pression of several disease entities, and until the precise molecular defect(s) is identified, it is prudent to discuss the disorder in general terms. It was, of course, impossible for Dr Schlegel to include all available data in such a brief commentary; however,

few points were made that are at variance with the literature. Cytoplasmic granules of neutrophils are discussed in the third paragraph. It appears that the term "lysosomes" is used to encompass all types of neutrophilic cytoplasmic granules. These structures have been divided by Bainton et al1 into two broad groups and labeled as primary (azurophilic) and secondary (specific). Although both types are membrane-limited, it is somewhat imprecise to classify the latter as lysosomes since they do not contain the lysosomal acid hydrolases. The terms "primary" and "azurophilic" are generally used in¬ terchangeably and refer to the same group of granules. It is the secondary or specific type that are observed in stained smears of mature neutrophils from the peripheral blood. The azu¬ a

rophilic type are not as easily seen in similar preparations because they

fewer in number and stain less in¬ the specifics.1 In the same paragraph, it was stated that an abnormality of degranulation in chronic granulomatous disease was "firmly established" by studies measuring the exocytosis of granule contents. It is unlikely that this controversy is settled, because a similar study published at about the same time reported normal exocytosis in this disorder.2 In the fifth paragraph, it is stated that "the increase in oxygen con¬ sumption following stimulation of the neutrophils is due to anaerobic glycolysis through the Embden Meyerhoff pathway, and to hexose monophosphate pathway activity." In neither of these metabolic pathways is oxygen directly consumed. The ex¬ act mechanism for the postphagocytic increase in oxygen consumption is a matter of controversy, but probably involves reduced nadide (NADH) oxi¬ dase, reduced nadide phosphate (NADPH) oxidase, or the amino acid oxidases.34 The pathways mentioned by Dr Schlegel may be indirectly re¬ lated, however, because they provide NADH and NADPH for interaction with their respective oxidases. are

tensely than

Ronald G. Strauss, MD St Jude Children's Research



1. Bainton

DF, Ullyot JL, Farquhar MG: The developneutrophilic polymorphonuclear leukocytes in human bone marrow. J Exper Med 134:907, 1971. 2. Ulevitch RJ, Henson P, Holmes B, et al: An in vitro study on exocytosis of neutrophil granule enzymes in chronic granulomatous disease neutrophils. J Immunol 112:1383, 1974. 3. DeChatelet LR, Wang P, McCall CE: Hexose mono\x=req-\ phosphate shunt activity and oxygen consumption during phagocytosis: Temporal sequence. Proc Soc Exper Biol Med 140:1434, 1972. 4. Johnston RB Jr, Baehner RL: Chronic granulomatous disease: Correlation between pathogenesis and clinical findings. Pediatrics 48:730, 1971. ment of

Duchenne Muscular


To the Editor.\p=m-\In Duchenne muscular

dystrophy, walking on the toes is commonly seen in later stages of the disease. This is generally attributed to contracture or shortening of the heel cords. It is conceded, however, that toe-walking may be seen early, long before any contracture or weak-

in the calf muscles sets in. up numerous children with Duchenne muscular dystrophy, I believe that toe\x=req-\ walking, in nearly all cases, precedes and results in contracture of the heel cords. The reason for toe-walking is an adjustment for the marked lumbar hyperlordosis and weakness of the hip flexors. Thus, the child makes a postural adjustment and finds it easier to get up on his toes to walk. It is possible that early weakness of the foot dorsiflexors also contributes to this posture. If one should put himself in the position of marked lumbar hyper\x=req-\ lordosis, it can be realized that rising on the toes compensates for this awkward posture and makes walking eas¬ ier. Obviously, a child who has weak¬ ness of his sural muscles cannot rise on his toes, and thus the problem is not attributable to weakness of the calf muscles or early dystrophic pro¬ cess within these muscles. The calf muscles, in fact, remain strong until the late stages of the disease. ness

Having carefully followed

Kamal Sadjadpour, MD Midland Hospital Center

Midland, Mich

Uses of Nomenclature To the Editor.\p=m-\I'mwriting to say how much I enjoyed the book review (231:982, 1975) in which Marjorie C. Meehan, MD, reviewed Models of Madness, Models of Medicine by Miriam Siegler and Humphrey Osmond (Macmillan, 1974). I agree that in our clinical effort to get at the causes of aberrant behavior and function, clinicians have generated nomenclature expressing that same predominately causal focus so succinctly expressed by Dr Meehan.

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Unfortunately, when third parties preoccupied themselves with generating categories of individuals regarded as deserving of funds, they have

have borrowed from clinical nomenclature and established categorical

funding according to etiologic categories. In the state of Ohio, accusations of misappropriation of funds may be made if mental retardation funds go for the operation of mental


agencies. Champions of each category jealously guard funds from dispersal to agencies caring for individuals similarly incapacitated and functionally capable of benefiting

from programs of treatment designed for patients in their own cate¬ gory even though patients may have arrived at their incapacity from a dif¬ ferent cause. From these thoughts I am led to re¬ flect that the adoption of etiologically focused clinical patterns of nomencla¬ ture, by parties whose principal pre¬ occupation is funding rather than clinical care, may be a serious admin¬ istrative error, the correction of which may require the development of an entirely differently focused no¬ menclature dealing with patterns of incapacity that are the end result of the operation of varying causal forces. I have long wondered how clinical assistance might be separated from financial assistance. The aware¬ ness of functional relationships may be a beginning. Carl G. Madsen, Jr, MD Painesville, Ohio

Pronunciation and Acoustics To the Editor.\p=m-\Recently,I attended the convention of the American College of Physicians and heard some presentations concerning the B- and


Possibly because I do not possess the same degree of auditory acuity that I had previously, or more likely because of the inadequacies of the speaking system and acoustics in lecture halls, I was unable to determine whether the speaker said "T" or "B." Therefore, may I suggest that these two lymphocytes be renamed as "beta" or "tau." Perhaps in written communications that won't be necessary, but in oral presentations I think it would help, as I do not think that I am the only one sometimes unable to distinguish "B" and "T" as they come over the microphone. Julian Love, MD

Arcadia, Calif

Letter: Uses of nomenclature.

pression of several disease entities, and until the precise molecular defect(s) is identified, it is prudent to discuss the disorder in general terms...
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