LETTERS AND CORRECTIONS

CONTENTS Percutaneous Transluminal Coronary Angioplasty D. H. Spodick 850 L G. Bentivoglio 850 Cholesterol and Clinical Decisions B. R. Zimmerman 851 Geriatric Medicine T. Harris 851 S. C Werch 852 Warfarin and Phenytoin Interaction J. M. Nappi 852 Heroin and Thrombocytopenia D. H Ryan 852 Hepatitis and Leukemia F. Rosner 853 References on Sodium-Retaining Potency of Corticosteroids L. Parker, A. Kutas, M. Bolognese, andR. Skowsky 853 Alkaline Phosphatase and Hyperthyroidism D. G. Oreopoulos 854 Myalgia and Elevated Creatine Phosphokinase with Danazol® in Hereditary Angioedema W. B. Spaulding 854 Hypothermia and Adrenocortical Function J. V. Felicetta and W. L Green 855 Salmonella Gastroenteritis in Older Patients M. I. Bowmer 855 Infections in Long-Term Care Facilities F. T. Sherman andL S. Libow 855

Interstitial Lung Disease and Cancer Chemotherapy J. R. Cohn Tube Feeding and Pyriformsinusotomy M. Block, T. J. Carmody, and J. T. Carson Colonoscopy and Barium Enemas R. H. Marshak F. J. Tedesco and J. D. Waye Oxacillin and Hepatitis C. Taylor, K. Corrigan, S. Steen, and C. Craig Cimetidine, Cloxacillin, and Pancytopenia E. L Westerman Psoriasis During Hemodialysis G. O. Perez, J. R. Oster, C A. Vaamonde, and K. M. Halprin Computed Tomography and Contrast Enhancement J. O. Greenberg, H. Houser, G. Shepherd, H. Harris, A. Alves, I. Mier, and G. Morley Epidural Lipomatosis from Corticosteroids B. R. Paull

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.

REFERENCES

Percutaneous Transluminal Coronary Angioplasty

T o T H E EDITOR: In their well-written editorial note in the February issue, Engel and Meister (1) raise appropriate caveats about the mixed blessings and potential dangers of the promising new mechanical procedure for coronary artery disease, transluminal balloon angioplasty. They also appropriately note its successes but include a well-reasoned caution. This was a needed analysis, yet it was profoundly disappointing not to find any reference to the need for appropriately designed controlled clinical trials with random allocation of comparable patients. If we are to compare this with any other treatment or with no treatment, trial-and-error is no longer acceptable. Surely, the F D A would not use this method for a new tablet or injection (2). The continuing immunity of surgical treatments and other mechanical procedures testifies to this "schizoid behavior'* of large segments of the medical profession (3). Lest we get into years of controversy over treatments such as the Vineberg operation, aortocoronary bypass, radical versus simple mastectomy, or the myriad procedures for peptic ulcer disease, we must not prematurely let this new genie out of its bottle. Since the publication bottleneck is the most efficient place to check the spread of unscientific (hence unethical) treatment evaluations, editorial matter should consistently and unflinchingly insist on appropriately designed controlled clinical trials. D A V I D H.

SPODICK, M.D.,

D.SC.

St. Vincent Hospital; Worcester, M A 01604 850

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Correction: Locations of Legionnaires' Disease Clusters 7". F. Tsai, D. W. Fraser, C. M. Helms, J. P. Viner, W. J. Hierholzer, R. J. Corry, E. D. Renner, and L A. Wintermeyer Correction: Temperature Correction for Oxygen Tension J. B. Reuler Correction: Annotated Bibliography

856 856 856 857 857 858

858

858 859

859 859 859

1. ENGEL TR, MEISTER SG: Coronary percutaneous transluminal angioplasty. Ann Intern Med 90:268-269, 1979 2. SPODICK DH: Numerators without denominators. There is no F D A for the surgeon. JAMA 232:35-36, 1975 3. SPODICK DH: The surgical mystique and the double standard: controlled trials of medical and surgical therapy for cardiac disease. Analysis, hypothesis, proposal. Am Heart J 85:579-583, 1973

T o T H E EDITOR: I read with interest the editorial note in the February issue by Drs. Engel and Meister (1) on percutaneous transluminal coronary angioplasty (PTCA), a fair account based on presentations at the American Heart Association Scientific Session in November 1978. Being directly involved in PTCA and in contact with the three other cardiologists using the technique, I write to update some of the data, sharpen the focus of comments in the note, and provide additional information. Since the first coronary dilatation by A. Griintzig in September 1977 (2), PTCA has been attempted in 158 patients in Europe and the United States. Dilatation has been successful in 88 patients, while in 70 the stenosis could not be relieved because of inability to [a] reach the lesion due to tortuosity of the vessel; [b] advance the catheter past the lesion due to eccentricity or excessive degree of stenosis; or [c] relieve the blockage by balloon inflation after proper positioning of the catheter because of excessive hardness of the plaque. Complications developed in nine of the 70 unsuccessful attempts, characterized angiographically by further narrowing or occlusion of the stenosis and clinically by chest pain and ST segment changes. Penetration and disruption of the plaque by the dilating catheter was the probable mechanism in eight patients. Seven underwent emergency coronary bypass surgery that was successful, without lasting sequelae; one patient died postoperatively after unsuccessful PTCA complicated by a small myocardial infarction. In the ninth patient the guiding catheter dissected the left main coronary artery, causing death on the table. Three deaths have occurred months after successful coronary dilation, two in pa-

tients with severe left main disease. Follow-up findings have been encouraging. Although stenosis has recurred in some patients, in most the diameter of the dilated lumen has either not varied or has seemed to widen further. How the inflating balloon relieves the stenosis is unknown at present; we favor the concept that the plaque contents are redistributed within the vessel wall, but expression of water from the atheroma and outward stretching of the vessel probably play a role. Mobilization of the displaced components of the plaque within the wall followed by scarring and retraction could take place subsequently. Balloon dilatation of the coronary arteries of cadavers has revealed instances of rupture of the plaque wall and release of its contents distally. Whether this has occurred in patients is not known; death does lead to vessel distortion and progressive, irreversible alterations in the entire body, including the arterial wall. Although the contents of an atheroma may embolize distally, especially during complicated PTCA, the complete lack of discomfort and ECG changes in most patients during and after the successful dilatation is against the frequent occurrence of this phenomenon. Some reports can be added to those referenced in the editorial note; see References 3-6 below. The small group of cardiologists initially entrusted with the balloon catheters have adhered to a fairly rigid protocol governing technique and indications. The responsibility of regulating this yet experimental technique in the United States logically falls on a government agency. The National Heart, Lung, and Blood Institute in Bethesda, Maryland, is in fact initiating a registry of cardiologists who have engaged in trials of PTCA to collect information on patients treated, indications, results, and complications. The trials of PTCA should be thereby disciplined, collection of meaningful data enhanced, and evaluation of data hastened; a PTCA workshop will be held in June. Besides its effectiveness in selected cases of coronary artery disease, little else is known about PTCA. Some likely avenues of research and possible applications have been outlined elsewhere (6). The ultimate value of PTCA vis-a-vis medical and surgical approaches remains to be ascertained. If PTCA is finally accepted for general clinical use, the impact on patient suffering and hospital costs could be substantial. In the meanwhile, those investigators involved in PTCA are proceeding with caution and care. L A M B E R T O G. B E N T I V O G L I O , M . D .

Medical College of Pennsylvania; Philadelphia, PA 19129 REFERENCES

1. E N G E L TR, MEISTER SG: Coronary percutaneous transluminal angioplasty. Ann Intern Med 90:268-269, 1979 2. G R U N T Z I G A: Transluminal dilatation of coronary-artery stenosis (letter). Lancet 1:263, 1978 3. G R U N T Z I G A, M Y L E R RK, H A N N A ES, T U R I N A MI: Coronary translu-

minal angioplasty (abstract). Circulation

56(suppl III):III-84, 1977

4. G R U N T Z I G A, M Y L E R R, S T E R T Z E R S, K A L T E N B A C H M, B E N T I V O G L I O

LG: Percutaneous transluminal coronary angioplasty—a study (abstract). Am J Cardiol 43:384, 1979

cooperative

5. G R U N T Z I G AR, S E N N I N G A, S I E G E N T H A L E R W: Non-operative dilata-

tion of coronary artery stenosis: percutaneous transluminal coronary angioplasty (PTCA). N Engl J Med, in press 6. BENTIVOGLIO LG: Bypassing the bypass with percutaneous transluminal coronary angioplasty (letter). Am J Cardiol 43: 866-867, 1979

Cholesterol and Clinical Decisions T o T H E EDITOR: Kannel and associates in the January issue provide an excellent review of the epidemiologic data relating lipids and lipoproteins to atherosclerosis (1). On the whole, the statistical significance obtained in these studies is impressive. Unfortunately, I believe that in the segment of their paper relating to clinical implications, the difference between statistical and clinical significance is not emphasized strongly enough and their recommendations will lead to an unnecessary increase in medical costs. A s can be clearly seen in their Figure 2, most patients with or without coronary heart disease have total serum cholesterol values ranging from 150 to 300 mg/dL. Cur-

rently there is no drug or dietary therapy that has been shown to be safe or effective in reducing atherosclerosis in patients with cholesterol values in the upper part of this range. Obtaining a high-density lipoprotein cholesterol value in these patients does not improve our ability to treat them and may lead to false security, allowing the patient and physician to ignore the risk indicators clearly shown to be more important than lipids in Figure 1. Total cholesterol and triglyceride determinations are adequate screening for patients with values greater than the 95th percentile where lipids may be the major risk indicators. Quantitative lipoprotein analysis may be helpful in some of these patients but not otherwise. Yearly screening with cholesterol and triglyceride determinations, and even more so with high-density lipoprotein cholesterol, in patients previously shown to have normal lipids, with a negative family history, and with no major change in their health is to be deplored. It serves no purpose except to enrich laboratories. The time for the "technology transfer" is not imminent. B R U C E R. Z I M M E R M A N , M . D .

Mayo Clinic; Rochester, M N 55901 REFERENCE 1. K A N N E L WB, C A S T E L L I WP, G O R D O N T: Cholesterol in the prediction

of atherosclerotic disease. New perspectives based on the Framingham study. Ann Intern Med 90:85-91, 1979

Geriatric Medicine T o THE EDITOR: As a recent medical school graduate interested in a career in geriatric medicine, I applaud Dr. Beeson's editorial in the February issue (1) and agree on many of the issues he raises. Medical educators are not, however, disinterested in responding to the needs of the elderly. Whether taught how to care for elderly persons or not, medical students are influenced by their experiences with these patients. Spence and associates (2) have documented that negative attitudes towards older persons grow from the first to the fourth year of medical school. Kutner (3) has found that experiences with the chronically ill and with older patients influence a student's specialty choice. A s the proportion of these patients increases on the wards, they will play an even greater factor, especially in the choice of internal medicine as a career. I am at present conducting a study of specialty choices and attitudes towards the elderly in graduating seniors that I hope will further document this and serve as an additional impetus towards change in medical education. Dr. Beeson cites the lack of quality nursing home facilities in which medical students and house staff can rotate for exposure to long-term care as a limitation in our ability to teach geriatric medicine. If only 20% of elderly persons ever reside in longterm care facilities, I question the wisdom of basing a teaching program around these patients, probably the most incapacitated and socially isolated of the "gerontocrats" of our society. Alternatively, I believe that the forum for teaching geriatric medicine already exists. Rather more representative are the older people who crowd into the ambulatory care facilities associated with many medical centers and often have house officers as their primary care physicians. Also more characteristic are older persons admitted to tertiary care facilities as acute admissions. For these patients we need to revamp our approach, not only to provide multisystem medical care, but also to mobilize relevant knowledge from psychiatry, rehabilitation, and social science from the outset with the aim of restoring the patient to the highest level of independent functioning he or she desires and is capable of achieving. Studies have shown that there is interest in geriatric medicine among physicians (4). I strongly urge that this education begin now, with the patients we serve at present as our resource. TAMARA HARRIS, M.D.

Montefiore Hospital; Bronx, N Y 10467 REFERENCES

1. BEESON PB: Training doctors to care for old people. Ann Intern Med 90:262-263, 1979 Letters and Corrections

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851

2. S P E N C E D, F E I G E N B A U M E, F I T Z G E R A L D F, R O T H J: Medical student

attitudes toward the geriatric patient. J Am Geriatr Soc 16:976-983, 1968 3. K U T N E R N: Medical students' orientation toward the chronically ill. / MedEduc 53:111-118, 1978 4. G R U B E R H: Geriatrics—physician attitudes and medical school training. J Am Geriatr Soc 25:494-496, 1977

T o THE EDITOR: The importance of a geriatric rotation in a general internal medicine residency is being widely recognized. Training in general internal medicine should include experience in the diagnosis and treatment of multiple chronic diseases in a single patient, as well as experience in the medical care of acute problems of the aged. A well-established geriatric institution is where such experiences are best secured. The plan for a geriatric rotation in general internal medicine at the Iowa Veterans Home and Geriatric Center may be of interest to your readers. It covers a period of 2 months, and the rotation can be included in the senior year as part of the established program or as an elective rotation. The Iowa Veterans Home and Geriatric Center is a progressive geriatric institution located in a park-like setting in a pleasant, central Iowa city of 29 000. Veterans and their spouses, or surviving spouses, now numbering 600 and increasing to 750 by 1980, are offered medical care and rehabilitation. Since the institution is a home for the patients, ambulatory as well as intermediate and extended medical care is included. Members of the departments of social service, activities, and occupational, physical, and speech therapy contribute to the team approach. Residents are assigned in rotation to ambulatory, intermediate, and extended medical care units, where they function under the supervision of experienced internists but where independent decisions are fostered in respect for their mature clinical judgment. Seminars introduce the residents, in the first week of the seminar program, to geriatric medicine and the aging process. The second week's topics deal with the psychosocial factors in aging. During the third and fourth weeks the focus is on medicine and aging. During the sixth week geriatric research, as well as nutrition and dentistry in the aged, is discussed. The practical problems of geriatric care are considered during the last 2 weeks of the rotation. Residents are given a collateral reading list for the above seminar topics, and the staff library, in the charge of a professional librarian, is available to them evenings and weekends, as well as during the day. The library is classified according to the National Library of Medicine Classification and includes not only the core list of books and journals recommended for hospital health-science libraries by the University of Iowa, but much more. The library bibliography, dated July 1978, not only has books related to geriatric medicine but also many others in relevant categories not included in the basic list from the University of Iowa. S. C. W E R C H , M . D .

Iowa Veterans Home and Geriatric Center; Marshalltown, IA 50158 Warfarin and Phenytoin Interaction T o THE EDITOR: In their excellent review on antiepileptic drugs in the February issue, Drs. Penry and Newmark (1) note that dicumarol may prolong the half-life of phenytoin. The potential interaction of warfarin and phenytoin was not mentioned and deserves attention, since both of these drugs are commonly prescribed. The package insert (2) does not list phenytoin as a drug that can influence the prothrombin time of a patient maintained on warfarin therapy. Deykin (3), however, includes phenytoin in a group of drugs that may potentiate the action of warfarin, presumably by inhibiting its metabolism. Koch-Weser (4) has reported this drug interaction to be clinically significant. Recently I have seen two patients who were stabilized on maintenance doses of warfarin and had significant elevations of their prothrombin times when phenytoin was added to their regimen. In one case the patient had been receiving 2.5 mg of 8 5 2

May 1979

• Annals of Internal Medicine • Volume 90 • Number 5

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warfarin 5 days a week and 5 mg of warfarin 2 days a week. Prothrombin times were never greater than 21 seconds, with a control time of 12 seconds. Phenytoin, 300 mg daily, was added for arrhythmia control, and even though warfarin was decreased to 2.5 mg daily the patient's prothrombin time was 32 seconds (control value, 12 seconds) within a month. Phenytoin therapy was discontinued, and the patient's prothrombin time was again controlled on his former warfarin regimen. It is difficult to ascertain to what extent phenytoin influences the metabolism of warfarin. It is thought that warfarin may inhibit the metabolism of phenytoin (5). Clinicians should be alerted to the potential drug interaction between phenytoin and warfarin and, as with any drug added to a patient maintained on warfarin, should monitor prothrombin times at frequent intervals. J E A N M. N A P P I ,

PHARM.D.

School of Pharmacy; University of Wisconsin Madison, WI 53706 REFERENCES 1. P E N R Y JK, N E W M A R K ME: The use of antiepileptic drugs. Ann

2. 3. 4. 5.

Intern

Med 90:207-218, 1979 Product information. Garden City, New York, Endo Laboratories, Inc., March 1977 D E Y K I N D: Warfarin therapy. N Engl J Med 283:801-803, 1970 K O C H - W E S E R J: Hemorrhagic reactions and drug interactions in 500 warfarin-treated patients (abstract). Clin Pharmacol Ther 14:139, 1973 Adverse interactions of drugs. Med Lett Drugs Ther 21:5-12, 26 January 1979

Heroin and Thrombocytopenia T o THE EDITOR: We wish to add our experience to those reported by Adams and colleagues in their paper "Thrombocytopenia and Intravenous Heroin Use" in the September 1978 issue (1). In 1976 and 1977 we saw five active intravenous heroin users (all men) who had profound thrombocytopenia, increased megakaryocytes in the bone marrow, and rapid response during hospitalization with steroid treatment or splenectomy, or both. When one patient again injected heroin, his thrombocytopenia recurred. Nonimmunologic causes were excluded. None of the patients had evidence of hypersplenism. Laboratory results excluded disseminated intravascular coagulation. All five patients had normal prothrombin and partial thromboplastin times. None of the five had fragmentation of erythrocytes. Fibrinogen level was normal in the two patients in whom it was measured. None of the patients had had an antecedent viral illness. All five patients were treated with prednisone, 40 to 60 mg/m 2 , and four patients underwent splenectomy 3 to 6 days after admission. Platelet counts were normal immediately after splenectomy in those four patients and on Day 6 in the fifth patient. In two patients, platelet aggregometry studies (2) were done with serum, normal platelets, and quinine and quinidine in an attempt to detect activity of antiplatelet antibodies induced by these two common heroin adulterants known to cause immunologic thrombocytopenia. The results of these tests were negative. Our experience with one patient provided strong evidence that heroin was causing the thrombocytopenia. When that patient used intravenous heroin 5 months after diagnosis, at a time when his platelet count was elevated, we documented the occurrence of thrombocytopenia with recovery of platelet count to normal in 1 week. Unlike Adams and associates, we found no clustering of cases within a short interval. In a retrospective analysis, however, we could find no cases of thrombocytopenia in heroin users at Charity Hospital at New Orleans before 1976, although substantial numbers of heroin addicts with various other medical problems had been encountered in earlier years. We think a change in the composition of heroin might account for thrombocytopenia as a new finding. Harold C. Patin, chief of compli-

ance of the local Drug Enforcement Administration, reports a gradual change in the character of confiscated heroin in our area from pure white heroin imported through Europe to brown heroin imported from Mexico. All confiscated heroin in the New Orleans area since 1976 has been brown heroin. We think heroin itself or the classic adulterants quinine or quinidine are unlikely to be responsible for thrombocytopenia in our patients because that complication is a recent finding in our addict population. T h e occurrence of such cases since 1976 leads us to suspect a recently added constituent of heroin as the causative factor, perhaps related to the influx of brown heroin in our area. D O N N A H. R Y A N , M . D .

Louisiana State University Medical Center; New Orleans, L A 70112 REFERENCES 1. ADAMS WH, RUFO RA, TALARICO L, SILVERMAN SL, BRAUER MJ:

Thrombocytopenia and intravenous heroin use. Ann Intern Med 89:207211, 1978 2. DEYKIN D, HELLERSTEIN LJ: The assessment of drug-dependent and

isoimmune antiplatelet antibodies by the use of platelet aggregometry. / Clin Invest 51:3142-3153, 1972 Hepatitis and Leukemia T o T H E EDITOR: Barton and Conrad suggest in the February issue (1) that hepatitis may have a beneficial effect in acute myelocytic leukemia. They postulate that hepatitis may directly suppress the leukemia or that leukemic patients with hepatitis may be those with "greater immunocompetence and thus a better prognosis." Several additional hypotheses should be considered. Patients with increased S G O T levels may not have hepatitis at all; rather their hepatocytes (and their leukemic cells) may be more sensitive to the antileukemic chemotherapy. For example, these patients may be lacking in cytarabine deaminase, thus accounting for higher and more prolonged cytarabine levels. Another explanation of Barton and Conrad's findings might be that the hepatitis virus potentiates entry of antileukemic drugs into leukemic (and perhaps liver) cells, thus accounting for a longer remission duration. The well-known association of aplastic anemia after hepatitis (2, 3) has not been emphasized by Barton and Conrad. Perhaps the hepatitis virus is as lethal to leukemic cells as it is to normal hematopoietic tissue in patients whose bone marrow cells are suppressed by this virus.

References on Sodium-Retaining Potency of Corticosteroids T o T H E EDITOR: There are two major reasons to measure accurately the mineralocorticoid potency of a corticosteroid preparation. First, a corticosteroid must be used for its anti-inflammatory effect without inducing excessive sodium retention that causes edema and congestive heart failure. Second, the choice of replacement therapy in a patient with primary adrenal insufficiency depends on the ratio of glucocorticoid to mineralocorticoid activity. A corticosteroid preparation with little or no sodium-retaining properties must often be supplemented with a more potent mineralocorticoid to prevent hyperkalemia, hypotension, or vascular collapse. Comparison of the reported mineralocorticoid potencies of some widely used corticosteroids, as listed in standard reference works (1-11), revealed numerous discrepancies. T h e data are tabulated in Table 1, with hydrocortisone standardized as " 1 . 0 " (1-8) or "2 + " (9-11). One standard reference listed no table but stated that prednisone "has no significant mineralocorticoid activity . . . [and is] inadequate as the sole agent in the treatment of adrenocortical insufficiency" (12). This conflicts with data in Table 1. These discrepancies may result in part from the different assay systems and dosages used to test the mineralocorticoid potency of the corticosteroid preparations. Further, not all of the standard references used studies in the human model, but rather in other species such as rats, mice, and dogs (13-16). Many of the standard sources do not give references for their mineralocorticoid data tables. We suggest that to avoid unnecessary confusion among physicians and to avoid excessive morbidity and mortality in patients receiving corticosteroid preparations, tables of mineralocorticoid potency should [a] reference their data, [b] reference human studies only, and [c] list mineralocorticoid potency specifically at physiologic glucocorticoid replacement dosages as compared with pharmacologic dosages. LAWRENCE PARKER, ALEX KUTAS, M I C H A E L BOLOGNESE, R O N A L D SKOWSKY,

Veterans Administration Medical Center; Long Beach, C A 90822 REFERENCES

1. GOODMAN LS, GILMAN A: The Pharmacological Basis of Therapeutics, 5th ed. New York, Macmillan Publishing Co., Inc., 1975, p. 1491 2. THORN GW, ADAMS RD, BRAUNWALD E, ISSELBACHER KJ, PETERS-

F R E D ROSNER, M.D.

Queens Hospital Center Affiliation of Long Island Jewish-Hillside Medical Center; Jamaica, N Y 11432 REFERENCE'S

3. 4. 5.

1. BARTON JC, CONRAD ME: Beneficial effects of hepatitis in patients with acute myelogenous leukemia. Ann Intern Med 90:188-190, 1979 2. ROSNER F: Aplastic anemia and viral hepatitis. Lancet 2:1080, 1970 3. HAGLER L, PASTORE RA, BERGIN JJ: Aplastic anemia following viral hepatitis. Report of two fatal cases and literature review. Medicine (Baltimore) 54:139-164, 1975

M.D. M.D. M.D. M.D.

6. 7.

DORF RG (eds.): Harrison's Principles of Internal Medicine, 8th ed. New York, McGraw-Hill Book Co., 1977, p. 554 WILLIAMS RH (ed.): Textbook of Endocrinology, 5th ed. Philadelphia, W. B. Saunders Company, 1974, p. 246 BONDY PK, ROSENBERG LE (eds.): Duncan's Diseases of Metabolism, 7th ed. Philadelphia, W. B. Saunders Co., 1974, p. 1131 ROSENFELD MG (ed.): Manual of Medical Therapeutics (Washington University) 22nd ed. Boston, Little, Brown and Co., 1977, p. 351 HOLLANDER JL, MCCARTY DJ JR: Arthritis and Allied Conditions: A Textbook of Rheumatology, 8th ed. Philadelphia, Lea and Febiger, 1972, p. 503 GARDNER LI (ed.): Endocrine and Genetic Diseases of Childhood and Adolescence. Philadelphia, W. B. Saunders Co., 1975, p. 532

Table 1. Relative Mineralocorticoid Potency

Corticosteroid

Hydrocortisone (Cortisol) Prednisone Methylprednisolone (Solu- Medrol®) Dexamethasone U-desoxycorticosterone (DOC) Fludrocortisone (Florinef®)

Reference 1

2

3

4

5

6

7

8

9

10

11

1.0 0.8 0.5 0 100 125

1.0 0.3 0 0

1.0 0.7 0.5 2.0 20 400

1.0 1.3 0.7 0 33 140

1.0 0.8 0.5 0.5

1.0 0.8 0 0

1.0 0.3

1.0 0.8 0 0

2+ 1+ 0 0

2+ 1+ 0 0

2+ 140 0

0 15

Letters and Corrections

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853

8. Medical Letter. New York, The Medical Letter, Inc., 1977, p. 100 9. THORN GW, LAULER DP: Clinical therapeutics of adrenal disorders. Am J Med 53:673-684, 1972 10. FAUCI AS, D A L E DC, B A L O W JE: Glucocorticosteroid therapy: mechanisms of action and clinical considerations. Ann Intern Med 84:304-315, 1976 11. M O V E R CA (ed.): Surgery: Principles and Practice. Philadelphia, J. B. Lippincott Co., 1965, p. 725 12. AM A D E P A R T M E N T OF D R U G S : AMA Drug Evaluations. Littleton, Massachusetts, Publishing Sciences Group, Inc., 1977, p. 526 13. L I D D L E GW: Studies of structure-function relationships of steroids. Metabolism 7:405-415, 1958 14. M A R C U S F, R O M A N O F F LP, PINCUS G: The electrolyte-excreting activi-

ty of adrenocortical substances. Endocrinology

50:286, 1952

15. L I D D L E GW, P E C H E T MM, B A R T T E R FC: Enhancement of biological

activities of corticosteroids by substitution of halogen atoms in 9 «-position. Science 120:496, 1954 16. TOLKSDORF S: Laboratory evaluation of anti-inflammatory steroids. Ann NY Acad Sci 82:829, 1959

Alkaline Phosphatase and Hyperthyroidism T o T H E EDITOR: Dr. Cooper and colleagues mention in their recent article "Alkaline Phosphatase Isoenzyme Patterns in Hyperthyroidism" in the February issue (1), that "bone healing in patients with hyperthyroidism may take a prolonged period"; they also observed that "serum alkaline phosphatase may not return to normal for 18 to 24 months after treatment." Further, they mention that the enzyme pattern of alkaline phosphatase from normal before treatment converts to predominant bone in origin after treatment. Velentzas and colleagues (2) have shown that patients with hyperthyroidism have significantly lower plasma levels of 25 hydroxy-vitamin D than do normal controls subjects. Possibly the changes they describe are the result of vitamin D depletion and the healing process is accelerated with administration of vitamin D . D . G. O R E O P O U L O S , M . D . , P H . D . Toronto Western Hospital; Toronto, O N M5T 2S8, Canada REFERENCES

The patient was begun on Danazol therapy, 200 mg three times daily. Medication was continued for nearly a year (Figure 1). During this time she had no episodes of abdominal pain or swelling. Dental work was carried out uneventfully. However, a few days after the start of Danazol therapy she had recurrent, superficial, right-sided chest pain radiating to her arms and back and lasting about 20 minutes. When the dose of Danazol was reduced to 200 mg twice daily, the aching pain decreased in frequency to once or twice a week, lasting about 5 minutes. Sometimes she had aching or cramps in the lower limbs. During the last half of her treatment with Danazol, cramps and aches occurred about once a month. Coincident with Danazol therapy, C P K was elevated or high normal with a peak of 531 I U / L of plasma. At the same time the CI esterase inhibitor activity and C4 levels rose towards or entered the low normal range (Figure 1). When Danazol was withdrawn, the attacks of abdominal pain recurred every 2 or 3 weeks. The level of CPK fell to normal. There was a fall in the levels of CI esterase inhibitor and C4. Danazol is being used increasingly in the management of endometriosis. It suppresses the midcycle surge of luteinizing and, follicle stimulating hormones and may produce anovulation. Generally the drug is well tolerated and can be administered for long periods. I report this case to draw attention to myalgia and an elevated CPK level as a side effect of Danazol. Muscle spasms or cramps have been reported in 28 of 704 patients (4%), mainly in a dose of 800 mg daily (4), and in a similar percentage in another group of 452 patients (3). The finding of an elevated CPK level in conjunction with myalgia is presumptive evidence of damage to voluntary muscle. Further observations are needed to document the nature and severity of the change in muscle. W I L L I A M B. S P A U L D I N G , M . D . McMaster University; Hamilton, O N L8S 4J9, Canada

REFERENCES

1. POTTS GO: Pharmacology of danazol. / Int Med Res 5(suppl 3): 1-14, 1977 2. G E L F A N D JA, SHERINS RJ, A L L I N G DW, F R A N K MM: Treatment of

hereditary angioedema with danazol. Reversal of clinical and biochemical abnormalities. TV Engl J Med 295:1444-1448, 1976 3. Y O U N G MD, BLACKMORE WP: The use of danazol in the management of endometriosis. J Int Med Res 5(suppl 3):86-91, 1977 4. SPOONER JB: Classification of side-effects to danazol therapy. / Int Med Res 5 (suppl 3): 15-17, 1977

1. COOPER DS, K A P L A N MM, R I D G W A Y EC, M A L O O F F, D A N I E L S G H :

Alkaline phosphatase isoenzyme patterns in hyperthyroidism. Ann Intern Med 90:164-168, 1979 2. V E L E N T Z A S C, OREOPOULOS DG, F R O M G, P O R R E T B, R A P O P O R T A:

Vitamin-D levels in thyrotoxicosis (letter). Lancet 1:370-371, 1977

Myalgia and Elevated Creatine Phosphokinase with Danazol® in Hereditary Angioedema

T o T H E EDITOR: Danazol®, a synthetic steroid that inhibits pituitary gonadotropins (1), is effective in preventing attacks of hereditary angioedema (2). Side effects are minor, the commonest being menstrual irregularities or amenorrhea, weight gain, edema, and acne (3). Muscle aching has been mentioned without reference to the plasma level of creatine phosphokinase (CPK) (3, 4). The following summary describes the case of a patient with hereditary angioedema whose attacks stopped when she took Danazol but who had muscle cramps and aching with elevated CPK levels until Danazol was withdrawn. The patient, a 40-year-old woman, began to have bouts of abdominal colic at age 10. The colic would be severe for 24 h, sometimes associated with vomiting, and then subside over a couple of days. Abdominal attacks occurred about once every 3 weeks. Since age 24 she had had attacks of swelling involving her hands, feet, arms, face, throat, and vulva. The swellings that occurred every few months would spread over 24 h, then subside. They tended to occur a few days after menses. Throat and facial swellings had occurred after dental work and indirect laryngoscopy. Plasma levels of CI esterase inhibitor and the fourth component of complement (C4) were below normal. Only three relatives, the mother and two siblings, were available for study. None had a history of angioedema or low levels of CI esterase inhibitor. 854

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Figure 1 . Increases in serum concentrations of creatine phosphokinase (CPK), C I esterase inhibitor (CI EST INH), and the fourth component of complement (C4) during treatment with Danazol®.

Hypothermia and Adrenocortical Function T o T H E EDITOR: In his review of hypothermia in the October 1978 issue, Reuler (1) includes a diagram that suggests cold exposure stimulates the pituitary gland, which in turn stimulates secretion by the thyroid and adrenal glands. Although increased thyroid-stimulating hormone output in response to cold has been demonstrated in other species and in the human neonate, several investigators have been unable to document this phenomenon in the adult human (2). Acute cold exposure does stimulate Cortisol secretion. In hypothermic patients, however, we have found (3) that adrenal responsiveness to ACTH is lost and Cortisol levels may be in the normal range despite severe stress. Adrenal unresponsiveness to ACTH has been demonstrated in hypothermic dogs (4); also, Cortisol levels are relatively low during hypothermic surgery (5). One point we have made from these findings is that a diagnosis of chronic adrenal insufficiency should not be based on results of ACTH testing during hypothermia. A second possible conclusion is that hypothermia leads to a functional adrenal insufficiency for which glucocorticoid treatment is appropriate; such treatment has been used in Great Britain for some time (6). A controlled study of the efficacy of glucocorticoid treatment in hypothermic patients has not been done but deserves consideration. J A M E S V. F E L I C E T T A , M . D . W I L L I A M L. G R E E N , M . D .

University of Washington; Seattle, WA 98195 REFERENCES

1. REULER JB: Hypothermia: pathophysiology, clinical settings, and management. Ann Intern Med 89:519-527, 1978 2. WOOLF PD, HOLLANDER CS, MITSUMA T, LEE LA, SCHALCH DS: Ac-

cidental hypothermia: endocrine function during recovery. / Clin Endocrinol Metab 34:460-466, 1972 3. FELICETTA JV: False diagnosis of decreased adrenal reserve in the hypothermic subject (abstract). Clin Res 27:20A, 1979 4. GANONG WF, BERNHARD WF, MCMURRAY JD: The effect of hypother-

mia on the output of 17-hydroxycorticosteroids from the adrenal vein in the dog. Surgery 38:506-512, 1955 5. SWAN H, JENKINS D, HELMREICH ML: The adrenal Cortisol response to

surgery. III. Changes in plasma corticosteroid levels during hypothermia in man. Surgery 42:202-217, 1957 6. EXTON-SMITH AN: Accidental hypothermia. Br Med J 4:727-729, 1973 Salmonella Gastroenteritis in Older Patients T o T H E EDITOR: I read with interest the recent paper by Cohen and colleagues in the December 1978 issue (1) but was extremely concerned about their final statement that antibiotics may be indicated for the treatment of acute salmonella gastroenteritis in patients older than 50 years. Although their retrospective study does appear to identify this age group as being at high risk for endothelial infection, their criteria for selection identified only adult patients with bacteremia. We are not given the total number of patients with salmonella gastroenteritis for the same period and, specifically, the number of patients who are older than 50 years of age. Their own review of the literature from 1958 to 1974 provided only 46 cases of salmonella arteritis. Cherubin and co-workers (2) in their study of more than 5800 cases of salmonellosis reported a 5% incidence of septicemia. They recognized that patients who were older than 60 years of age constituted a high-risk group. Even so, only 18% of patients over 60 with acute salmonella gastroenteritis actually had septicemia. Since Cohen and colleagues (1) also identify the high-risk group as including those with infection evident before hospital admission, perhaps a better recommendation would be that patients with acute salmonella gastroenteritis who are over 50 years of age and have underlying disease should be recognized as a high-risk group. Close follow-up of these patients is needed, and blood cultures should be part of that investigation.

With Cherubin's figures and Cohen's current recommendation, more than 80% of patients would be treated unnecessarily, but in view of the prolonged fecal excretion of salmonella and the increased frequency of resistant stool isolates (3), the approach suggested by the authors raises a definite question of cost and risk versus benefit. M. I A N B O W M E R , M . D .

Memorial University of Newfoundland; St. John's, N F A1B 3V6, Canada REFERENCES 1. COHEN PS, O'BRIEN TF, SCHOENBAUM SC, MEDEIROS AA: The risk of

endothelial infection in adults with salmonella bacteremia. Ann Intern Med 89:931-932, 1978 2. CHERUBIN CE, NEU HC, IMPERATO PJ, HARVEY RP, BETTEN N: Sep-

ticemia with non-typhoid salmonella. Medicine (Baltimore) 53:365-376, 1974 3. ASERKOFF B, BENNETT JV: Effect of antibiotic therapy in acute salmonellosis on fecal excretion of salmonellae. N Engl J Med 281:636-640, 1969 Infections in Long-Term Care Facilities T o THE EDITOR: We have just completed our report on infection surveillance in a skilled nursing facility (1) and were struck by the absence of such a focus in the National Institute of Allergy and Infectious Disease's recent symposium, "The Impact of Infection on Medical Care in the United States: Problems and Priorities for Future Research" (2). The symposium addressed itself mainly to bacterial infections acquired in the community as well as in the one million acute hospital beds in this country. None of the authors who discussed problems needing clinical investigation referred to infection surveillance or control among approximately 2.2 million patients per year who occupy the 1.3 million beds in 18 300 nursing homes. Neither the State of New York in its Hospital Code, nor the Federal government in discussing infection control in its Medicare regulated facilities, nor the Joint Commission on Accreditation of Hospitals in its Accreditation Manual for Long-Term Care, adequately defines the common infection control problems, provides for infection surveillance, or mandates the implementation of cost-effective measures to prevent problems in infection control among this predominantly elderly population. Recently, there have been reports of investigations into the change in oropharyngeal flora of patients and staff in long-term care facilities (3), and the bacteriologic characteristics of pneumonia in elderly patients admitted to acute hospitals from nursing homes (4). Our own preliminary data suggest that urinarytract infections are the most commonly reported infections in skilled-nursing facilities and that the pathogen is different depending on whether the patient was hospitalized in the weeks before admission {Escherichia coli or Pseudomonas aeruginosa) or had been residing in the institution for a more prolonged period (E. coli or Proteus species). Continued efforts are needed to provide a data base for defining the characteristics and scope of the problem. We recommend the following. 1. The term "nonsocomial infection" should be expanded to include not only infections acquired in acute hospitals but also in long-term care facilities. The National Nosocomial Infections Study should include a representative sample of the various types (intermediate care and skilled nursing) and sizes of longterm care facilities, so that the bacteriologic characteristics of infections affecting these groups of elderly, chronically ill, institutionalized patients can be explored and cost-effective control measures can be implemented to prevent such infections. 2. Because one third of all admissions to nursing homes and three quarters of all admissions to skilled-nursing facilities come from acute hospitals, clarifying the impact of hospital-acquired flora on the flora and specific infection rates in nursing home residents is important. The use of potent antibiotics may have far-reaching effects outside the realm of the acute hospital. Letters and Corrections

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Upper and lower respiratory-tract infections and asymptomatic bacteriuria require specific attention. 3. Based on surveillance data and controlled trials, attempts should be made to ascertain the most reliable, reasonable, and cost-effective methods to control influenza, pneumonia, and gastroenteritis among nursing home residents, staff, and visitors. Guidelines should be developed for the prevention and treatment of these infections in long-term care facilities to avoid unnecessary hospitalization. When indicated, procedures and concepts gleaned from the acute hospital experience should be applied. Otherwise, recommendations should be implemented based on an organized, planned approach to infection surveillance and control in longterm care facilities. F R E D R I C K T. S H E R M A N , M . D . L E S L I E S. L I B O W , M . D .

Division of Geriatric Medicine, Jewish Institute for Geriatric Care at Long Island Jewish Hillside Medical Center, School of Medicine, State University of New York at Stony Brook; New Hyde Park, N Y 11042 REFERENCES

1. SHERMAN FT, T u c c i V, L I B O W LS: Nosocomial urinary tract infections in a skilled nursing facility. 31st Annual Scientific Meeting of the Gerontological Society 1978 2. K U N I N CM, EDELMAN R (eds.): The impact of infections on medical care in the United States. Problems and priorities for future research. Ann Intern Med 89:737-866, 1978 3. V A L E N T I WM, T R U D E L L R G , B E N T L Y DW: Factors predisposing to

oropharyngeal colonization with gram-negative bacilli in the aged. N Engl J Med 298:1108-1 111, 1978 4. G A R B JL, B R O W N RB, G A R B JR, T U T H I L L RW: Differences in etiology

of pneumonias in nursing 240:2169-2173, 1978

home and community

patients.

JAMA

Interstitial Lung Disease and Cancer Chemotherapy T o T H E EDITOR: Dr. Durant and his associates in the Southeastern Cancer Study Group (SECSG) reported in the February 1979 issue (1) 10 patients who developed an interstitial pulmonary disease while undergoing multiple-agent antineoplastic regimens that included bischlorethylnitrosourea (BCNU). Their patients presented with signs and symptoms of respiratory distress, resting hypoxia, diffusion abnormalities, a restrictive pattern on pulmonary function testing, and, frequently, infiltrates found on chest roentgenogram. Nine of their patients were concurrently receiving cyclophosphamide. As they noted, this agent has already been implicated as a cause of drug-induced pulmonary disease (1-5). The clinical, laboratory, and pathologic findings in the previous cases of cyclophosphamide toxicity are essentially identical to those found by the SECSG in their patients who received both cyclophosphamide and BCNU. All are nonspecific abnormalities and have been associated with bisulfan and bleomycin use, as well (2). The one difference between this most recent series and previous reports of cyclophosphamide toxicity is the relatively high mortality, 60%, found by the SECSG. Most (3) but clearly not all (4-6) patients with cyclophosphamide-induced pulmonary disease improve with cessation of the drug. This single disparity is too small and the circumstances too diverse, however, to foster any new conclusions. Overall, apparently a strong case can be made for cyclophosphamide as the cause of the pulmonary toxicity reported. Whether there is an additive or synergistic toxic effect from B C N U is a question that will only be answered by further experience and detailed analyses. Unfortunately, there is little comparative basis for examining the 1.1% frequency of pulmonary toxicity found by the SECSG. Telling whether this supports an argument for combined toxicity, or, conversely, represents a "protective" effect from the concurrently administered prednisone, a drug that has been used to treat this type of fibrosis, is impossible. Interestingly, the authors of this paper believed that their rate of pulmo8 5 6

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nary toxicity was lower than that reported by others. Dr. Durant and his colleagues deserve much credit for their extensive study. One hopes it will inspire others to do likewise, so that these questions can be resolved. J O H N R. C O H N , M . D .

Jefferson Medical College, Thomas Jefferson University; Philadelphia, PA 19107 REFERENCES 1. D U R A N T JR, N O R G A R D MJ, M U R A D TM, BARTOLUCCI AA, L A N G -

FORD K.H: Pulmonary toxicity associated with bischloroethylnitrosourea (BCNU). Ann Intern Med 90:191-194, 1979 2. ROSENOW EC: The spectrum of drug-induce pulmonary diseases. Ann Intern Med 77:977-991, 1972 3. P A T E L AR, SHAH PC, R H E E HL, SASOON H, R A O K P : Cyclophospham-

ide therapy and interstitial pulmonary fibrosis. Cancer 1976

38:1542-1549,

4. D O H N E R VA, W A R D HP, S T A N D A R D RE: Alveolitis during procarba-

zine, vincristine and cyclophosphamide therapy. Chest 62:636-639, 1972 5. T O P I L O W AA, R O T H E N B E R G SP, C O T T R E I L TS: Interstitial pneumonia

after prolonged treatment with cyclophosphamide. Am Rev Respir Dis 108:114-117, 1973 6. Case records of the Massachusetts General Hospital (Case 12-1978). N Engl J Med 1978; 13:729-736

Tube Feeding and Pyriformsinusotomy T o T H E EDITOR: Heymsfield and colleagues in the January 1979 issue (1) have recently described various enteral modalities of alimentation. In addition to nasogastric enteral feeding tubes we have found the use of tube-feeding via the pyriformsinusotomy procedure described by Schumrick (2) to be useful. With swallowing abnormalities resulting from cerebrovascular accidents and other conditions, this procedure offers the advantages of reduced risk of aspiration and subsequent pneumonitis in long-term alimentation; also, because the tube may be removed between meals and reinserted with little difficulty, the complications inherent with long-term nasogastric intubation are avoided, that is, esophageal erosion, ulcers, tracheoesophageal fistula formation, and so forth. We have found in patients requiring long-term enteral alimentation that the pyriformsinsusotomy approach is more acceptable and better tolerated than the more conventional alternatives of long-term nasogastric intubation or gastrostomy. M A L C O L M BLOCK, M.D. T H O M A S J. C A R M O D Y , M . D . J. T U R N E R C A R S O N , M . D .

The Good Samaritan Hospital and Health Center; Dayton, OH 45406 REFERENCES 1. H Y M E S F I E L D S, B E T H E L RA, A N S L E Y J D , N I X O N DW, R U D M A N D:

Enteral hyperalimentation: an alternative to central venous hyperalimentation. Ann Intern Med 90:63-71, 1979 2. SHUMRICK D: Pyriformsinusotomy. Arch Surg 94:277-279, 1967

Colonoscopy and Barium Enemas T o THE EDITOR: I write to respond to the article by Tedesco and associates in the December 1978 issue (1). The validity of this study should be questioned because (as the author states in the Material and Methods section), the barium enema results were taken from reports on hospital charts in a retrospective study. That some of the films were reviewed but the number of cases that were reviewed or the identity of the reviewers is not given is stated. Roscoe Miller (2) has published an article citing 54 colonoscopic errors. Rather than encouraging cooperation with radiologists, the article stirs a controversy. Barium enemas done by myself or my peers approach 100% accuracy. If the colon is thoroughly cleansed and proper technique is used, barium enema examinations done by competent radiologists interested in the gastrointestinal tract should yield similar results. The one-line state-

ment in the discussion that colonoscopy and contrast barium enemas should be complementary does not alter the main thrust against radiology. A presumed error rate of 41.5% would be regrettable and certainly does not reflect the experience of competent radiologists throughout the country. R I C H A R D H.

MARSHAK,

M.D.

Mt. Sinai School of Medicine, Mt. Sinai Hospital, New York, NY 10028

bleeding site has not been found by proctosigmoidoscopy or a barium enema roentgenographic examination. F R A N C I S J. T E D E S C O ,

M.D.

Medical College of Georgia; Augusta, G A 30901 JEROME D. W A Y E ,

M.D.

Mt. Sinai Hospital; New York, N Y 10028 REFERENCES 1. SWARBRICK ET, FEVRE DI, HUNT RH, THOMAS BM, WILLIAMS CB:

REFERENCES 1. TEDESCO FJ, WAYE JD,

RASKIN JB, MORRIS SJ, GREENWALD

RA:

Colonoscopic evaluation of rectal bleeding. A study of 304 patients. Ann Intern Med 89:907-909, 1978 2. MILLER RE, LEHMAN G: Polypoid colonic lesions undetected by endoscopy. Radiology 129:295-297, 1978 In comment: Dr. Marshak has seemed to miss the point of our article. We have shown that patients with rectal bleeding need further evaluation if a previous proctosigmoidoscopy and single-contrast barium enema fail to show the cause of bleeding. In our studies, all barium enemas were done either by competent radiologists in private practice or at university centers. We used the reports rendered by the radiologists as would most physicians using their services. We were not attempting to initiate a "controversy" but rather to define the approach to a patient with unexplained rectal bleeding after proctosigmoidoscopy and barium enema. It is indeed "regrettable" that Dr. Marshak seized upon the number of 41.5% as the amount of "error rate" of barium enemas. That is erroneous and a misinterpretation of the facts in this article. This article states that colonoscopy can significantly increase the diagnostic yield in unexplained rectal bleeding, and when all other diagnostic methods fail to find the bleeding site, colonoscopy will identify a bleeding site in 41.5% of those patients. Dr. Marshak might be interested in seeing how our data compare with those from three studies in England (Table 1). A large number of the barium studies in these reports were double-contrast studies. A review of the barium enemas would be worthwhile if an attempt were actually made to compare the two modalities of roentgenogram and colonoscopy. However, the intent of this paper was to start with a dilemma that the clinician is faced with, that is, a report of a "normal barium enema or one showing only diverticulosis" in a patient with unexplained rectal bleeding. Although Dr. Marshak states that "barium enemas done by myself or my peers approach 100% accuracy," radiologists, in fields other than gastroenterology, do not consider it a "lack of cooperation" when endoscopic methods are used to visualize body cavities in bleeding patients where radiology has not shown the site of bleeding. Are Sanderson and Zavala (5, 6) guilty of not cooperating because they have found a significant number of carcinomas in patients with hemoptysis and negative chest roentgenograms? Are urologists not "cooperating" when they cystoscope patients with hematuria and a negative intravenous pyelogram? Should gastroenterologists "cooperate" and stop causing "controversies" by discontinuing upper gastrointestinal endoscopy for patients with hematemesis? We believe that we have shown the desirability and effectiveness of further investigation in the bleeding patient whose Table 1. Colonoscopy in Unexplained Rectal Bleeding References

Patients, no. Lesions found, % Polyps, % Cancer, % Inflammatory bowel disease, /o

1

2

3

4

239 40 16 10 10

215 41 14 13 7

258 41.5 15.1 11 7.4

561 42 14 11 10

Colonoscopy for unexplained rectal bleeding. Br Med J 2:1685-1687, 1978 2. TEAGUE RH, THORNTON JR, MANNING AP, SALMON PR, READ AE:

Colonoscopy for investigation of unexplained rectal bleeding. Lancet 1:1350-1352, 1978 3. TEDESCO FJ, WAYE JD,

RASKIN JB, MORRIS SJ, GREENWALD

Oxacillin and Hepatitis T o THE EDITOR: We report a case that sheds further light on the anicteric hepatitis induced by intravenous high-dose oxacillin therapy, reviewed by Onorato and Axelrod in the October 1978 issue (1). A 24-year-old man was hospitalized due to a 2-week history of severe pain in the left sacral area, associated with fever to 39.5 °C and shaking chills. He reported a recent laceration of the left foot that healed slowly, with erythema and exudate. There was no past history of hepatitis, jaundice, intravenous drug use, allergies, blood transfusions, exposure to hepatotoxins, or significant alcohol consumption. Physical examination showed temperature of 39.5 °C, normal results of funduscopic examination, grade 2/6 coarse apical systolic murmur not previously heard on examination 6 d before admission, nonpalpable liver and spleen, normal results of neurologic examination, no sacral tenderness, and negative straight-leg-raising test. Several days after admission, two oral mucosal petechiae and a subungual splinter hemorrhage were noted. On admission, laboratory values included hematocrit, 37%; leukocyte count, 12 000/mm3 with 69% segmented neutrophils (with toxic granulation), 2% band forms, 26% lymphocytes, 3% monocytes; and erythrocyte sedimentation rate, 83 mm/h (Westergren), with Rouleaux formation of the erythrocytes on peripheral smear. Urinalysis findings were normal, hepatitis B surface antigen, negative; serum glutamic-oxalacetic transaminase (SGOT), 49 IU (normal, 0 to 41); serum glutamic-pyruric transaminase (SGPT), 123 IU (normal, 0 to 45); lactic dehydrogenase (LDH), 238 IU (normal, 60 to 200); alkaline phosphatase, 252 IU (normal, 30 to 115); and total bilirubin, 0.6 mg/dL. Four blood cultures drawn initially were all positive for Staphylococcus aureus, resistant to penicillin and ampicillin, but sensitive to oxacillin. Results of chest film, ECG, echocardiogram, lumbosacral spine films, and plain films and tomograms of the left sacroiliac joint were normal, but on bone scan and gallium scan, abnormal uptake of the tracer in the left sacral and sacroiliac joint areas was noted. Treatment for S. aureus osteomyelitis and endocarditis was instituted with oxacillin, 2 g intravenously every 4h, with resolution of fever by the third day of oxacillin therapy and of sacral pain by the tenth day of treatment. The murmur was reduced to grade 1/6 by the fifth day of oxacillin, then remained unchanged. The SGOT, SGPT, LDH, and alkaline phosphatase levels returned to normal by the 12th day of treatment. On the 27th day of oxacillin treatment, after a total dose of 324 g, a diffuse, nonpruritic maculopapular rash was noted, leukocyte count was 5 000 mm1 with 10% eosinophils, and SGOT had risen to 101 IU, SGPT to 226 IU, and LDH to 230 IU; alkaline phosphatase and bilirubin levels were normal. The patient remained afebrile and was otherwise asymptomatic without hepatic enlargement or tenderness. He had received no other medication or transfusion. Oxacillin was withdrawn and intravenous nafcillin begun, 2 g every 4 h initially for 9 d, then 1.5 g every 4 h for another 7 d to complete 6 weeks of treatment. Resolution of the rash followed withdrawal of oxacillin in 3 d, eosinophilia resolved in 10 d, and the liver chemistry values returned to normal by thefinalday of nafcillin treatment. This case suggests hepatocellular injury due to a hypersensitivity reaction to oxacillin and provides further information about choice of an alternative antibiotic. One of the patients reported by Onorato and Axelrod was treated with nafcillin twice after each of two episodes of oxacillin-induced hepatitis Letters and Corrections

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RA:

Colonoscopic evaluation of rectal bleeding. A study of 304 patients. Ann Intern Med 89:907-909, 1978 4. HUNT RH: Rectal bleeding. Clin Gastroenterol 7:719-740, 1978 5. ZAVALA DC: Diagnosticfiberopticbronchoscopy: techniques and results of biopsy in 600 patients. Chest 68:12-16, 1975 6. SANDERSON DR: Bronchofiberscopy—fiberoptic bronchoscopy (editorial). Chest 68:2, 1975

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"without further deterioration in his liver function tests." Dismukes (2) reported a case of oxacillin-induced hepatitis that resolved after change to intravenous penicillin, and Bruckstein (3) reported another case in which therapy was initially changed to nafcillin, but then because of phlebitis, changed again to cephalothin after an unspecified time, with resolution of the liver chemistry derangements. The case presented here clearly shows that the hypersensitivity reaction is a distinctive response to oxacillin and will resolve despite continued treatment with nafcillin. This is significant information in light of the restricted number of drugs effective in treatment of S. aureus endocarditis and the significant toxicities associated with alternative antibiotics, for example, vancomycin, gentamicin, and rifampin. The increasing awareness of oxacillin-induced hepatitis should prompt further reports, one hopes with detailed ultrastructural and immunologic study. CHARLES TAYLOR, M.D. K A T H Y CORRIGAN, M.D. SUSAN STEEN, M.D. CHARLES CRAIG, M.D.

University of South Florida College of Medicine; Tampa, FL 33612 REFERENCES

1. ONORATO IM, AXELROD JL: Hepatitis from intravenous high-dose oxacillin therapy. Findings in an adult inpatient population. Ann Intern Med 89:497-500, 1978 2. DISMUKES W.: Oxacillin-induced hepatic dysfunction. JAMA 226:861863, 1973 3. BRUCKSTEIN AH, ATTIA AA: Oxacillin hepatitis. Two patients with liver biopsy, and review of the literature. Am J Med 64:519-522, 1978 Cimetidine, Cloxacillin, and Pancytopenia T o T H E EDITOR: I disagree with the conclusion reached in the report by deGalocsy and deStrihou (1) in the February 1979 issue claiming cimetidine caused pancytopenia in their patient who was also receiving intravenous cloxacillin. In their letter they stated, "We have not found any report of pancytopenia associated with cloxacillin." Westerman, Bradshaw, and Williams (2) have reported a case of agranulocytosis that occurred during therapy with oral cloxacillin. Almost all the penicillins have been found to cause agranulocytosis. The mechanism involved in the phenomenon is unclear; but the data indicate that this is not immunologically mediated but is, rather, a direct toxic effect on the marrow. This is substantiated by the cases described by Reyes, Palutke, and Lerner (3). Pancytopenia has not been reported as often with the penicillins as has neutropenia; however, if one hematopoetic series (myeloid) can be suppressed apparently pancytopenia could also occur. I submit that in view of the data that deGalocsy reported, one cannot conclude that the cimetidine caused the pancytopenia. E R I C L. W E S T E R M A N , M . D .

Hillcrest Medical Center; Tulsa, OK 74104 REFERENCES

1. DEGALOCSY C, VAN YPERSELE DE STRIHOU C: Pancytopenia with cim-

etidine (letter). Ann Intern Med 90:274, 1979 2. WESTERMAN EL, BRADSHAW MW, WILLIAMS TW: Agranulocytosis

during therapy with orally administered cloxacillin. Am J Clin Pathol 69:559-560, 1978 3. REYES MP, PALUTKE M, LERNER AM: Granulocytopenia associated

with carbenicillin. Am J Med 54:413-418, 1973. Psoriasis During Hemodialysis T o T H E EDITOR: Recent uncontrolled trials of dialytic therapy of psoriasis suggest a remarkable clinical improvement (1-3). However, this disease may manifest spontaneous improvements and exacerbations (4); thus, assessment of the effects of dialysis is difficult to interpret. In this regard, Friedman and Delano have described in the January 1979 issue (5) a case of psoriasis 858

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developing de novo during hemodialysis. We report the clinical course of two patients who began dialysis several years after the onset of psoriasis. A 43-year-old man with diabetic nephropathy developed typical cutaneous lesions of psoriasis in 1976. The diagnosis was confirmed by skin biopsy. During mid-1978, renal function deteriorated progressively, and the patient began maintenance hemodialysis in September 1978. Since then, the skin lesions have remained unchanged despite continued dialytic therapy. A 60-year-old man with psoriasis involving the scalp and all four extremities since 1940, and chronic renal failure secondary to obstructive uropathy, began maintenance hemodialysis in November 1970. Within approximately 2 months of the initiation of hemodialysis, the patient noted a gradual almost total clearing of the skin lesions. This remarkable remission, unique in the patient's experience, lasted for about 6 months. Afterward, during a period of about 6 months, the psoriasis regressed to its original state and remained essentially stable. The patient underwent a subtotal parathyroidectomy in June 1977 because of progressive bone pain. In September 1978 the patient moved to Florida and has continued his home hemodialysis treatments without changes in his skin condition. The clinical course of these two patients with psoriasis receiving maintenance hemodialysis underscores the difficulties in evaluating the effects of therapy on the natural course of a disease characterized by spontaneous remissions and exacerbations. Although the second patient appeared to improve shortly after the initiation of dialysis, the disease recurred after a few months and is currently active despite 9 years of hemodialysis. Controlled trials will be necessary to document the effect of dialysis, if any, on the natural history of psoriasis. G U I D O O. P E R E Z , M . D . J A M E S R. O S T E R , M . D . C A R L O S A. V A A M O N D E , M . D . K E N N E T H M. H A L P R I N , M . D .

Veterans Administration Medical Center, University of Miami School of Medicine; Miami, FL 33125 REFERENCES 1. TWARDOWSKI ZJ, NOLPH KD, RUBIN J, ANDERSON PC: Peritoneal

2. 3. 4. 5.

dialysis for psoriasis. An uncontrolled study. Ann Intern Med 88:349351, 1978 BUSELMEIER TJ: Dialysis and psoriasis (letter). Ann Intern Med 88:842, 1978 MUSTON HL, CONCEICAO S: Remission of psoriasis during haemodialysis. Br Med J 1:480-481, 1978 VAN SCOTT EJ, FARBER EM: Psoriasis in Dermatology in General Medicine. New York, McGraw Hill Book Company, 1971, p. 230 FRIEDMAN EA, DELANO BG: Psoriasis developing de novo during hemodialysis (letter). Ann Intern Med 90:132, 1979

Computed Tomography and Contrast Enhancement T o T H E EDITOR: At the Second Annual Meeting of the Society For Computerized Tomography and Neuro-Imaging held at Hilton Head, North Carolina, 29 October 1978, the subject of contrast enhancement in computed tomography (CT) scanning was discussed. The generally agreed upon indications for the use of intravenous contrast to help delineate lesions of the brain are as follows: 1. Previously treated brain tumors. 2. Abnormal isotope scans, cerebral arteriograms, or other positive neurodiagnostic tests. 3. Possible posterior fossa lesions, especially cerebellar pontine angle tumor. 4. Metastatic disease. 5. Arteriovenous malformations or aneurysms. 6. Patients with focal central nervous system signs. 7. Sellar and parasellar lesions. Contrast enhancement is being used excessively throughout this country as a routine. Contrast enhancement can lead to reactions in 5% of patients and mortality in anywhere from one in 30 000 to 50 000 cases. Hence, contrast should only be given when central nervous system disease is strongly suspected, when one of the aforementioned criteria is present, or in both circumstances. The diagnostic problems in which contrast is least productive are congenital lesions, degenerative diseases,

infarct, and trauma. Caution should be exercised in patients older than 70 years of age, in those with cardiac disease (especially failure), and any seriously ill patient. Computerized tomography is an expensive procedure, and there are times when the physician is forced to order it in spite of the fact that it is very unlikely that a lesion is present, for example, with persistent headaches. The routine C T scan without contrast yields a lot of information. T h e use of contrast should be carefully considered and used only when indications are present. In this way, a remarkable diagnostic procedure without any morbidity or mortality will not become a procedure with the possibility of complications. JACK O. G R E E N B E R G , M.D., C H A I R M A N HARRIS HOUSER, M.D. GEORGE SHEPHERD, M.D. HENRY HARRIS, M.D. A N G E L O ALVES, M.D. IMMANUEL MIER, M.D. G E R A L D MORLEY, M.D. C O M M I T T E E FOR U T I L I Z A T I O N A N D P E E R R E V I E W , SOCIETY FOR C O M P U T E R I Z E D T O M O G R A P H Y & N E U R O - I M A G I N G ; 25

Prescott Street; Atlanta, G A 30308

2. L E E M, LEKIAS J, GUBBAY SS, H U R S T PE: Spinal cord compression by extradural fat after renal transplantation. Med J Aust 1:201-203, 1975

Correction: Locations of Legionnaires' Disease Clusters T o T H E EDITOR: In the editorial, " T h e Diagnosis of Legionnaires' Disease," in the September issue (1), Iowa was incorrectly listed as a location of a Legionnaires' disease cluster in renalhomograft recipients. The correct list is Kansas, Ohio, and Vermont, in addition to Los Angeles. Case reviews at the University of Iowa Hospitals, the state's only transplantation center, have discovered no cluster. However, three isolated cases of Legionnaires' disease in renal-homograft recipients in the past 3 years have been identified. T H E O D O R E F. TSAI, M . D . D A V I D W. F R A S E R , M . D .

Center for Disease Control; Atlanta, G A 30333 C H A R L E S M. H E L M S , M.D.,P H . D . J O H N P. V I N E R , M . D . W A L T E R J. H I E R H O L Z E R , J R . , M . D . R O B E R T J. C O R R Y , M . D . E D W A R D D. R E N N E R , PH.D.

University of Iowa, Iowa City, IA 52242 L A V E R N E A. W I N T E R M E Y E R , M . D .

Epidural Lipomatosis from Corticosteroids T o T H E EDITOR: The interesting case of corticosteroid-induced epidural lipomatosis reported by Drs. Butcher and Sahn in the January 1979 issue (1) is very similar to that reported in a renal transplant recipient (2). In the latter case as well, the myelog r a p h y findings indicated an entirely posterior extradural block from T, .2 to T„, which proved at surgery to be due to normal fat tissue. A laminectomy from C7 to L4 with removal of the ligamentum flavum and extradural fat resulted in cord pulsation only after the dura was slit. This suggests that the fat deposits encircled the dura asymmetrically, necessitating an extensive surgical procedure to decompress the cord and restore neurologic function. A review of the 14 renal transplant recipients at our institution who have had computed tomography of the lumbar or thoracic spine showed no cases of cord displacement or unusual fat deposition within the spinal canal. Recognition of the need to minimize high-dose steroid therapy to reduce the risk of infection has also reduced the risk of epidural lipomatosis in transplant recipients. Drs. Butcher and Sahn should be thanked for reminding us that this complication may be seen in patients exposed to corticosteroids for other reasons as well. B A R R Y R. P A U L L , M . D .

Mallinckrodt Institute of Radiology, Washington University School of Medicine; St. Louis, M O 63110 REFERENCES 1. BUTCHER DL, SAHN SA: Epidural lipomatosis: a complication of corticosteroid therapy. Ann Intern Med 90:60, 1979

Iowa State Department of Health; Des Moines, I A 50319 REFERENCE 1. TSAI TF, FRASER DW: The diagnosis of Legionnaires' disease (editorial). Ann Intern Med 80:413-414, 1978

Correction: Temperature Correction for Oxygen Tension T o T H E EDITOR: A commentary from me in the February 1979 issue (1) contains an error I failed to detect in the original manuscript. The error occurs in the example I used to illustrate blood gas correction. It should read, " F o r example, a patient with a core temperature of 27 °C and a p H of 7.10 and a Po 2 of 75 m m H g would have, with correction for temperature, a tissue-level p H of 7.25 and a Po 2 of 20 m m H g . " The original listed the first Po 2 as 20 m m Hg. J A M E S B. R E U L E R , M . D .

Veterans Administration Hospital, Portland, O R 97207 REFERENCE 1. R E U L E R JB: Hypothermia (letter). Ann Intern Med 90:273, 1979

Correction: Annotated Bibliography The name of the journal in Reference 63 in the "Annotated Bibliography for Allergy and Immunology" {Ann Intern Med 90:138, 1979) is incorrect. The correct reference is T A U B R N , D E U T S C H V: Antilymphocytic serum. Pharmacol Ther (A) 2:89-111, 1977.

Letters and Corrections

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