Although corticosteroids are effective in the treatment of hypercalciuria and hypercalcemia in chronic sarcoidosis, complications of their long-term use frequently limit therapy. We studied the efficacy of chloroquine in two patients with sarcoidosis who were unable to tolerate the dosage of corticosteroids required to control hypercalciuria and prevent the formation of renal stones. Over a three-year period, each patient received a 6-month and a 10-month course of oral chloroquine phosphate (500 mg per day) while continuing to receive corticosteroids at a fixed dose. Chloroquine therapy was associated with a significant reduction in levels of serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and urinary calcium. We observed a direct correlation between serum 1,25-(OH)2D levels and 24-hour urinary calcium excretion, supporting the hypothesis that excessive serum 1,25-(OH)2D is responsible for the hypercalciuria in sarcoidosis. Serum levels of 25-hydroxyvitamin D (25-(OH)D) did not change with therapy, suggesting that chloroquine may act by inhibiting the conversion of 25-(OH)D to 1,25-(OH)2D. Current dosage guidelines and ophthalmologic-surveillance techniques, which allow chloroquine to be administered with little risk of retinopathy, should permit an expanded role for this agent in the treatment of the calcium abnormalities of sarcoidosis.

On the basis of almost 15 years of experience with thiazide treatment in 346 patients with calcium stones, we believe that the following conclusions are justified: 1) Stone progression ceases in at least 90% of patients who take hydrochlorothiazide (50 mg, twice daily) on a regular basis. 2) A reduced dose of hydrochlorothiazide, i.e., 25 mg twice daily, appears to be effective in a significant proportion of patients. 3) Thiazides are effective in normocalciuric as well as hypercalciuric patients and in most patients with tubular ectasia (medullary sponge kidney). 4. Side effects necessitate discontinuation of thiazide treatment in approximately 7% of patients. The incidence and severity of side effects is reduced by initiating treatment with a small dose and by increasing the dose progressively until the full maintenance dose is achieved. A trial with a reduced dose is warranted in patients who are unable to tolerate the regular maintenance dose. 5) The therapeutic efficacy of thiazides in stone prevention cannot be accurately predicted by the degree of hypocalciuric response. Stone prevention may cease despite a minimal hypocalciuric response, whereas stone progression may occur when an adequate hypocalciuric response has taken place. 6) In addition to the hypocalciuric action, thiazides reduce urine oxalate excretion and increase urine zinc and (probably) magnesium; these effects probably contribute to the efficacy of this agent in stone prevention.

We measured urinary oxalate and glycolate excretion before and during pyridoxine administration (2 to 200 mg per day) in four patients with primary hyperoxaluria. In two patients with type I primary hyperoxaluria, urinary oxalate and glycolate excretion fell markedly in response to a physiologic dose of pyridoxine of 2 mg per day and became completely normal when the dose was increased to 25 mg per day. In the other two patients, who had a different type of primary hyperoxaluria (normal urinary glycolate excretion), there was no response to 2 mg of pyridoxine per day. In one of these patients, doses of 25 and 50 mg per day were also ineffective, but a moderate reduction in oxalate excretion took place with 200 mg per day; in the other patient there was a moderate reduction in oxalate excretion with 25 mg of pyridoxine per day. Our findings suggest that the degree of hyperoxaluria in this disorder may be only slight or moderate if the patient has been ingesting a pyridoxine-rich diet or multivitamin tablets containing small amounts of pyridoxine. Our results also suggest that smaller doses of pyridoxine than those heretofore employed should be tried in patients with primary hyperoxaluria.