SUMMARY OF TRANSLATION OF SECTIONS CONCERNING HIV AND AIDS FROM THE IMMODAL KRALLENDORN BOOKLETS FOR DOCTORS AND PATIENTS

(NOTE:  Krallendorn treatment is extract from Uña de Gato, uncaria tomentosa, or Cat’s Claw)

From the Information for Patients

Three groups of patients with HIV infections were treated with Krallendorn medication.  The first group was comprised of patients who, although HIV-positive at the time of treatment, were nonetheless clinically healthy.  The second group consisted of patients with abnormal blood values and the first signs of AIDS.  In the third group were patients who had all the symptoms of AIDS.

The patients of the first group have been treated for five years with Krallendorn.  The treatment was effective with almost all of these patients in preventing the disease from progressing.

The patients of the second group have been treated for six years with Krallendorn.  The treatment worked with almost all of these patients.  The abnormal blood values were bettered inside of one year from the time of initial treatment, and the patients lost their symptoms of clinical illness.  This good condition has been maintained to this day.

The patients of the third group have been treated for one year with Krallendorn and AZT.  The treatment was effective with almost all patients in preventing the appearance of side effects of AZT therapy.  Abnormal blood values were improved and clinical symptoms were lessened.

From the Information for Doctors and Pharmacists

Therapy of HIV Patients in the CDC A1 and CDC B2 Stages of the Disease

Patients and Methods:

In the time period from 1987 to 1991 a total of 32 HIV-infected patients were informed of the possibility of participating in an experimental therapy with the test medicine (i.e. Krallendorn).  Of these, 14 regularly provided us with data about the progression of their disease.  The only criterion for inclusion in the test therapy was definite presence of HIV-infection demonstrated in two independent tests.  The only criterion for exclusion was a lack of compliance on the part of the patient in making the health data on his/her illness available to us.

The length of observation per patient amounted to a minimum of 12 months, a maximum of 72 months and on average 36 months.  None of the patients had taken AZT or any other HIV therapy before the beginning of the test therapy.  None of the patients had used a prophylactic therapy against opportunistic infections before the start of the test therapy.  The ascertaining of the parameters of the progression of the disease took place every 3-6 months, regardless of the condition of the patient.

Medication:  During the period of observation the patients took a Krallendorn capsule containing 160 ug oxindolalkaloid-hydrochloride.  When an additional infection was present the patients also received antibiotic treatment.  When CD4-cells sank under 200/ul the patient was advised of this circumstance and recommended to go on AZT and a prophylactic therapy for opportunistic infections.

Clinical Examination:  The data on the clinical condition of the patients were made available to us by the patients.

Laboratory Examination:  The carrying out of the laboratory examinations followed in most cases an interval of 3-6 months, although in single cases with a shorter or longer interval.  The following parameters were regularly examined:  erythrocytes, hemoglobin, hematocrit, leukocytes, thrombocytes, differential blood profile, CD4/CD8-subtyping and ratio, serum-neopterin W-Blot HIV-1, recombinant Blot HIV-1 and -2, HIV-1 antigen immunelectrophorese.  In irregular intervals the liver values SGOT, SGPT, and GGT, kidney values, blood fats, blood sugar and electrolytes, testing of germs in body fluids and virus serology were examined.

Statistics:  The statistical processing of the data limited itself to the use of the descriptive statistics to calculate the medians and quartiles of each measurement parameter to each measurement period for the comparison of the disease progression findings with the respective base values, as well as the calculation of the correlation coefficient for the ascertaining of possible correlations between the increase of the CD4-cells and the development of leukocytes, lymphocytes and CD8-cells.

Discussion

With up to six years of continuous use of the therapy it appears to be atoxic, and the therapy seems to not be burdened with side effects.  Serious side effects that would have necessitated the cessation of the therapy were not observed in any case.  The therapy with the test medicine seemed to have a delaying influence on the progression of the symptoms of the illness and the development of full-blown AIDS.

Most impressively visible is this effect on two female patients.  One female patient from the CDC A1 group was infected with HIV five years before the beginning of the therapy.  The time of the first diagnosis was in the year of infection.  This patient had at the time of evaluation of these data just concluded her fifth year with the test therapy.  Ten years after infection with HIV this patient is still clinically asymptomatic and has 600 CD4-cells/ul.  The only female patient from the CDC B2 group was infected with HIV also five years before the start of the therapy.  At the time of evaluation of these data this patient had concluded her sixth year on the test therapy.  Eleven years after infection this woman has a count of 250 CD4/ul a value close to the base value of 300/ul at the start of the therapy.  Except for recurring vaginal candidiasis she is clinically symptom free.

The mechanism of action of the test medicine is still far from clear.  The replication inhibiting effect of the alkaloids for HIV in primary lymphocyte cultures of 33.5% HIV-RNA observed in-vitro does not seem to be sufficient to explain the prominent clinical effects on retroviral infected cats and the patients with HIV-infection.  A possible beginning of an explanation could be in the strongly positive correlation found between the CD4 cell count and the leukocyte count, as well as the somewhat weaker correlation between the CD4 cell count and the lymphocyte count, that is the CD4 count and the CD8 count. The discovered positive correlation between the CD4 cell count and the CD8 cell count with r=0.7 explains why no appreciable improvement in the T4/T8 ratio can be expected.  Parallel to the growth of the CD4 cell count is the growth of the CD8 count.  In our CDC B2 group it was clear that the increase of the CD4 cells to the level of up to 500 CD4-cell/ul under the influence of the test medicine was not an isolated course of events but rather the expression of a growth in all leukocyte populations.  Herewith the growth of the leukocytes in the therapy appears to be most decisive, since the most prominently positive correlation is between the leukocyte count and the CD4 cell count with a correlation coefficient of r=0.9.  With the leukocyte subtypes only the absolute number appears to be relevant.  Between the lymphocyte count and the CD4 count also exists a positive correlation with a correlation coefficient of r=0.8, while no correlation was found between CD4 cell counts and the %-lymphocytes and %-granulocytes (r=0.2 and r=0.1 respectively).

The correlation between CD4 cell counts and leukocytes, lymphocytes and CD8 cell counts (r=0.3, r=0.3 and r=0.2 respectively) was relatively slight in the CDC A1 group with its more stabile CD4 cell counts and the considerably slighter CD4 cell count fluctuations.

Return to Science & Research