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HYDROXOCOBALAMIN ACETATE
| Flammability | 1 | |
| Toxicity | 2 | |
| Body Contact | 1 | |
| Reactivity | 1 | |
| Chronic | 2 | |
| SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 | ||
In the treatment of of pernicious anemia and cobalamin, Vitamin B12 or cobalt
deficiencies. Usually administered by intramuscular injection. Deficiencies may occur as a
result of inadequate diet including one which totally abstains from animal products.
Naturally occuring cobalamins in man and animal include hydroxocobalamin,
adenosylcobalamine and methylcobalamin. Because of the serious discrepancies between the
results of microbiological and radioisotopic assay for total cobalamins, together with the
recommendation that laboratories should specify the assay method used, it has been
suggested that the term " Vitamin B12" be abandoned in preference fot " the cobalamins" .
Generally given by injection. Although it has been sugested that hydroxocobalamine may be
suitable for the treatment of cynide poisoning existing preparations proved to be
unsuitable.
C64-H91-Co-N13-O16-P, "cobinamide, acetate (salt) hydroxide dihydrogen phosphate (ester),
", "inner salt, 3'-ester with 5, 6-dimethyl-1-alpha-D-ribofuranosylbenzimidazole",
"inner salt, 3'-ester with 5, 6-dimethyl-1-alpha-D-ribofuranosylbenzimidazole", "alpha-
(dimethyl-5, 6-benzimidazolyl)hydroxocobamide acetate", "alpha-(dimethyl-5, 6-
benzimidazolyl)hydroxocobamide acetate", acetatocobalamin, "Vitamin B12a acetate; Vitamin
B12b acetate"
Although ingestion is not thought to produce harmful effects, the material may still be damaging to the health of the individual following ingestion, especially where pre- existing organ (e.g. liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally based on doses producing mortality (death) rather than those producing morbidity (disease, ill-health). Gastrointestinal tract discomfort may produce nausea and vomiting. In an occupational setting however, ingestion of insignificant quantities is not thought to be cause for concern. Cobalamins are absorbed from the gastrointestinal tract but may be irregularly absorbed when given in large therapeutic doses. Absorption is impaired in the absence of Castles Intrinsic Factor. Cobalamins are stored in the liver, excreted in the bile and undergo some hepatoenteric recirculation; part of the dose is excreted in the urine. In toxic doses soluble cobalt salts produce stomach pain and vomiting, flushing of the face and ears, rash, ringing in the ears, nervous deafness and reduced blood flow to the extremities.
Although the material is not thought to be an irritant, direct contact with the eye may produce transient discomfort characterized by tearing or conjunctival redness (as with windburn). The dust may produce eye discomfort causing smarting, pain and redness.
The material is not thought to produce adverse health effects or skin irritation following contact (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting.
The material is not thought to produce adverse health effects or irritation of the respiratory tract (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting. Not normally a hazard due to non-volatile nature of product. Persons with impaired respiratory function, airway diseases and conditions such as emphysema or chronic bronchitis, may incur further disability if excessive concentrations of particulate are inhaled.
Principal routes of exposure are by accidental skin and eye contact andinhalation of generated dusts. Though the cobalamins are generally well tolerated, allergic hypersensitivity reactions have followed the administration of the Vitamin B12 factors, cyanocobalamin and hydroxocobalamin. Vitamin B12 rapidly increases the rate of cell maturation, in vivo, and as a consequence increases the rate of nucleic acid degradation which in turn increases blood uric acid levels; this may produce gout in susceptible individuals. Inhalation of cobalt powder can induce asthma, chest tightness and chronic inflammation of the bronchi. Chronic exposure to cobalt causes increase in blood hemoglobin, increased production of cells in the blood marrow and thyroid gland, discharge from around the heart and damage to the alpha cells of the pancreas. Long-term administration has caused goiter (overactivity of the thyroid) and reduced thyroid activity. Allergic inflammation of the skin may appear following exposure to cobalt, usually exhibited as red patches. Injection of cobalt can cause cancer at the site of entry.
