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Adverse reactions & toxicity :
Adverse reactions to sulfonamides may be due to hypersensitivity or direct toxic effects. Possible
hypersensitivity reactions include urticaria, angioedema, anaphylaxis, skin rashes, drug fever,
polyarthritis, hemolytic anemia, and agranulocytosis. Keratitis sicca is a recognized adverse
effect. The allergic response targets, in part, metabolites of the aryl amine of sulfonamides.
Because dogs are deficient in acetylation, they may be at risk of increased formation of phase I
metabolites associated with adverse effects. Crystalluria with hematuria, and even tubular
obstruction, is not common in veterinary medicine. Acute toxic manifestations may be seen after
too rapid IV administration or if an excessive dose is injected. Clinical signs include muscle
weakness, ataxia, blindness, and collapse. GI disturbances, in addition to nausea and vomiting,
may occur when sulfonamide concentrations are sufficiently high in the tract to disturb normal
microfloral balance and vitamin B synthesis. Sulfonamides depress the cellulolytic function of
ruminal microflora, but the effect is usually transient (unless excessively high concentrations are
reached). Several adverse effects have been reported after prolonged treatment, including bone
marrow depression (aplastic anemia, granulocytopenia, thrombocytopenia), hepatitis and icterus,
peripheral neuritis and myelin degeneration in the spinal cord and peripheral nerves,
photosensitization, stomatitis, conjunctivitis, and keratitis sicca. Mild follicular thyroid
hyperplasia may be associated with prolonged administration of sulfonamides in sensitive
species such as dogs, and reversible hypothyroidism can be induced after treatment with high
doses in dogs. Several sulfonamides can lead to decreased egg production and growth. Topically,
the sulfonamides retard healing of uncontaminated wounds.
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**Interactions:
Sulfonamide solutions are incompatible with calcium- or other polyionic-containing fluids as
well as many other preparations. Sulfonamides may be displaced from their plasma-protein-
binding sites by other acidic drugs with higher binding affinities. Antacids tend to inhibit the GI
absorption of sulfonamides. Alkalinization of the urine promotes sulfonamide excretion, and
urinary acidification increases the risk of crystalluria. Some sulfonamides act as microsomal
enzyme inhibitors, which may lead to toxic manifestations of concurrently administered drugs
such as phenytoin.
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