Drugs: Helpful but Also Harmful

• Share

From the first sulfa compounds of the 1930s to the latest molecular manipulation of penicillin, the wonder drugs of modern medicine have carried a high price tag. And the bill keeps getting bigger. Patients are paying it with an increased number of drug-induced diseases.

Each drug is designed to act upon a particular organ or upon particular tissues. But as Lieut. Colonel Robert H. Moser of the Army Medical Corps told a Palo Alto, Calif., symposium on "Diseases of Medical Progress": "We are inclined to forget that the drug is also in contact with other tissues. Effects in those areas are not immediately evident: subtle influences may be at work and may become manifest only later." Such long-range effects, Dr. Moser warned, may never be traced to the drug that caused them. "This is a shadow world of pathophysiology, where relation of cause to effect is at best diffi cult to assess."

Despite that difficulty, Moser made a devastating indictment of almost every class of new drug. The cortisone-type hormones, familiar for their wide use, particularly in rheumatic disorders, have long since been convicted of causing or exacerbating peptic ulcers, of giving users a fattened "moon" face, and growing mustaches on women. Colonel Moser emphasized two severe unpleasant side effects that may go undetected. Given to victims of leukemia or Hodgkin's disease, he said, these hormones predispose the patients to fungus infections, and they leach the calcium out of the bones of the bedridden elderly.

Malaria & Anemia. Newer, and far more mysterious, is a set of disease reactions that doctors describe as "pharmacogenetic." In these cases a drug may have no detectable harmful effect upon the vast majority of members of one ethnic group; yet because of a hereditary quirk, some individuals will be made gravely ill. Best example, said Dr. Moser, is the tendency—rare in the general U.S. population—to a blood-destroying anemia that can develop after taking aspirin or phenacetin (compounded together in the familiar APC tablets), some sulfonamides, and drugs for the relief of peptic ulcer.

The underlying cause of the trouble is a deficiency in a red-blood-cell enzyme (as complex as its name): glucose-6-phosphate dehydrogenase (G-6-PD). And, strangely, a deficiency of G-6-PD is not necessarily bad. It confers a definite survival value in areas where malaria is rife, and it has evolved into a common condition among the peoples of the Mediterranean basin and West African Negroes. But if these malaria survivors take to modern medicine, they often find their enzyme peculiarity a grave liability. Widely prescribed drugs may throw them into a devastating, life-threatening anemia.

Even the most universally useful anti-TB drug, isoniazid, is harmless only if the patient's enzyme system can break it down readily: if not, he is likely to develop a generalized neuritis, or even an acute form of rheumatism.

Making matters even more complicated, some drugs increase the potency of enzyme activity. This leads to the bizarre situation in which a heart patient needs more of the anticlotting coumarin drugs if he is also taking barbiturates to allay his anxiety. The "barbies" hasten the breakdown of coumarin, and they have the same effect on some antiepilepsy and antifungal drugs.