involving him in costly and emotionally draining legal proce¬ dures? This is a matter to ponder lest without

all too

soon

we

enter the

era

of

George Orwell's 198b. Jonathan M. Williams, MD Silver Spring, Md

To the Editor.\p=m-\Thecase that Dr. Williams describes involved a 1972 Mental Retardation Administration Law of Maryland. If the litigation concerning the question of Maryland's being named the legal guardian of the deformed infant had proceeded to judgment, some of Dr. Williams' questions would have been answered. The 1972 Law has not been interpreted by the Maryland courts. In the absence of such interpretation, attempts to outguess how the civil rights of the mentally retarded individual will be balanced by the courts against the obligations of the state and the interests of the natural parents or relatives are speculative at best. The provisions of the 1972 Law give the Director of the Mental Retardation Administration the authority and the obligation to have the infant evaluated and to protect the infant's civil rights. Protection of the civil rights of mentally retarded or incompetent individuals is an area of the law that has been before the courts with increasing frequency. The courts today are requiring active treatment and appropriate medical care for those committed to state in¬ stitutions either voluntarily or invol¬ untarily. To protect the civil rights of such individuals, someone other than a concerned and involved parent would have to be appointed to repre¬ sent the individual. Otherwise, the mentally retarded infant would not have proper representation or protec¬ tion. The parents, hard as they might try, would have a degree of emotional involvement that might or might not assure protection of the interests or needs of the mentally retarded child. The preceding is an explanation of the purpose of the law. Whether the law "worked" as it should in the case in question evidently involves a dif¬ ference of medical (and perhaps socio¬

logical) opinion.

Betty Jane Anderson, JD

AMA Office of the General Counsel

Chicago

Marathon

Running After Myocardial Infarction To the Editor.\p=m-\Asif in answer to Bruce's editorial question (229:1637,

1974), "has any patient submitted to surgical revascularization done as well?" (ie, completed a 42-km run), two cardiac patients have subsequently done so! These two patients were official entrants in the marathon

runs in Santa Oct 13, and in Dec 15,1974. One patient

Barbara, Calif,

on

Honolulu on had undergone triple-bypass surgery. The other had had his internal mammary artery anastomosed to one coronary vessel. Both continue to enjoy their new hobby of distance running. Both of these marathons were part of a regular meeting of the American Medical Joggers Association (AMJA), which uses distance running to improve the life-style of physicians and patients. The 42-km run is used because AMJA has been unable to substantiate a single ischemic heart disease death among marathon finishers of any age. Although longevity studies have a while to run, we remain enthusiastic for the use of this form of vigorous exercise in controlled situations sim¬ ply because of the improved quality of life the patients experience. Sev¬ eral other bypass patients are in training and expect to complete 42 km in the coming year. The Honolulu Marathon was de¬ signed specifically for cardiac pa¬ tients. Nineteen such patients fin¬ ished on Dec 15,1974. Each received a "noncompetitive trophy" from the Hawaii Heart Association. Thomas J. Bassler, MD Jack H. Scaff, Jr., MD

American Medical Joggers Association North Hollywood, Calif

Phosphates

and

Hypercalcemia

To the Editor.\p=m-\Intheir short review of the treatment of hypercalcemia, Newmark and Himathongkam (230: 1438, 1974) recommend the intravenous administration of inorganic phosphate. The risk of ectopic calcification as a consequence of the treatment was only touched on, not warned against. In several articles, serious side effects have been described.1-5 Goldsmith and Ingbar,6 proponents of phosphate therapy, made autopsy observations of ectopic calcifications in five of seven phosphate-treated patients. In a later report they recommended avoidance of this therapy in patients with increased serum phosphate concentration and decreased kidney function.7 Tubular calcification as a consequence of phosphate

Downloaded From: http://jama.jamanetwork.com/ by a New York University User on 05/26/2015

infusions in hypercalcemic patients leading to decreased glomerular filtration rate is to be considered an extremely serious and sometimes fatal complication. Bernheim and Vischer1 observed an increase of serum creatinine concentration, from 8 to 116 mg/liter, in a patient with estrogen\x=req-\ induced hypercalcemia treated with a 100-millimol phosphate infusion over 13 hours. In another patient, a fatal decrease of glomerular filtration rate might have been caused by an exces¬ sive infusion rate of the phosphate solution.4 Halver5 described a hyper¬ calcémie patient in whom nephrocalcinosis and numerous small kidney stones developed following the ad¬ ministration of six doses of 50-millimol phosphate solution. Creatinine clearance fell from 30 to 10 ml/min despite normalization of the serum calcium concentration. Bent Halver, Maribo, Denmark 1. Bernheim C, Vischer T: Nephropathie tubulaire aigu\l=e'\et calcifications radiologiques vasculaires tardives apr\l=e`\straitment d'une hypercalcemie par administration intraveineuse de phosphates. Schweiz Med Wochenschr 98:641-645, 1968. 2. Breuer RI, Le Bauer J: Caution in the use of phosphates in the treatment of severe hypercalcemia. J Clin Endocrinol Metab 27:695-698, 1967. 3. Carey RW, Schmitt GW, Kopald HH, et al: Massive extraskeletal calcification during phosphate treatment of hypercalcemia. Arch Intern Med 122:150-155, 1968. 4. Shackney S, Hasson J: Precipitous fall in serum calcium, hypotension, and acute renal failure after intravenous phosphate therapy for hypercalcemia: Report of two cases. Ann Intern Med 66:906-916, 1967. 5. Halver B: Metastatiske Kalcifikationer efter intra-

fosfatbehandling af hyperkalcaemi. Ugeskr Laeg 134:1667-1669, 1972. 6. Goldsmith RS, Ingbar SH: Inorganic phosphate treatment of hypercalcemia of diverse etiologies. N Engl J Med 274:1-7, 1966. 7. Goldsmith RS, Bartog H, Hulley SB, et al: Phosvenos

phate supplementation as an adjunct in the therapy of multiple myeloma. Arch Intern Med 122:128-133, 1968. Dr. Newmark writes that he fully agrees with Dr. Halver.-ED.

Omitted. \p=m-\Inthe "Guillain-Barr\l=e'\Syn-

Acknowledgement BRIEF REPORT

drome in Heroin Addiction," lished in the March 31 issue

pub-

(231: 1367-1368, 1975), an acknowledgment was omitted. Stanley van den Noort, MD, Dean, UCI-CCM, made a major contribution to that study.

Lindbergh's

Birthplace. \p=m-\In the "The Lone Eagle's Last Flight," published in the May 19 issue (232:715,1975), the last sentence incorrectly indicated that Charles Lindbergh was born in MinCOMMENTARY

nesota. Although Lindbergh's boyhood was spent in Minnesota, he was born in Detroit.

Letter: Phosphates and hypercalcemia.

involving him in costly and emotionally draining legal proce¬ dures? This is a matter to ponder lest without all too soon we enter the era of G...
183KB Sizes 0 Downloads 0 Views