Monograph: |
Glutamic Acid
A white crystalline powder or colourless crystals. Freely sol-
uble in boiling water: slightly soluble in cold water; practical-
ly insoluble in alcohol, in acetic acid. in acetone, and in
ether.
Protect from light.
Glutamic acid hydrochloride, which releases hydrochloric
acid in the stomach, has been used in the symptomatic treat-
ment of achlorhydria or hypochlorhydria in usual doses by
mouth of 0.5 to I g with meals.
Parenteral nutrition. Profound depletion of glutamine in
skeletal muscle is characteristic of injury, and suggestions
that glutamine is involved in the regulation of muscle protein
synthesis have led to studies of supplementation with levo-
glutamide or more stable peptide derivatives in parenteral nu-
trition regimens for patients with injury and infection.
Supplementation of parenteral nutrition regimens with levo-
glutamide has been shown to reduce clinical infection in
patients who have undergone bone-marrow transplantation
or who have suffered multiple trauma. A further study has
shown improved mortality among intensive-care patients giv-
en parenteral feeds supplemented with glutamine.
The use of levoglutamide coupled with alanine (L-alanyl-L-
glutamine: Ala-GIn) has been described.' In patients under-
going major uncomplicated surgery on the lower gastro-inies-
tinal tract, a significantly better postoperative nitrogen
balance was achieved in those whose total parenteral nutrition
regimen had been supplemented with about 29 g daily of this
dipeptide (equivalent to about 12 g daily of glutamine) when
compared with a control group. Others' have shown that sup-
plementation of total parenteral nutrition solutions with a
glutamine dipeptide (glycyl-t-glutamine), in quantities
equivalent to 0.23 g of glutamine per kg body-weight daily.
prevented the increased intestinal permeability and atrophic
changes in the intestinal mucosa associated with unsupple-
mented solutions. Such changes may be associated with de-
creased immunity and bacteraemia. which may explain the
reduction in clinical infection mentioned above.
It has also been postulated that muscle protein catabolism af-
ter trauma may be due to a shortage of a-ketoglutarate rather
than glutamine: glutamine is formed from a-ketoglutarate.
which has the same carbon skeleton. Wemerman and co-
workers* have shown that supplementation of total parenteral
nutrition with a-ketoglutarate or a dipeptide. omithine-a-
ketoglutarate. reduces muscle protein depletion and suggest-
ed this may be a more physiological way of providing
glutamine.
Vincristine neurotoxicity. Neurotoxicity is a relatively
common adverse reaction experienced with vincristine . A double-
blind placebo-controlled randomised study
involving 84 patients found that the administration of glutam-
ic acid 1.5 g daily by mouth in divided doses during a 6-week
induction chemotherapy course decreased vincristine-in-
duced neurotoxicity. The mechanism by which glutamic acid
may inhibit vincristine toxicity was not known although var-
ious proposals were discussed and further trials were consid-
ered warranted.
Inadvertent intrathecal administration of vincristine has re-
sulted in paralysis and death although there has been one case
where this was prevented. One of the manufacturers of vinc-
ristine (Lilly) has stated that details of this case will be in-
cluded in data sheets and package inserts, adding though that
the role of glutamic acid cannot be determined. Successful
treatment included removal of cerebrospinal fluid and flush-
ing the subarachnoid space with lactated Ringer's solution to-
gether with the administration of glutamic acid lO g
intravenously over 24 hours followed by 500 mg three limes
daily by mouth until neurological dysfunction stabilised.
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