Incidence

vs

Prevalence

measures:

To the Editor.\p=m-\Thearticle in the Archives (112:1397-1399,1976) by Drs Carter and Jegasothy on alopecia areata in patients with Down's syndrome was interesting and useful. The authors

reported alopecia areata in 19 patients, and the authors reported the incidence of the disease of 214

to be 17.4% in females and 3.1% in

males. I am writing to call attention to the difference between the terms "incidence" and "prevalence." Incidence is the number of new cases per year per a fixed unit of population. For example, the incidence of melanoma might be reported as 6.5 cases per 100,000 population for the year 1973 in Alameda, Calif. In contrast, prevalence refers to the number of patients affected with a particular disease in a unit population at one specific point in time. I think the authors of this article used incidence where prevalence would have been more accurate. This is a common error in dermatologic literature. John R. Tkach, MD Bozeman, Mont

Reply.\p=m-\Wethank Dr writing to clarify the In

Tkach for distinction

between incidence and prevalence. The word prevalence should have been used to describe the percent of persons in our series who were affected with vitiligo at the time of the study. D. Martin Carter, MD Brian V. Jegasothy, MD New Haven, Conn

Immunotherapy

for

Leprosy

To the Editor.\p=m-\Inthe March 1977 issue of the Archives (113:345-352), Drs Rea and Levan reviewed the current concepts in the immunology of leprosy. They noted the work of Lim et al1 with respect to the treatment of leprosy patients with intravenous infusions of leukocytes from normal persons. Rea and Levan stated, "Lim et al reported improvement in lepromatous patients associated with the administration of deliberately mismatched leukocytes. To our knowledge, the confirmatory studies have not been reported." In the article by Lim et al,1 the patients who were treated were three lepromatous patients and one tuberculoid patient. The authors reported remission of the patients' leprosy as measured by the following three

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teriologic.

clinical, histologic, and bac-

Rea and Levan used the term "de-

liberately mismatched leukocytes" in referring to the whole WBC infusions. This may imply to the reader a major incompatibility with possibly ABO

blood types. In the study by Lim et al,1 the normal persons who were used as donors had their blood types matched against the patients' blood types with respect to the standard blood bank techniques of ABO tests. In addition, an attempt was made to select the best possible histocompatible donor by leukocyte agglutination tests, since other histocompatibility tests were not available. It is obvious that the WBC infusions were incompatible to some histocompatibility antigens, but under these circumstances, it appears that the immunologie capacity of patients with lepromatous and tuberculoid leprosy is not sufficiently reduced to allow the occurrence of graft-vs-host (GVH) reaction. In each of the patients who were treated, GVH reactions were not observed. Patients with leprosy who receive blood transfusions for other medical reasons have not shown any evidence of GVH reaction. With respect to the comment of the failure of any evidence in the litera¬ ture of a confirmatory nature, it should be noted that in early 1975,2 results of a study confirmed the effi¬ cacy of whole WBC transfusions in clearing patients with leprosy of their disease without symptoms of GVH reactions. In addition, a parallel study by the same group noted the essential total failure of transfer factor in the immunotherapy for patients with

leprosy. Obviously,

much work needs to be done in the area of the immuno¬ therapy for leprosy. The immuno¬ therapy for patients who have leprosy with whole WBC infusions may offer a more promising avenue for research than the present effort that is being directed to transfer factor, especially since there have been two consecutive reported failures with transfer fac¬ tor.23

Ramon M.

Omaha

Fusaro, MD,

PhD

1. Lim SD, Fusaro R, Good RA: Leprosy: VI. The treatment of leprosy patients with intravenous infusions of leukocytes from normal persons. Clin Immunol Immunopathol 1:122-139, 1972. 2. Saha K, Mittal MM, Maheshwari HB: Passive transfer of immunity into leprosy patients by transfusion of lymphocytes and by transfusion of Lawrence's transfer factor. J Clin Microbiol 1:279-288, 1975. 3. Bullock WE, Fields JP, Brandriss MW: An evaluation of transfer factor as immunotherapy

for patients with lepromatous Med 287:1053-1059, 1972.

leprosy.

N

Engl J

In Reply.\p=m-\Wechose the phrase "deliberately mismatched leukocytes" for two reasons. Drs Lim, Fusaro, and Good1 indicated their awareness that the tests they used were incomplete measures of histocompatibility and that donor-recipient leukocyte incompatibility, in terms of histocompatibility antigens, was a virtual certainty. Indeed, one of the hypotheses offered by these investigators to explain their results depended on the presence of donor-recipient leukocyte incompatibility. Lim et al1 stated:

possibility is that the allogenic lymphocytes react against the host as in the initiation of a graft vs host Another attractive

act as an response of the host's cells and substitute for a T-cell requirement in an immune response.

reaction. Such

a

reaction

can

adjunct to a vigorous immune

We regret any ambiguity that arose from our choice of words. We thank Dr Fusaro for pointing out the work of Saha et al.2 To Dr Saha and his colleagues in particular, and to the authors of other inadvertently neglected papers, we extend our sincere apologies. Thomas H. Rea, MD Norman E. Levan, MD Los Angeles 1. Lim SD, Fusaro R, Good RA: Leprosy: VI. The treatment of leprosy patients with intravenous infusions of leukocytes from normal persons. Clin Immunol Immunopathol 1:122-139,

1972. 2. Saha K, Mittal MM, Maheshwari HB: Passive transfer of immunity into leprosy patients by transfusion of lymphocytes and by transfusion of Lawrence's transfer factor. J Clin Microbiol 1:279-288, 1975.

Systemic Steroids

for Treatment of

Alopecia Areata

To the Editor.\p=m-\Thisis a rebuttal to the rejection of corticosteroid therapy in treatment of alopecia areata by Winter et al in the November 1976 Archives (112:1549-1552). I have treated the conditions of over a dozen patients with systemic steroids, with clearing of the disease in every instance and only one instance of untoward side effect, ie, a readily controlled peptic ulcer. My protocol is to use intralesional steroids once weekly for three weeks in cases of patchy alopecia areata. If no regrowth of hair is noted, I begin treatment with combination of intralesional and intramuscular steroids\p=m-\usuallybetamethasone valerate suspension. This last medication I frequently use on an every-other-week basis, because the duration of effect of intramuscular

betamethasone is approximately one week. At times I have used intramuscular triamcinalone acetonide suspension, but this drug is less successful, perhaps because of the lower steroid blood level. Before placing the patient on a regimen of steroids, I carefully outline the side effects in a realistic manner. All of my patients have accepted the steroid treatment after the side-effect discussion, which is a reflection of how serious the patients consider their problem to be. No patient has had to be on a course of systemic steroids for more than four months, and all patients have had resolution of their alopecia areata condition. A few patients have had a recurrent patch of alopecia that has rapidly been aborted with intrale¬ sional steroids. I have used courses of systemic steroids in three patients with alope¬ cia areata totalis. Two of the patients have had conspicuous hair regrowth, but loss of hair began again after the systemic steroid course was stopped. Thus, I doubt whether courses of systemic steroids are useful once the patient has reached the stage of alopecia areata totalis. I believe that in most cases progres¬ sion of patchy alopecia areata to total hair loss can be prevented by the use of intralesional steroids, and if neces¬ sary, by the judicious use of systemic steroids. Not to offer the patient the therapeutic option of systemic ste¬ roids when patchy alopecia areata does not respond to local treatment, is doing the patient a disservice by permitting the progression of a cosmetically disfiguring and psychologi¬ cally scarring disease. All my patients who have required regimens of sys¬ temic steroids have been adults; the conditions of the children that I have treated for alopecia areata have responded to intralesional steroids or to

phenolization. I am surprised that Winter and his

co-workers did not use intralesional steroids or phenolization in the treat¬ ment of the conditions of their

patients. Both forms of medication are accepted and virtually harmless, and these forms of therapy have a reasonably high success rate. In conclusion, I believe vigorous initial treatment of patchy alopecia areata, using systemic steroids if

necessary, can prevent the progres¬ sion of the disease to the untreatable, and often psychologically disastrous, alopecia areata totalis or universalis

forms.

David A.

Fisher, MD Antioch, Calif

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Alopecia Areata and Regrowth of Hair To the Editor.\p=m-\DrsWinter, Kern, and

Blizzard are to be congratulated for their observations on prednisone therapy for alopecia areata (Arch Dermatol 112:1549-1552,1976). Their findings concerning various subgroups of alopecia areata (AA) treated with systemic steroids fit well with my experience, ie, in most cases, systemic steroids do not alter the course of AA, although one may occasionally obtain gratifying results. I do, however, disagree with the pronouncement by these authors of a generally poor prognosis for patients with AA. Winter et al quote Muller and Winkelmann1 for this information, but I believe closer reading of the article will show that Muller and Winkelmann were referring to "extensive" patchy AA, alopecia totalis, and (presumably) alopecia universalis. In my experience, the majority of patients with AA have one patch or a few small patches on their scalp where the hair has been lost; the hair will almost invariably regrow in these areas. Muller and Winkelmann seem to agree with me; they write: "The overwhelming tendency is for regrowth of hair, usually within a few months; but often the regrown hair was less profuse."

True, recurrences are common, even

in the patient with mild AA. However, I believe that it is wrong to portray such a grim outlook for AA in general when, in the majority of cases, small patches of alopecia are regrown readi¬ ly without benefit of treatment except that of giving reassurance to the patient. Dan A. Bovenmyer, MD Davenport, Iowa 1. Muller

SA, Winkelmann RK: Alopecia areapatients. Arch Dermatol

ta: An evaluation of 736

88:290-297, 1963.

In

Reply.\p=m-\Itis certainly true, as Dr Bovenmyer states, that "the majority of patients with AA have one patch or a few small patches on their scalp where the hair has been lost; the hair will almost unvariably regrow in these areas." However, it is also true that recurrences are common.

In the study by Muller and Winkelmann,1 80% of the children and 65% of the adults who

were

followed for five

years or longer had recurrences. In the very next sentence after the one WinkelmannDr Bovenmyer, Muller and Winkelmann state that "After re-

growth, subsequent episodes of alopecia were frequent in most cases, though occasionally 20 years sepa-

rated mild occurrences." Our follow\x=req-\ up evaluation2 revealed that only five of eighteen patients (28%) who were treated with alternate-day prednisone therapy had lasting regrowth of hair, and the evaluation is thus consistent with the previously cited data. However, both of these studies evaluated patients who were referred to large hospitals, and thus, the studies may only represent a subgroup of AÀ patients who have a poorer prognosis than is generally seen in the private practice of dermatology. Interestingly, Dr Bovenmyer's ex¬ perience, which suggests that no treatment except reassurance is nec¬ essary for patients with mild AA, is directly countered by Dr Fisher's experience, in which early, aggressive therapy is recommended. Well de¬ signed clinical research attempts, ulti¬ mately, to resolve this sort of discrepancy. Our study was not designed to evaluate topical, intrale¬

or parenteral steroid therapy. Our study was designed to monitor the clinical and laboratory response to oral prednisone in a fastidious fash¬ ion. A major impact of our study is that the incidence of side effects to oral prednisone therapy is disturb¬ ingly high. In that regard, we would be interested to know whether routine blood pressure determinations, ophthalmological evaluations, and evalua¬ tions of adrenocorticotropic hormone reserve are part of Dr Fisher's "proto¬ col." Dr Fisher does not indicate the period of follow-up after resolution of the alopecia, nor the steroid dosages used. We strongly disagree with Dr Fisher's statement that intralesional

sional,

steroid therapy is "virtually harm¬ less." Topical and intralesional steroid therapy, as well as systemic steroid therapy, all have the potential to cause severe and debilitating side effects, particularly in children in whom growth can be affected.3 4 We totally concur with Dr Fisher that progression of this disorder is "cosmetically disfiguring and psycho¬ logically scarring." Unfortunately for us as physicians as well as for our patients, no form of therapy has been proved effective in producing longterm remission. If Dr Fisher has data to the contrary from a well-designed, controlled study, we heartily urge him to

publish

same.

Robert J. Winter, MD Frank Kern, MD Robert M. Blizzard, MD

Chicago

1. Muller SA, Winkelmann RK: Alopecia areata: An evaluation of 736 patients. Arch Dermatol 88:290-297, 1963.