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PubMed1996

[Effect of the Nucleus CMP forte in 46 patients with progressive spastic paraparesis. Randomized and blind study].

BACKGROUND: Idiopatic or HTLV-1 associated progressive spastic paraparesis does not have a clear etiology or treatment. AIM: To assess the effects of a medication containing cytidinmonophosphate, uridintriphosphate and vitamin B 12 in the treatment of progressive spastic. PATIENTS AND METHODS: Patients with the disease were randomly assigned to receive the Nucleus CMP forte (containing dysodic cytidinmonophosphate 5 mg, trisodic uridintriphosphate 3 mg and hydroxicobalamin 2 Mg) tid or placebo during six months. Gait, spasticity, degree of neurogenic bladder and somatosensitive evoked potentials were assessed during treatment. RESULTS: Forty six patients aged 25 to 79 years old were studied, 24 were female and 29 HTLV-1 positive. Twenty two were treated with the drug and the rest with placebo. Gait and spasticity improved in 7 of 22 patients receiving the drug and 1 of 24 receiving placebo (p < 0.05). Neurogenic bladder improved in 10 of 22 receiving the drug and 4 of 24 receiving placebo (NS) Somatosensitive evoked potentials improved in four of seven patients treated with the drug and in two of seven treated with placebo. CONCLUSIONS: The medication caused a modest improvement in patients with progressive spastic paraparesis and was free of side effects.

Adult↗
PubMed1997

Cyanocobalamin [c-lactam] inhibits vitamin B12 and causes cytotoxicity in HL60 cells: methionine protects cells completely.

The [c-lactam] derivative of cobalamin antagonizes vitamin B12 in vivo. Therefore, we investigated its effects in tissue culture to develop a model in which to study vitamin B12-deficient hemopoiesis. HL60 cells were cultured in medium containing either methionine or L-homocysteine thiolactone, and various concentrations of 5-methyltetrahydrofolate or pteroylglutamic acid. In medium with L-homocysteine thiolactone, 5-methyltetrahydrofolate, and dialyzed serum, cyanocobalamin [c-lactam] caused cell death, reversible by additional vitamin B12. Pteroylglutamic acid did not prevent this cytotoxic effect. Methionine completely protected cells against cyanocobalamin [c-lactam] for periods of up to 4 months of culture, irrespective of the folate source. Cyanocobalamin [c-lactam] reversibly impaired the incorporation of 5-[14CH3]-tetrahydrofolate and [1-(14)C] propionic acid by intact cells, consistent with inhibition of methionine synthase and methylmalonyl-CoA mutase. A substantial proportion of 5-[14CH3]-tetrahydrofolate uptake could not be suppressed by methionine and may, therefore, have occurred outside of the methionine synthase pathway. These findings are the first indication that cyanocobalamin [c-lactam] antagonizes vitamin B12 in vitro and causes cell death from methionine deficiency. The model should be valuable for investigating the biochemical pathology of vitamin B12-deficient hemopoiesis. The results suggest that methylfolate is not trapped when methionine synthase is inhibited in HL60 cells, but they do not disprove the methylfolate trap hypothesis as applied to normal blood cells.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1998

[Polyneuropathy caused by vitamin B12 deficiency secondary to chronic atrophic gastritis and giardiasis].

INTRODUCTION: In chronic atrophic gastritis atrophy of the stomach glands leads to intrinsic factor deficit, with consequent failure to absorb vitamin B12 and gastric achylia, which predisposes to Giardia infection which in itself leads to depletion of vitamin B12. We describe the case of a patient with peripheral and central nervous system pathology due to lack of vitamin B12 secondary to the combined effect of these two disorders. CLINICAL CASE: A 54 year old woman consulted us for paraesthesia and weakness of the legs which had been progressive for the previous two years. She presented with tactile hypoaesthesia, hypoparaesthesia, distal hyperreflexia and dysymmetry of the legs, ataxic-spastic gait and a positive Romberg sign. The investigations carried out showed the serum vitamin B12 level to be 3 pg/ml (N: 180-900), hemoglobin 13 g/dl and MCV 111 fl with MCHC 348/dl; neurophysiological studies: compatible with demyelinating motor polyneuropathy. Schilling test: deficit of absorption of vitamin B12 which was corrected on administration of intrinsic factor; gastroscopy; atrophic gastritis which confirmed the morbid anatomy findings. There was also flora containing Helicobacter and massive Giardia infection. Replacement and antibiotic therapy was followed by complete remission of the clinical picture. CONCLUSION: We emphasize the excellent clinical response to treatment in spite of the time elapsed since onset of symptoms.

Amoxicillin↗