Complete Immunophenotypic Reversal of Chronic Lymphocytic Leukemia with
High Dose Parenteral Methylcobalamin.
Abstract
Background: Supposed ‘spontaneous’ remissions in chronic
lymphocytic leukemia/CLL are extremely rare. By the most stringent
immunophenotypic criteria, there are only seven cases to date of
unexplained, immune system effected cures. A historic review of this
phenomenon is presented as context for this eighth case of CLL
immunophenotypic reversal. Case history: A 59-year-old,
molecular biologist, stage I CLL, whose diagnosis and recovery were both
thoroughly documented, not content to watch and wait, chose to treat
himself, after individual tumour susceptibility testing, with evidence
based, biological response modifiers, which initially seemed to keep his
CLL stable. This included 1mg of hydroxocobalamin injected i.m. daily.
However, after some years his lymphocytosis began slowly to drift
upwards. At that point, he was persuaded to change his injection
protocol to methylcobalamin, at 50 mg i.m. a day, a dose whose clinical
safety is sufficiently well established, and a form of cobalamin that
the research literature shows has anticancer actions. Outcome:
This change in cobalamin form and dose proved a critical turning point.
Complete disappearance of the lymphocytosis also coincided with a severe
infection and an even further temporary increase of the parenteral
methylcobalamin dose, both catalytic factors. In the 4th & 5th years
following this, the patient’s repeated immunophenotyping showed no
clonal disease present. A brief review of the field of cobalamin in
cancer research and treatment is given, with discussion of the various
mechanisms by which cobalamins may impact on cancer/CLL. Historic
analysis reveals that cyanocobalamin is generally cancer promotional,
whereas hydroxocobalamin, methylcobalamin and adenosylcobalamin are
cancer protective and cytotoxic. It is hypothesised that the actions of
cobalamin in cancer aetiology and oncogenesis/progression are
intertwined with those of nitric oxide, which tumours regulate to dupe
the immune system to their presence, by causing a functional cobalamin
deficiency in the host.