No abstract

Lithium salts are widely used in psychiatric practice and are known to induce thyroid dysfunction. Lithium-induced parathyroid dysfunction is rare. We are reporting a case of hyperparathyroidism in a 28-year-old female patient who was on lithium carbonate for 2 years, when she developed osteopenia and girdle girdle-type muscle weakness. Biochemical parameters showed hyperparathyroidism with shift of calcium creatinine clearance ratio to 0.013, indicating an error in threshold of calcium sensing receptor. The patient eventually required parathyroidectomy and the histology of the gland showed atypical features.

The effect of hypo- and hyperthyroidism on vitamin B-12 metabolism in the rat was studied by measuring methylmalonic acid excretion, B-12 content of liver and oxidation of 2-[14C]histidine. Ten percent pectin was added to increase severity of B-12 deficiency. The addition of thiouracil to a diet containing 10% pectin decreased the excretion of methylmalonic acid suggesting an amelioration of the B-12 deficiency. It was found that part of this decreased methylmalonic acid excretion was due to a decreased food consumption with a correspondingly decreased intake of branched-chain amino acids which are precursors of methylmalonic acid. When attempts were made to increase the protein intake of animals receiving thiouracil so their amino acid intake was equal to that of the control animals, methylmalonic acid excretion was still lower than that of the controls. It was also found that the vitamin B-12 content of the liver was higher in the animals receiving thiouracil than in the controls. Thyroidectomy had the same effect as feeding thiouracil. Liver B-12 levels are rapidly depleted on a B-12 deficient diet containing 10% pectin. It appears that hypothyroidism, induced either by thyroidectomy or by feeding thiouracil, slows the rate of depletion of hepatic B-12 which in turn facilitates the metabolism of methylmalonic acid and decreases its excretion in the urine.

SummaryHypothyroidism results in decreased urinary excretion of folates leading to enhanced tissue retention of folates. The proportion of polyglutamylfolates, which are better retained by tissues, is elevated in liver, blood, and bone marrow of hypothyroid rats. The hypothyroid condition is discussed in the light of the enhanced proportion of polyglutamylfolate cofactors and increased in vivo oxidation of histidine possibly resulting in under-utilization of one-carbon units of the folate pool leading to a decrease in weight gain.Key Words:hypothyroidism, polyglutamylfolates, histidine oxidationMetabolism of folic acid and vitamin B12 is enhanced by hypothyroidism as evidenced by the increased in vivo oxidation of [2-14C] histidine to 14C02 and decreased excretion of formiminoglutamic acid [1], a metabolite of histidine with the 2-carbon of histidine forming the formimino-group; formiminoglutamic acid is metabolized through the folate one-carbon [1-C] pool after conversion to formiminotetrahydrofolate. The 1-C groups of folate pool, which are freely interconvertible, are utilized in various biosynthetic reactions; the excess 1-C units are oxidized to CO2 via the 10-formyltetrahydrofolate: NADP oxidoreductase [2]. In hypothyroidism the proportion of nonmethyltetrahydrofolates is increased in liver [1,3], and urinary excretion of methylmalonic acid is decreased [4]; the disorder also results in increased hepatic folate and vitamin B12 content [4,5] and altered levels of various folate-metabolizing enzymes [3,6].Folylpolyglutamates are more active than monoglutamate as cofactors in various folate-mediated reactions [7] and have a special function in the reactions

SummaryThe effects of the hormones thyroxine, glucagon and hydrocortisone, and of protein level on hepatic histidase, urocanase, and certain folate enzymes were studied in rats. Hypothyroidism, induced either by feeding thiouracil or by thyroidectomy, increased histidase, urocanase, and the folate dependent enzyme formiminotransferase, and increased histidine metabolism as measured by oxidation of the 2-ring carbon of histidine to carbon dioxide. Hyperthyroidism, produced by feeding thyroid powder, decreased histidine oxidation and liver levels of this enzyme. Glucagon and hydrocortisone increased histidine oxidation and increased levels of histidase, urocanase and formiminotransferase . Elevated levels of casein and soy protein produced four to eight fold increases in histidase and urocanase, and 50% increases in formiminotransferase. Thus, increases in histidase and urocanase involved in the formation of formiminoglutamic acid (FIGlu) were accompanied by increases in the FIGlu metabolizing enzyme formiminotransferase.