 month without Hypericum. At the end of the 4-month study, p24 antigenaemia disappeared in 2 of 6 initially positive patients,both also using AZT. CD4 cell changes differed, depending on AZT usage, in thesubgroup of 10 pt who had never taken AZT, none had developed AIDs, the mean CD4count increased 13% from the base line after 1 month of Hypericum and maintainedthis increase for 4 months. These increases were not statistically significant. Bycontrast however, in those using Hypericum and AZT throughout the study, CD4counts fell significantly after initial mild rise.Details of the patients are minimal and there was no control group; size samplewas small and duration short. So, again, a study might not have any significance,however this is the first pointer towards that hp might interfere with theanitiviral AZT and as a consequence lower CD4 count.A study was carried out to assess the toxicity and possible anti-HIV activity ofhypericin; there was no CD4 count criteria for entry (Fumer et al 1991). Fourdifferent daily dosage levels of hypericin were administered (0.5mg, 2mg, 4mg,8mg) to cohorts, often HIV-infected men, all HIV positive, no details of whatstage of disease, for a period of 12 weeks. No indication is given on the baselinedifferences between the different groups. Possibly observed toxicities includedmild diarrhoea and indigestion, and infrequent itchy rash, and fatigue ordepression. An idiosyncratic, reversible elevation of hepatic transaminases wasalso observed. No early, marked anti-HIV activity was found. The authors concludedthat at doses of 2mg per day given to HIV infected individuals, hypericin appearsto be safe for the majority of subjects observed so far (Moraleda et al 1993).Duration of treatment was 12 weeks, which might be too short to notice anybeneficial effects. However the conclusion that 2 mg was a safe dose for themajority of patients is important to look at.

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