LETTERS AND CORRECTIONS "The power and the beauty of science do not rest upon infallibility, which it has not, but on corrigibility, without which it is nothing."—HOWARD E. GRUBER*
Letters submitted for publication must be typed double-spaced. Text length must not exceed 500 words, and no more than five references may be used. Complete references must be furnished, as specified in "Information for Authors" (page 1-6). Specific permission to publish should be appended as a postscript. Publication depends on availability of space: We give preference to comment on recent content and to new information. Letters for this section should be concise—the Editor reserves the right to shorten them and make changes that accord with our style.
ing their definitions to equivalency with primary care. Several studies of the characteristics of clinical encounters are underway under the aegis of various investigators. The potential importance of these studies lies in educational and training matters, in manpower distribution, and in the delivery of cost-effective, high-quality medical care. Advances will come faster if there is consensus on operating definitions. In a world of increased dependence on computers and numbers we hope that the definitions provided in the Mendenhall study will not compromise or confuse the accepted definition of primary care. For the American Board of Internal Medicine
Classification of Patient Care R I C H A R D J. R E I T E M E I E R , M . D .
T o T H E EDITOR: The paper by Mendenhall and associates titled " A National Study of Internal Medicine and Its Specialties: Primary Care in Internal Medicine" (Ann Intern Med 1979;91:275-87) classifies care encounters into first, episodic, principal, specialized (or limited), and consultative. This is a valuable and carefully performed study which provides much real and valuable data for the examination of manpower issues. The categories of care, however, raise problems since they are not separately or in combination precisely congruent with existing definitions of primary care. In their study "principal care" may be equated with the more widely accepted term primary care. Primary care is well defined elsewhere (1, 2). The Federated Council for Internal Medicine has defined a primary care physician as one who is [1] the physician of first contact; [2] the physician who makes the initial assessment of the patient's problems and who attempts to solve as many problems as are in realm of his competence; [3] the physician who coordinates the health care team, including health care extenders and consultants; and [4] the physician who assumes responsibility for continuing and comprehensive care. MendenhalFs study excludes first visits from "principal care," although such a visit may be the initial encounter for continuing and comprehensive care. Thus, a first visit by a patient for comprehensive evaluation and therapy for a severe respiratory infection is not "principal care." Furthermore, the categories "episodic care" and "principal care" differ depending on whether the patient is a regular patient. T h e periodic care of a mildly hypertensive individual could conceivably be assigned to either category. Many physicians assume continuing responsibility for patients seen only occasionally, and thus these two categories are not distinct. Concurrent care by two or more physicians to a single patient is not categorized. Telephone encounters, simple or complex, are not specifically included in this paper, although they were reported elsewhere. For the above reasons the Mendenhall category of "principal care" is an underestimate of primary care to the extent that some first, episodic, consultative, concurrent, and telephone encounters do, indeed, satisfy the established definitions of primary care. Further, no allowance is made for the differences in the comprehensiveness or the complexity of care provided for the same disease when managed by generalists, specialists, or subspecialists. Therefore, although we admire and welcome the contribution of this extensive and thorough study, we urge caution in extendG R U B E R H E . T h e origin of the origin of species. Review of Darwin and the Mysterious Mr. X: New Light on the Evolutionists. By E I S E L E Y L. The New York Times Book Review 1979 July 22: 16. 924
For the American College of Physicians R I C H A R D W. V I L T E R , M . D .
For the American Society of Internal Medicine M O N T E MALACH, M.D.
For the Association of Professors of Medicine J O S E P H E. J O H N S O N III, M . D . REFERENCES 1. Position papers on the internist and primary care. Bull Am Coll Physicians. 1976;17:2-11. 2. Primary care: toward a universal definition. Internist. March 1976;6.
In comment: The authors of " A National Study of Internal Medicine and Its Specialties: Primary Care in Internal Medicine" (1) concur with the caveat issued by Reitemeir and his associates on the pitfalls of treating our "principal care" measure as ipso facto equivalent to any of the many definitions of primary care. Indeed, in the referenced article and in an earlier more complete discussion of problems related to measurement of primary care, we take a similar position (2). Though the principal care category used in the study incorporates many aspects of "primariness," only one element in a fivefold classification scheme goes beyond a simple primary/nonprimary dichotomy. The advantage of this elaborated care classification lies in the fact that it is not necessary to adopt a particular concept of primary care; rather, the five categories can be considered individually or in some combination to conform to one model or another of primary medical care. The usefulness of our classification scheme becomes particularly apparent when one considers the lack of correspondence between various definitions of primary care. The Institute of Medicine's (IOM) comprehensive analysis of the literature identified 33 definitions of primary care. Based on their analysis, they derived a composite definition comprising four unique primary care attributes: access, comprehensiveness, coordination, and continuity (3), each of which is incorporated either directly or by inference in our principal care category. Reitemeier and his associates cite the possibility of a particular encounter falling into more than one of the types of care as a potential problem. In fact, though, one of the strengths of the classification scheme is that it does not require the physician to judge the proper classification type; rather, it is based solely on several characteristics that the physician reports about a particular patient-encounter. As a result, each encounter is unambiguously assigned by the algorithm to only one class without requiring any interpretive decisions on the part of the physician or researcher. Further, the classification system is totally independent of the specific diagnosis and associated testing and treatment regimen, leaving such clinical issues for a further level of analysis. Without question, there are differences in the
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clinical profile subsumed under each type of care when specialties are examined in comparative context; however, the provision of types of care as identified by the care classification remains constant. Clearly, then, the question of a possible underestimation (or overestimation) of the provision of primary care by internists is more a function of the particular conceptual model(s) applied to the care classification than of the empirical tractability of the categories themselves. Therefore, while we join Reitemeier and his associates in cautioning against the use of the care classification as an unqualified index of the relative provision of primary care, we believe that the classification constitutes an important vehicle for such comparisons provided that the underlying assumptions of the user's particular model of primary care are made explicit. R O B E R T C. M E N D E N H A L L , M . S . A L V I N R. T A R L O V , M . D . R O G E R A. G I R A R D , P H . D . J A N E T K. M I C H E L , M.S. S T E P H E N E. R A D E C K I , M . A .
University of Southern California School of Medicine; Los A n geles, C A 90033 REFERENCES 1. M E N D E N H A L L RC, TARLOV AR, G I R A R D RA, M I C H E L JK, RADECKI SE. A national study of internal medicine and its specialties: II. Primary care in internal medicine. Ann Intern Med. 1979;91:275-87. 2. M E N D E N H A L L RC, L E W I S CE, D E F L O R I O GP, G I R A R D RA. A national study of medical and surgical specialties: III. An empirical approach to the classification of patient care. JAMA. 1979;241:2180-5. 3. INSTITUTE O F M E D I C I N E . Primary Care in Medicine: A Definition. Washington, D.C.: National Academy of Sciences; 1977.
Primary Care Training T o T H E EDITOR: T h e paper by Goldenberg and colleagues (1) represents an important contribution to the large literature that can be expected to emerge from the development of primary care pathway training programs for medical residents. T h e authors point out that once the residents have been admitted to the primary care track, a high proportion of them remain committed to general internal medicine thereafter. This contrasts with findings for residents in the traditional pathway in the same institution. T h e authors intend to d o a longitudinal study to determine the relation between their findings and the ultimate career work of the trainees who have emerged from their program. We are skeptical, however, of the major conclusion of their work—"thus, the primary care pathway reinforced the career plans of trainees in general internal medicine, whereas traditional training influenced potential generalists toward subspecialty medicine." This conclusion does not take into account the admissions requirements into these two different tracks. Individual medical students apply to the particular pathway most compatible with their career plans established during medical school, or possibly before. Those persons w h o elect the primary care pathway are committed before entering the program to a career in general internal medicine, whereas those who enter the traditional pathway need make no such commitment before entering their program. Nevertheless, Weil and Schleiter present analyses that suggest factors other than residency training account for the decision to pursue either general internal medicine or a subspecialty (unpublished data). The purpose of this letter is not to denigrate the importance of the paper by Goldenberg and colleagues. W e simply wish to caution the reader on the interpretation of the data. T h e caution is doubly indicated because of the important relevance of this subject to matters of public policy.
REFERENCE 1. GOLDENBERG DL, POZEN JT, C O H E N AS. The effect of a primary-care pathway on internal medicine residents' career plans. Ann Intern Med. 1979;91:271-4.
Controlled Trials of Hemoperfusion for Intoxication T o T H E EDITOR: T h e following summary prepared by participants in the recent International Workshop on Hemoperfusion held in Haifa, Israel, is submitted in response to the report by Lorch and Garella that appeared in the August 1979, issue (1). Conservative medical management with support of vital systems represents the treatment of choice for most patients with toxic ingestions. F o r patients with serious intoxications fulfilling the following criteria, charcoal or resin hemoperfusion is indicated: [1] severe clinical intoxication leading to hypoventilation, hypothermia, hypotension, and nonresponsiveness despite supportive clinical measures; [2] lethal blood concentration of one or more potentially adsorbable drugs; and [3] prolonged coma associated with pneumonitis or known severe chronic pulmonary disease. T h e value of hemoperfusion for the treatment of ingestions of drugs having large volumes of distribution with slow intercompartmental transfer rates (for example, tricyclic antidepressants) or drugs associated with severe acid-base derangements (for example, aspirin, methanol, ethylene glycol) is not established. Patients fulfilling the above criteria should be considered for hemoperfusion, and controlled clinical trials are encouraged. 0 . S. B E T T E R G. B R U N N E R T. M. S. C H A N G J. M. C O U R T N E Y P. C . FARRELL M. C. G E L F A N D A. G I M S O N
H. J. G U R L A N D E. H O F F E R K. M A E D A R. M A I N I J. L . R O S E N B A U M S. S I D E M A N U. T A I T L E M A N J. F . W I N C H E S T E R
REFERENCE 1. LORCH J A, GARELLA S. Hemoperfusion to treat intoxications. Ann In-
tern Med. 1979;91:301-4. T o T H E EDITOR: T h e recently published paper on hemoperfusion for the treatment of intoxications is an excellent "think piece." Lorch and Garella (1) carefully reviewed their experience to suggest that this attractive form of therapy is not necessarily the panacea that anecdotal reports would suggest. The larger issue here, as with any kind of therapy, is simply that "a treatment is a treatment is a treatment" (pace Gertrude Stein). Every promising treatment deserves appropriately designed controlled clinical trials. T h e detailed case for controlled trials has been made elsewhere and need not be repeated (2, 3). Lorch and Garella emphasize the need of such an approach for hemoperfusion. T h u s far its promise exceeds its performance. Moreover, any hazards must yet be identified. Consequently, after first deciding which patients might benefit from it, patients should be randomly assigned to hemoperfusion, in the hope that these questions can be settled. D A V I D H. SPODICK, M.D., D.SC.
St. Vincent Hospital; Worcester, M A 01604 REFERENCES 1. LORCH JA, G A R E L L A S. Hemoperfusion to treat intoxications. Ann Intern Med. 1979;91:301-4. 2. SPODICK D H . Revascularization of the heart—numerators in search of denominators. Aw Heart J. 1971;81:149-57. Editorial. 3. SPODICK DH, A R O N O W W, BARBER B, et al. Controlled trials in surgery. Lancet. 1978;1:1213-4. Letter.
A L V I N R. T A R L O V , M . D .
University of Chicago, Chicago, I L 60637 PETER WEIL, PH.D. M A R Y K A Y SCHLEITER, M.A.
National Study of Internal Medicine Manpower
Tests of Urinary Excretion of Uric Acid T o T H E EDITOR: As practicing clinicians, we were delighted to see an article promising a simple convenient test to measure Letters and Corrections
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uric acid excretion (1). W e were dismayed, however, by the authors' failure to compare their test to the standard one (24-h urine uric-acid excretion) and by their unsupported statement that their test is more physiologic than the standard one. The 24-h urine excretion of uric acid is physiologic because it accurately reflects production and is clinically useful because it is a good predictor of renal stone formation (2). The authors do not supply any data as to whether their test is equally predictive. In fact, we wonder what their test truly measures. The authors refer to the excretion of uric acid relative to glomerular filtration rate ( G F R ) as a physiologic relation. W e believe that the important physiologic and clinical measurement is the excretion of uric acid in a given time period (usually 24 h), since processes regulating homeostasis seem to be modulated to maintain the steady state by equating excretion to intake or production. Factoring excretion by G F R may be misleading. Although G F R may diminish from aging or chronic renal disease, the excretion of substances such as uric acid remains equal to production since the patient remains in the steady state. Therefore, if uric-acid excretion is divided by a number that is decreasing over time ( G F R ) , then the resultant value (which the authors call uric-acid excretion in m g / d L - G F R ) will increase although total daily excretion remains constant. If, for example, one of the authors were to donate a kidney for transplantation, would he suddenly become an overexcretor of uric acid? Using the authors' test he would. If his uric-acid excretion were 660 m g / d and his G F R 180 L / d (or 1800 d L / d ) , then his uric-acid excretion as expressed by the authors would be 660 mg/1800 d L = 0.36 m g / d L G F R . After donating a kidney his uric-acid excretion would still be 660 mg. If his G F R were now only 900 d L / d , then his uric-acid excretion would be 660 m g / 900 d L = 0.73 m g / d L G F R . Voila, an overexcretor! Obviously, this test can be quite misleading. We believe it is the responsibility of the peer review process to carefully screen and evaluate articles before they are published. That process has failed here. STEPHEN M. SELTZER, M.D. N E I L SMITHLINE, M.D. 608 Tucson Medical Park; Tucson, A Z 85712
phasize the etiologic roles of low urine p H and flow rate in their report. These points do not gainsay the value of finding that minority of hyperuricemic people who significantly overexcrete uric acid. They are intended only to retain some reasonable perspective about the value of our traditional tools. Readers of this correspondence may judge for themselves whether uric-acid excretion is consistently evaluated in their hyperuricemic patients and whether a "standard" 24-h method is sufficiently clear in its dietary restrictions, normal limits, experimental precision, and practicality to justify continuing uncritical acceptance. Those who share our dissatisfaction may wish to further consider our midmorning technique or to propose and evaluate yet another alternative. PETER A SIMKIN, M.D.
University of Washington School of Medicine; Seattle, W A 98195 REFERENCES
1. SORENSEN LB. Role of the intestinal tract in the elimination of uric acid. Arthritis Rheum. 1965;8:694-706. 2. YD T-F, G U T M A N AB. Uric acid nephrolithiasis in gout: predisposing factors. Ann Intern Med. 1967;67:1133-48.
T o T H E E D I T O R : I a m writing about the paper "Uric Acid Excretion: Quantitative Assessment from Spot, Midmorning Serum and Urine Samples" which appeared in the July issue (1). This paper presents a very useful test for uric-acid secretion that overcomes the limitations of the conventional 24-h test. It does not, however, provide the appropriate information for clinicians to judge whether it is a valid test. The test is proposed to replace the 24-h urine uric-acid collection. Therefore, sensitivity/specificity data (in a 4 X 4 table) should be provided comparing values for the new test to the standard 24-h collection. The article presents data comparing normal to gouty/hyperuricemic men. Since the test is to be used to separate hyperexcretors within the single category of gout/hyperuricemia, the appropriate validation study would be between the two (normal excretion, hyperexcretion) subgroups of gouty/hypercemic persons, and not between normal persons and hyperuricemic patients. R I C H A R D GROSS, M.D., SC.M.
REFERENCES
Baltimore City Hospital; Baltimore, M D 21224
1. SIMKIN PA, H O O V E R PL, PAXSON CS, W I L S O N WF. Uric acid excretion:
quantitative assessment from spot, midmorning serum and urine samples. Ann Intern Med. 1979;91:44-7. 2. BROADUS AE, T H I E R SO. Metabolic basis of renal-stone disease. N Engl J Med. 1979;300:839-45.
In response: Unfortunately, those who propose new approaches to old problems can expect that a few more conservative colleagues will come after their heads. Seltzer and Smithline exceed conventional bounds, however, in wanting our kidneys as well. Most practicing clinicians, familiar with the effects of compensatory hypertrophy on glomerular filtration rate ( G F R ) , will recognize that Seltzer and Smithline's nephrectomy example is particularly ill-chosen. We call our experimental units milligram per decilitre of glomerular filtrate because that is what they are. Physicians more comfortable with a time reference may prefer to consider them milligrams per minute after normalization to a G F R of 1 d L / m i n . This formulation is more physiologic than one based on time alone because it provides a built-in correction for differences in body size. For quite some time, students of urate metabolism have known that uric-acid excretion provides only a rough approximation of its production. A variable degree of intestinal uricolysis provides the principal explanation for this finding (1). Not as well known is the fact that uric-acid excretion is a mediocre predictor of renal-stone formation. In the most extensive examination of this question, Yu and G u t m a n (2) studied the prevalence of urolithiasis in 923 gouty patients. Of those w h o had stones, 6 2 % excreted less than 700 mg and 8 7 % less than 900 mg of uric acid per day. All of these values are probably within the normal range. The authors quite appropriately chose to em926
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1979
REFERENCE 1. SIMKIN PA, H O O V E R PL, PAXSON CS, W I L S O N W F . Uric acid excretion:
quantitative assessment from spot, midmorning serum and urine samples. Ann Intern Med. 1979;91:44-7.
In response: The comments and questions of Dr. Gross rest on the concept that there is a generally accepted "gold standard" against which new tests of uric-acid excretion can and should be measured. I do not think this is so. Prevailing practices vary, but each rests heavily on a number of assumptions often unstated. Should there be dietary purine restriction, and, if so, how much and for how long? Should subjects be hospitalized, or can they be meaningfully evaluated as outpatients? Should urine be collected over a 24-h period, and, if so, how many times? These questions have been answered almost entirely by assertion rather than by systematic, comparative analysis. T h e recommendations of each author therefore reflect his or her experience, interests, and bias. My own bias favors the "state of nature" conditions of outpatient assessments during minimal purine restriction. Within this context, we chose to evaluate the precision both of 24-h urine collections and of a new technique using spot, midmorning serum and urine collections to express uricacid excretion per decilitre of glomerular filtrate. The 24-h technique, as we used it, is perhaps more widely employed than any other test of uric-acid excretion. It has not, however, been previously standardized by systematic study. We found 24-h collections to be much less convenient and somewhat less precise than our spot technique. In this setting, it seems inappropriate to assess the "validity" of the better technique by its degree of correlation with the poorer. Correlation
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coefficients are also highly dependent on the range of values in the population under study. Our normal men were closely grouped. In view of this factor and the variability in each approach, the tests would not be expected to correlate highly. Being aware of these points, we were neither surprised nor discouraged to find that the correlation between the two methods (r = 0.26) was not statistically significant. Dr. Gross is correct in observing that we did not directly address the questions of sensitivity and specificity. A s stated above, the principal reason for this omission was the lack of reliable standards of uric-acid excretion in ambulatory men with minimal purine restriction. As with any quantitative test, however, the objective of our method is to distinguish the small minority of hyperuricemic patients who "overexcrete" uric acid from the great majority who do not. In defining overexcretion as repeated findings more than 3 standard deviations above the normal mean, we believe our test will be highly specific but not overly sensitive. Until and unless more extensive studies establish the value of greater sensitivity, we believe this conservative approach is reasonable in everyday clinical practice.
male. Four of the five had abnormal sellar tomograms. Although there were some trends toward PRL suppression, none suppressed significantly or into the normal range. Symptoms of galactorrhea, if present, did not abate. In addition, growth hormone did not suppress significantly in the patient with acromegaly. We conclude that although serotonin may play a role in hypothalamic-pituitary function, blockade with cyproheptadine, in our cases, did not cause significant decrements in P R L in patients with pituitary adenomata but did cause a paradoxical rise in P R L in normal subjects. We continue to believe that when treatment of the amenorrhea-galactorrhea syndrome is considered, the two best choices are transsphenoidal adenectomy and bromocriptine. L O R E N I. D O L M A N , M . D .
Letterman Army Medical Center; San Francisco, C A 94129 REFERENCES 1. W O R T S M A N J, SOLER N G , H I R S C H O W I T Z J. Cyproheptadine in the man-
agement of the galactorrhea-amenorrhea 1979;90:923-5.
P E T E R A. SIMKIN, M . D .
University of Washington School of Medicine; Seattle, W A 98195
syndrome. Ann Intern
Med.
2. K R I E G E R DT, A M O R O S A L, LINICK F. Cyproheptadine-induced remis-
sion of Cushing's disease. N EnglJ
Med.
1975;293:893-6.
3. D O L M A N LI, J U B I Z W, T Y L E R F H . Effects on cyproheptadine on hor-
mone levels in normals and patients with hormone overproduction. In: International Society of Psychoneuroendocrinology: VHth International Congress, July 13-16, 1976, Strasbourg, France, p. 76. Abstract.
Cyproheptadine Effects on Pituitary Function T o THE EDITOR: The report of Wortsman and colleagues in the June issue (1) concludes that cyproheptadine in a dose of 16 to 24 mg/d for 8 to 16 weeks can effectively lower serum prolactin (PRL) levels and decrease symptomatic galactorrhea in patients with the galactorrhea-amenorrhea syndrome. In 1976 we were interested in the antiserotonin properties of cyproheptadine, noting evidence that serotonin probably plays a role in the release of pituitary PRL, growth hormone, and ACTH, as well as suppression of thyroid-stimulating hormone, luteinizing hormone, and follicle-stimulating hormone. The effects of the drug in suppressing ACTH release in Cushing's disease had recently been reported (2). We studied four normal subjects (Table 1), three patients with Addison's disease, and five patients with PRL-secreting pituitary adenomata (one who had coincident acromegaly) (3). After 4 weeks of cyproheptadine therapy, 4 mg four times daily, the four normal subjects complained of initial drowsiness; three had increased weight gain (2.2 to 11 kg), while the fourth lost 2.7 kg because of anorexia. In addition, three patients with Addison's disease, taking hydrocortisone, 30 mg/d, were treated with cyproheptadine. Baseline ACTH levels (0800 h before hydrocortisone dose) did not change significantly in this group. Five patients with PRL-secreting pituitary adenomata (PRL levels 28 to 85 ng/mL) were treated with cyproheptadine, 16 to 24 mg/d for up to 4 months. The group included four females (one with coincident growth-hormone hypersecretion) and one
Phentolamine for Primary Pulmonary Hypertension T o THE EDITOR: In the May issue, Ruskin and Hutter (1) reported a case of primary pulmonary hypertension in a patient who showed impressive symptomatic and hemodynamic improvement after a trial of phentolamine. We have studied another case using similar protocol and relate a different experience. A 21-year-old white woman was found to have abnormal chest roentgenogram and was referred for evaluation in 1975. At that time she was asymptomatic. She had a palpable second heart sound and grade II/VI ejection systolic murmur at base. Electrocardiogram findings were normal. Vectorcardiogram showed right ventricular hypertrophy. Chest roentgenogram revealed an enlarged pulmonary artery. Pulmonary function test findings were normal. Complete right and left heart catheterization and angiograms showed no evidence of valvular heart disease or shunt in any level. Pulmonary capillary wedge pressure was 1 mm Hg, while pulmonary arterial pressure was 55/25 mm Hg and left ventricular end-diastolic pressure, 7 mm Hg. For a few months before admission, she had noticed decreased exercise tolerance without any other symptoms. She was readmitted for a trial of phentolamine. She showed no change in findings on physical examination, ECG, and chest roentgenogram. Hemodynamic study was carried out at rest, during exercise, and with phentolamine. The work load of bicycle ergometer was increased from 25 W, 50 rpm, to 50 to 75 watts every 3 min until she developed dyspnea. After 50 mg of phentolamine was given intravenously at the rate of 0.3 mg/min, hemodynamic studies were repeated. The results are shown in Table 1.
Table 1. Findings in Four Normal Subjects Before and After Therapy with Cyproheptadine Baseline *
Subject ACTH B
A
Prolactin B
A
LH B
After Metyrapone (3 g Overnight)
TSH A
B
A
ACTH B
pg/mL 1 2 3 4 :
34.5 23.5 25.5 53.5
22.4 24.5 42.0 25.0
ng/mL 5.6 2.0 6.6 18.0
8.5 4.4 7.1 21.5
mlU/mL 3.4 6.1 5.9 8.0
7.2 10.4 8.2 14.7
nV/mL 3.6 4.7 2.5 4.2
5.4 5.8 2.9 5.3
11-Deoxycortisol B
A
14.0 17.0 17.3 14.0
8.9 11.0 11.6 13.6
A
pg/mL 244 131 219 432
121 37 117 273
After Dexamethasone (1 mg Overnight)
Letters submitted for publication must be typed double-spaced. Text length must not exceed 500 words, and no more than five references may be used. Complete references must be furnished, as specified in "Information for Authors" (page 1-6). Specific permission to publish should be appended as a postscript. Publication depends on availability of space: We give preference to comment on recent content and to new information. Letters for this section should be concise—the Editor reserves the right to shorten them and make changes that accord with our style.
ing their definitions to equivalency with primary care. Several studies of the characteristics of clinical encounters are underway under the aegis of various investigators. The potential importance of these studies lies in educational and training matters, in manpower distribution, and in the delivery of cost-effective, high-quality medical care. Advances will come faster if there is consensus on operating definitions. In a world of increased dependence on computers and numbers we hope that the definitions provided in the Mendenhall study will not compromise or confuse the accepted definition of primary care. For the American Board of Internal Medicine
Classification of Patient Care R I C H A R D J. R E I T E M E I E R , M . D .
T o T H E EDITOR: The paper by Mendenhall and associates titled " A National Study of Internal Medicine and Its Specialties: Primary Care in Internal Medicine" (Ann Intern Med 1979;91:275-87) classifies care encounters into first, episodic, principal, specialized (or limited), and consultative. This is a valuable and carefully performed study which provides much real and valuable data for the examination of manpower issues. The categories of care, however, raise problems since they are not separately or in combination precisely congruent with existing definitions of primary care. In their study "principal care" may be equated with the more widely accepted term primary care. Primary care is well defined elsewhere (1, 2). The Federated Council for Internal Medicine has defined a primary care physician as one who is [1] the physician of first contact; [2] the physician who makes the initial assessment of the patient's problems and who attempts to solve as many problems as are in realm of his competence; [3] the physician who coordinates the health care team, including health care extenders and consultants; and [4] the physician who assumes responsibility for continuing and comprehensive care. MendenhalFs study excludes first visits from "principal care," although such a visit may be the initial encounter for continuing and comprehensive care. Thus, a first visit by a patient for comprehensive evaluation and therapy for a severe respiratory infection is not "principal care." Furthermore, the categories "episodic care" and "principal care" differ depending on whether the patient is a regular patient. T h e periodic care of a mildly hypertensive individual could conceivably be assigned to either category. Many physicians assume continuing responsibility for patients seen only occasionally, and thus these two categories are not distinct. Concurrent care by two or more physicians to a single patient is not categorized. Telephone encounters, simple or complex, are not specifically included in this paper, although they were reported elsewhere. For the above reasons the Mendenhall category of "principal care" is an underestimate of primary care to the extent that some first, episodic, consultative, concurrent, and telephone encounters do, indeed, satisfy the established definitions of primary care. Further, no allowance is made for the differences in the comprehensiveness or the complexity of care provided for the same disease when managed by generalists, specialists, or subspecialists. Therefore, although we admire and welcome the contribution of this extensive and thorough study, we urge caution in extendG R U B E R H E . T h e origin of the origin of species. Review of Darwin and the Mysterious Mr. X: New Light on the Evolutionists. By E I S E L E Y L. The New York Times Book Review 1979 July 22: 16. 924
For the American College of Physicians R I C H A R D W. V I L T E R , M . D .
For the American Society of Internal Medicine M O N T E MALACH, M.D.
For the Association of Professors of Medicine J O S E P H E. J O H N S O N III, M . D . REFERENCES 1. Position papers on the internist and primary care. Bull Am Coll Physicians. 1976;17:2-11. 2. Primary care: toward a universal definition. Internist. March 1976;6.
In comment: The authors of " A National Study of Internal Medicine and Its Specialties: Primary Care in Internal Medicine" (1) concur with the caveat issued by Reitemeir and his associates on the pitfalls of treating our "principal care" measure as ipso facto equivalent to any of the many definitions of primary care. Indeed, in the referenced article and in an earlier more complete discussion of problems related to measurement of primary care, we take a similar position (2). Though the principal care category used in the study incorporates many aspects of "primariness," only one element in a fivefold classification scheme goes beyond a simple primary/nonprimary dichotomy. The advantage of this elaborated care classification lies in the fact that it is not necessary to adopt a particular concept of primary care; rather, the five categories can be considered individually or in some combination to conform to one model or another of primary medical care. The usefulness of our classification scheme becomes particularly apparent when one considers the lack of correspondence between various definitions of primary care. The Institute of Medicine's (IOM) comprehensive analysis of the literature identified 33 definitions of primary care. Based on their analysis, they derived a composite definition comprising four unique primary care attributes: access, comprehensiveness, coordination, and continuity (3), each of which is incorporated either directly or by inference in our principal care category. Reitemeier and his associates cite the possibility of a particular encounter falling into more than one of the types of care as a potential problem. In fact, though, one of the strengths of the classification scheme is that it does not require the physician to judge the proper classification type; rather, it is based solely on several characteristics that the physician reports about a particular patient-encounter. As a result, each encounter is unambiguously assigned by the algorithm to only one class without requiring any interpretive decisions on the part of the physician or researcher. Further, the classification system is totally independent of the specific diagnosis and associated testing and treatment regimen, leaving such clinical issues for a further level of analysis. Without question, there are differences in the
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clinical profile subsumed under each type of care when specialties are examined in comparative context; however, the provision of types of care as identified by the care classification remains constant. Clearly, then, the question of a possible underestimation (or overestimation) of the provision of primary care by internists is more a function of the particular conceptual model(s) applied to the care classification than of the empirical tractability of the categories themselves. Therefore, while we join Reitemeier and his associates in cautioning against the use of the care classification as an unqualified index of the relative provision of primary care, we believe that the classification constitutes an important vehicle for such comparisons provided that the underlying assumptions of the user's particular model of primary care are made explicit. R O B E R T C. M E N D E N H A L L , M . S . A L V I N R. T A R L O V , M . D . R O G E R A. G I R A R D , P H . D . J A N E T K. M I C H E L , M.S. S T E P H E N E. R A D E C K I , M . A .
University of Southern California School of Medicine; Los A n geles, C A 90033 REFERENCES 1. M E N D E N H A L L RC, TARLOV AR, G I R A R D RA, M I C H E L JK, RADECKI SE. A national study of internal medicine and its specialties: II. Primary care in internal medicine. Ann Intern Med. 1979;91:275-87. 2. M E N D E N H A L L RC, L E W I S CE, D E F L O R I O GP, G I R A R D RA. A national study of medical and surgical specialties: III. An empirical approach to the classification of patient care. JAMA. 1979;241:2180-5. 3. INSTITUTE O F M E D I C I N E . Primary Care in Medicine: A Definition. Washington, D.C.: National Academy of Sciences; 1977.
Primary Care Training T o T H E EDITOR: T h e paper by Goldenberg and colleagues (1) represents an important contribution to the large literature that can be expected to emerge from the development of primary care pathway training programs for medical residents. T h e authors point out that once the residents have been admitted to the primary care track, a high proportion of them remain committed to general internal medicine thereafter. This contrasts with findings for residents in the traditional pathway in the same institution. T h e authors intend to d o a longitudinal study to determine the relation between their findings and the ultimate career work of the trainees who have emerged from their program. We are skeptical, however, of the major conclusion of their work—"thus, the primary care pathway reinforced the career plans of trainees in general internal medicine, whereas traditional training influenced potential generalists toward subspecialty medicine." This conclusion does not take into account the admissions requirements into these two different tracks. Individual medical students apply to the particular pathway most compatible with their career plans established during medical school, or possibly before. Those persons w h o elect the primary care pathway are committed before entering the program to a career in general internal medicine, whereas those who enter the traditional pathway need make no such commitment before entering their program. Nevertheless, Weil and Schleiter present analyses that suggest factors other than residency training account for the decision to pursue either general internal medicine or a subspecialty (unpublished data). The purpose of this letter is not to denigrate the importance of the paper by Goldenberg and colleagues. W e simply wish to caution the reader on the interpretation of the data. T h e caution is doubly indicated because of the important relevance of this subject to matters of public policy.
REFERENCE 1. GOLDENBERG DL, POZEN JT, C O H E N AS. The effect of a primary-care pathway on internal medicine residents' career plans. Ann Intern Med. 1979;91:271-4.
Controlled Trials of Hemoperfusion for Intoxication T o T H E EDITOR: T h e following summary prepared by participants in the recent International Workshop on Hemoperfusion held in Haifa, Israel, is submitted in response to the report by Lorch and Garella that appeared in the August 1979, issue (1). Conservative medical management with support of vital systems represents the treatment of choice for most patients with toxic ingestions. F o r patients with serious intoxications fulfilling the following criteria, charcoal or resin hemoperfusion is indicated: [1] severe clinical intoxication leading to hypoventilation, hypothermia, hypotension, and nonresponsiveness despite supportive clinical measures; [2] lethal blood concentration of one or more potentially adsorbable drugs; and [3] prolonged coma associated with pneumonitis or known severe chronic pulmonary disease. T h e value of hemoperfusion for the treatment of ingestions of drugs having large volumes of distribution with slow intercompartmental transfer rates (for example, tricyclic antidepressants) or drugs associated with severe acid-base derangements (for example, aspirin, methanol, ethylene glycol) is not established. Patients fulfilling the above criteria should be considered for hemoperfusion, and controlled clinical trials are encouraged. 0 . S. B E T T E R G. B R U N N E R T. M. S. C H A N G J. M. C O U R T N E Y P. C . FARRELL M. C. G E L F A N D A. G I M S O N
H. J. G U R L A N D E. H O F F E R K. M A E D A R. M A I N I J. L . R O S E N B A U M S. S I D E M A N U. T A I T L E M A N J. F . W I N C H E S T E R
REFERENCE 1. LORCH J A, GARELLA S. Hemoperfusion to treat intoxications. Ann In-
tern Med. 1979;91:301-4. T o T H E EDITOR: T h e recently published paper on hemoperfusion for the treatment of intoxications is an excellent "think piece." Lorch and Garella (1) carefully reviewed their experience to suggest that this attractive form of therapy is not necessarily the panacea that anecdotal reports would suggest. The larger issue here, as with any kind of therapy, is simply that "a treatment is a treatment is a treatment" (pace Gertrude Stein). Every promising treatment deserves appropriately designed controlled clinical trials. T h e detailed case for controlled trials has been made elsewhere and need not be repeated (2, 3). Lorch and Garella emphasize the need of such an approach for hemoperfusion. T h u s far its promise exceeds its performance. Moreover, any hazards must yet be identified. Consequently, after first deciding which patients might benefit from it, patients should be randomly assigned to hemoperfusion, in the hope that these questions can be settled. D A V I D H. SPODICK, M.D., D.SC.
St. Vincent Hospital; Worcester, M A 01604 REFERENCES 1. LORCH JA, G A R E L L A S. Hemoperfusion to treat intoxications. Ann Intern Med. 1979;91:301-4. 2. SPODICK D H . Revascularization of the heart—numerators in search of denominators. Aw Heart J. 1971;81:149-57. Editorial. 3. SPODICK DH, A R O N O W W, BARBER B, et al. Controlled trials in surgery. Lancet. 1978;1:1213-4. Letter.
A L V I N R. T A R L O V , M . D .
University of Chicago, Chicago, I L 60637 PETER WEIL, PH.D. M A R Y K A Y SCHLEITER, M.A.
National Study of Internal Medicine Manpower
Tests of Urinary Excretion of Uric Acid T o T H E EDITOR: As practicing clinicians, we were delighted to see an article promising a simple convenient test to measure Letters and Corrections
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uric acid excretion (1). W e were dismayed, however, by the authors' failure to compare their test to the standard one (24-h urine uric-acid excretion) and by their unsupported statement that their test is more physiologic than the standard one. The 24-h urine excretion of uric acid is physiologic because it accurately reflects production and is clinically useful because it is a good predictor of renal stone formation (2). The authors do not supply any data as to whether their test is equally predictive. In fact, we wonder what their test truly measures. The authors refer to the excretion of uric acid relative to glomerular filtration rate ( G F R ) as a physiologic relation. W e believe that the important physiologic and clinical measurement is the excretion of uric acid in a given time period (usually 24 h), since processes regulating homeostasis seem to be modulated to maintain the steady state by equating excretion to intake or production. Factoring excretion by G F R may be misleading. Although G F R may diminish from aging or chronic renal disease, the excretion of substances such as uric acid remains equal to production since the patient remains in the steady state. Therefore, if uric-acid excretion is divided by a number that is decreasing over time ( G F R ) , then the resultant value (which the authors call uric-acid excretion in m g / d L - G F R ) will increase although total daily excretion remains constant. If, for example, one of the authors were to donate a kidney for transplantation, would he suddenly become an overexcretor of uric acid? Using the authors' test he would. If his uric-acid excretion were 660 m g / d and his G F R 180 L / d (or 1800 d L / d ) , then his uric-acid excretion as expressed by the authors would be 660 mg/1800 d L = 0.36 m g / d L G F R . After donating a kidney his uric-acid excretion would still be 660 mg. If his G F R were now only 900 d L / d , then his uric-acid excretion would be 660 m g / 900 d L = 0.73 m g / d L G F R . Voila, an overexcretor! Obviously, this test can be quite misleading. We believe it is the responsibility of the peer review process to carefully screen and evaluate articles before they are published. That process has failed here. STEPHEN M. SELTZER, M.D. N E I L SMITHLINE, M.D. 608 Tucson Medical Park; Tucson, A Z 85712
phasize the etiologic roles of low urine p H and flow rate in their report. These points do not gainsay the value of finding that minority of hyperuricemic people who significantly overexcrete uric acid. They are intended only to retain some reasonable perspective about the value of our traditional tools. Readers of this correspondence may judge for themselves whether uric-acid excretion is consistently evaluated in their hyperuricemic patients and whether a "standard" 24-h method is sufficiently clear in its dietary restrictions, normal limits, experimental precision, and practicality to justify continuing uncritical acceptance. Those who share our dissatisfaction may wish to further consider our midmorning technique or to propose and evaluate yet another alternative. PETER A SIMKIN, M.D.
University of Washington School of Medicine; Seattle, W A 98195 REFERENCES
1. SORENSEN LB. Role of the intestinal tract in the elimination of uric acid. Arthritis Rheum. 1965;8:694-706. 2. YD T-F, G U T M A N AB. Uric acid nephrolithiasis in gout: predisposing factors. Ann Intern Med. 1967;67:1133-48.
T o T H E E D I T O R : I a m writing about the paper "Uric Acid Excretion: Quantitative Assessment from Spot, Midmorning Serum and Urine Samples" which appeared in the July issue (1). This paper presents a very useful test for uric-acid secretion that overcomes the limitations of the conventional 24-h test. It does not, however, provide the appropriate information for clinicians to judge whether it is a valid test. The test is proposed to replace the 24-h urine uric-acid collection. Therefore, sensitivity/specificity data (in a 4 X 4 table) should be provided comparing values for the new test to the standard 24-h collection. The article presents data comparing normal to gouty/hyperuricemic men. Since the test is to be used to separate hyperexcretors within the single category of gout/hyperuricemia, the appropriate validation study would be between the two (normal excretion, hyperexcretion) subgroups of gouty/hypercemic persons, and not between normal persons and hyperuricemic patients. R I C H A R D GROSS, M.D., SC.M.
REFERENCES
Baltimore City Hospital; Baltimore, M D 21224
1. SIMKIN PA, H O O V E R PL, PAXSON CS, W I L S O N WF. Uric acid excretion:
quantitative assessment from spot, midmorning serum and urine samples. Ann Intern Med. 1979;91:44-7. 2. BROADUS AE, T H I E R SO. Metabolic basis of renal-stone disease. N Engl J Med. 1979;300:839-45.
In response: Unfortunately, those who propose new approaches to old problems can expect that a few more conservative colleagues will come after their heads. Seltzer and Smithline exceed conventional bounds, however, in wanting our kidneys as well. Most practicing clinicians, familiar with the effects of compensatory hypertrophy on glomerular filtration rate ( G F R ) , will recognize that Seltzer and Smithline's nephrectomy example is particularly ill-chosen. We call our experimental units milligram per decilitre of glomerular filtrate because that is what they are. Physicians more comfortable with a time reference may prefer to consider them milligrams per minute after normalization to a G F R of 1 d L / m i n . This formulation is more physiologic than one based on time alone because it provides a built-in correction for differences in body size. For quite some time, students of urate metabolism have known that uric-acid excretion provides only a rough approximation of its production. A variable degree of intestinal uricolysis provides the principal explanation for this finding (1). Not as well known is the fact that uric-acid excretion is a mediocre predictor of renal-stone formation. In the most extensive examination of this question, Yu and G u t m a n (2) studied the prevalence of urolithiasis in 923 gouty patients. Of those w h o had stones, 6 2 % excreted less than 700 mg and 8 7 % less than 900 mg of uric acid per day. All of these values are probably within the normal range. The authors quite appropriately chose to em926
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1979
REFERENCE 1. SIMKIN PA, H O O V E R PL, PAXSON CS, W I L S O N W F . Uric acid excretion:
quantitative assessment from spot, midmorning serum and urine samples. Ann Intern Med. 1979;91:44-7.
In response: The comments and questions of Dr. Gross rest on the concept that there is a generally accepted "gold standard" against which new tests of uric-acid excretion can and should be measured. I do not think this is so. Prevailing practices vary, but each rests heavily on a number of assumptions often unstated. Should there be dietary purine restriction, and, if so, how much and for how long? Should subjects be hospitalized, or can they be meaningfully evaluated as outpatients? Should urine be collected over a 24-h period, and, if so, how many times? These questions have been answered almost entirely by assertion rather than by systematic, comparative analysis. T h e recommendations of each author therefore reflect his or her experience, interests, and bias. My own bias favors the "state of nature" conditions of outpatient assessments during minimal purine restriction. Within this context, we chose to evaluate the precision both of 24-h urine collections and of a new technique using spot, midmorning serum and urine collections to express uricacid excretion per decilitre of glomerular filtrate. The 24-h technique, as we used it, is perhaps more widely employed than any other test of uric-acid excretion. It has not, however, been previously standardized by systematic study. We found 24-h collections to be much less convenient and somewhat less precise than our spot technique. In this setting, it seems inappropriate to assess the "validity" of the better technique by its degree of correlation with the poorer. Correlation
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coefficients are also highly dependent on the range of values in the population under study. Our normal men were closely grouped. In view of this factor and the variability in each approach, the tests would not be expected to correlate highly. Being aware of these points, we were neither surprised nor discouraged to find that the correlation between the two methods (r = 0.26) was not statistically significant. Dr. Gross is correct in observing that we did not directly address the questions of sensitivity and specificity. A s stated above, the principal reason for this omission was the lack of reliable standards of uric-acid excretion in ambulatory men with minimal purine restriction. As with any quantitative test, however, the objective of our method is to distinguish the small minority of hyperuricemic patients who "overexcrete" uric acid from the great majority who do not. In defining overexcretion as repeated findings more than 3 standard deviations above the normal mean, we believe our test will be highly specific but not overly sensitive. Until and unless more extensive studies establish the value of greater sensitivity, we believe this conservative approach is reasonable in everyday clinical practice.
male. Four of the five had abnormal sellar tomograms. Although there were some trends toward PRL suppression, none suppressed significantly or into the normal range. Symptoms of galactorrhea, if present, did not abate. In addition, growth hormone did not suppress significantly in the patient with acromegaly. We conclude that although serotonin may play a role in hypothalamic-pituitary function, blockade with cyproheptadine, in our cases, did not cause significant decrements in P R L in patients with pituitary adenomata but did cause a paradoxical rise in P R L in normal subjects. We continue to believe that when treatment of the amenorrhea-galactorrhea syndrome is considered, the two best choices are transsphenoidal adenectomy and bromocriptine. L O R E N I. D O L M A N , M . D .
Letterman Army Medical Center; San Francisco, C A 94129 REFERENCES 1. W O R T S M A N J, SOLER N G , H I R S C H O W I T Z J. Cyproheptadine in the man-
agement of the galactorrhea-amenorrhea 1979;90:923-5.
P E T E R A. SIMKIN, M . D .
University of Washington School of Medicine; Seattle, W A 98195
syndrome. Ann Intern
Med.
2. K R I E G E R DT, A M O R O S A L, LINICK F. Cyproheptadine-induced remis-
sion of Cushing's disease. N EnglJ
Med.
1975;293:893-6.
3. D O L M A N LI, J U B I Z W, T Y L E R F H . Effects on cyproheptadine on hor-
mone levels in normals and patients with hormone overproduction. In: International Society of Psychoneuroendocrinology: VHth International Congress, July 13-16, 1976, Strasbourg, France, p. 76. Abstract.
Cyproheptadine Effects on Pituitary Function T o THE EDITOR: The report of Wortsman and colleagues in the June issue (1) concludes that cyproheptadine in a dose of 16 to 24 mg/d for 8 to 16 weeks can effectively lower serum prolactin (PRL) levels and decrease symptomatic galactorrhea in patients with the galactorrhea-amenorrhea syndrome. In 1976 we were interested in the antiserotonin properties of cyproheptadine, noting evidence that serotonin probably plays a role in the release of pituitary PRL, growth hormone, and ACTH, as well as suppression of thyroid-stimulating hormone, luteinizing hormone, and follicle-stimulating hormone. The effects of the drug in suppressing ACTH release in Cushing's disease had recently been reported (2). We studied four normal subjects (Table 1), three patients with Addison's disease, and five patients with PRL-secreting pituitary adenomata (one who had coincident acromegaly) (3). After 4 weeks of cyproheptadine therapy, 4 mg four times daily, the four normal subjects complained of initial drowsiness; three had increased weight gain (2.2 to 11 kg), while the fourth lost 2.7 kg because of anorexia. In addition, three patients with Addison's disease, taking hydrocortisone, 30 mg/d, were treated with cyproheptadine. Baseline ACTH levels (0800 h before hydrocortisone dose) did not change significantly in this group. Five patients with PRL-secreting pituitary adenomata (PRL levels 28 to 85 ng/mL) were treated with cyproheptadine, 16 to 24 mg/d for up to 4 months. The group included four females (one with coincident growth-hormone hypersecretion) and one
Phentolamine for Primary Pulmonary Hypertension T o THE EDITOR: In the May issue, Ruskin and Hutter (1) reported a case of primary pulmonary hypertension in a patient who showed impressive symptomatic and hemodynamic improvement after a trial of phentolamine. We have studied another case using similar protocol and relate a different experience. A 21-year-old white woman was found to have abnormal chest roentgenogram and was referred for evaluation in 1975. At that time she was asymptomatic. She had a palpable second heart sound and grade II/VI ejection systolic murmur at base. Electrocardiogram findings were normal. Vectorcardiogram showed right ventricular hypertrophy. Chest roentgenogram revealed an enlarged pulmonary artery. Pulmonary function test findings were normal. Complete right and left heart catheterization and angiograms showed no evidence of valvular heart disease or shunt in any level. Pulmonary capillary wedge pressure was 1 mm Hg, while pulmonary arterial pressure was 55/25 mm Hg and left ventricular end-diastolic pressure, 7 mm Hg. For a few months before admission, she had noticed decreased exercise tolerance without any other symptoms. She was readmitted for a trial of phentolamine. She showed no change in findings on physical examination, ECG, and chest roentgenogram. Hemodynamic study was carried out at rest, during exercise, and with phentolamine. The work load of bicycle ergometer was increased from 25 W, 50 rpm, to 50 to 75 watts every 3 min until she developed dyspnea. After 50 mg of phentolamine was given intravenously at the rate of 0.3 mg/min, hemodynamic studies were repeated. The results are shown in Table 1.
Table 1. Findings in Four Normal Subjects Before and After Therapy with Cyproheptadine Baseline *
Subject ACTH B
A
Prolactin B
A
LH B
After Metyrapone (3 g Overnight)
TSH A
B
A
ACTH B
pg/mL 1 2 3 4 :
34.5 23.5 25.5 53.5
22.4 24.5 42.0 25.0
ng/mL 5.6 2.0 6.6 18.0
8.5 4.4 7.1 21.5
mlU/mL 3.4 6.1 5.9 8.0
7.2 10.4 8.2 14.7
nV/mL 3.6 4.7 2.5 4.2
5.4 5.8 2.9 5.3
11-Deoxycortisol B
A
14.0 17.0 17.3 14.0
8.9 11.0 11.6 13.6
A
pg/mL 244 131 219 432
121 37 117 273
After Dexamethasone (1 mg Overnight)
