gia paraesthetica is very conspicuous. N\l=a"\cke1 suffered from meralgia, and as early as 1895 he spoke of the hereditary disposition of this disease. Escat2 and Freud3 reported their own cases in
1895 and could not find a cause in their own cases even after many years of self-observation. Sigmund Freud, who reported that not only he himself but also one of his sons had the problem, stated that his was periodic and for months he did not feel anything and did not think of it. In 1944 Corlette4 mentions that his meralgia "has never been particularly troublesome, and only occasionally noticed." However, pain in meralgia may be severe and has been described as intolerable. Musser and Sailer5 in 1900 reviewed 99 cases in which ten were physicians, "an unduly large proportion." A plausible explana¬ tion for this was that the physician observes himself more carefully than the layman does and may report his observations to his fellow physicians. However, knowing the usual benign course of the disease may cause physi¬ cians to accept the bothersome neural¬ gia with less complaint. Finally, two of my own colleagues (physicians) on seeing my article have informed me that they suffer from
meralgia paraesthetica. I have no explanation for the unusu¬ al incidence of this mononeuropathy in physicians other than that mentioned previously, but I thought it might be interesting historically. Lt Comdr E. Wayne Massey, MC, USNR National Naval Medical Center Bethesda, Md 1. N\l=a"\ckeP: Beitrag zu den isolirt auftretenden Parasthesieen im Gebiete des N. cutaneus femoris externus. Neurol Centralbl 14:338, 1895. 2. Escat \l=E'\: Un cas de m\l=e'\ralgieparesth\l=e'\siquede Roth. Rev Neurol 3:577, 1895. 3. Freud S: \l=U"\berdie Bernhardt'sche Sensibilit\l=a"\tsst\l=o"\rung. Neurol Centralbl 14:491, 1895. 4. Corlette CE: Meralgia paraesthetica. Med J Aust 31:127, 1944. 5. Musser JH, Sailer J: Meralgia paraesthetica (Roth) with the report of ten cases. J Nerv Ment Dis 27:16, 1900.
Photodye Herpes Therapy To the Editor.\p=m-\We are referring to the recent article "Photodye Herpes Therapy\p=m-\CassandraConfirmed?" by Berger and Papa (238:133-134, 1977). A similar patient with multiple papules on the penis, with histologic features of squamous-cell carcinoma in situ, was recently reported by Kopf and Bart.1 This patient also had photochemotherapy for herpes simplex prior to the development of bowenoid papules of the penis. We will soon publish our experience with 11 young men who have multiple lesions of squamous-cell carcinoma in situ on the penis. Of great importance is the fact
that only three of the 11 patients received photodye treatments. Therefore, photochemotherapy is not related to this penile condition in most cases if, indeed, it is in any. Alfred W. Kopf, MD A. Bernard Ackerman, MD Thomas Wade, MD Robert S. Bart, MD New York University School of Medicine New York
Kopf AW, Bart RS: Tumor conference #11: Multiple papules of the penis: A new entity? J Derm Surg
Oncol 3:265-269, 1977.
Counterimmunoelectrophoresis and Bacterial Meningitis Editor.\p=m-\Having just reviewed experience with counterimmunoelectrophoresis (CIE), we read with To the
interest the letter from Denis et al
(238:1248, 1977) regarding CIE for the
diagnosis of bacterial meningitis. Our
observations are not in agreement with those of Denis et al, and the discrepancies have important clinical implications. Our procedure employs an electrophoresis chamber and tris-barbital buffer (pH 8.8) in 1% agarose. The antisera we use are group B Strepto-
coccus, Haemophilus influenzae type b, Neisseria meningitidis (groups A thru D and XYZ), and Streptococcus pneumoniae omnisera. Our laboratory began doing CIE on CSF samples shortly after the method was introduced for the diagnosis of bacterial meningitis.1,2 During this time, it gradually became apparent that our experience did not support the early optimism expressed in the literature. Use of commercial reagents was initially considered to be responsible
for the lack of
positive results in
patient specimens, but careful testing with purified antigens from S pneumo-
niae type 3 and from N meningitidis our methods were capable of detecting as little as 0.1 and 0.06 Mg/ml of antigen, respectively, in good agreement with literature re¬ ports.3 To quantify our general impres¬ sions, we reviewed all CIE data gen¬ erated in the Clinical Microbiology group C showed that
Laboratory of the University of Minne¬ sota Hospitals from June 1, 1976, to May 31,1977. In formulating the table, all in-hospital tests were included as
cases referred for CIE from outside hospitals when correlative cul¬ ture and smear results could be were
obtained. In contrast to the 98.6%
sensitivity reported by Denis et al, only 62% (8/13) of our culture-proved cases of meningitis caused by N meningitidis, H influenzae, and S pneumoniae were positive with CIE. Our results agree
well with the recent report from the Statens Seruminstitut'' in which specif¬ ic antigen was detected by CIE in 57% (72/126) of the CSF specimens from which the corresponding organism had been cultured. The cause of our two false-positives is not entirely clear. In these cases, the CSF produced a pecu¬ liar precipitin line against only one antisera after electrophoresis. On reex¬ aminaron of the slides, it was thought that these results most likely repre¬ sented nonspecific protein precipita¬ tion. The clinical history and culture results were consistent with this inter¬
pretation. Comparison of the data of Denis et al with ours points out the pitfalls in evaluating a new diagnostic test using known positives in advanced stages of a disease and a relatively small number of "healthy subjects" without other disease as controls. Our relatively large number of false-negatives may relate to the duration of the CNS infection at
the time of testing. Many of our posi¬ tive cultures were from cases with very early disease before the spinal fluid had become grossly purulent. In addi¬ tion, on review of culture, smear, and CIE results, only 10% of all CSF specimens submitted to us for CIE showed evidence of meningitis owing to organisms that could be tested with CIE. When a test with even very good specificity (approximately 98% for CIE in our hands) is used to screen large numbers of patients, most of whom do not have the disease in question, the number of false-positives becomes im¬
Smear and Culture Results in 157 Culture Positive
Cerebrospinal Fluids* CIE Positive
Negative Culture, Positive CIE
meningitidis_4_3_1_It_ 9 7 7 Haemophllus influenzae 1t
*CIE indicates counterimmunoelectrophoresis.
( Technical false-positive.
^Partially treated meningitis.
§One technical false-positive and
partially treated meningitis.
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In summary, the
only real advan¬ CSF culture are speed and usefulness in cases of partially treated meningitis. In our tages of CIE
hands, false-positives rarely do occur, and the sensitivity is only about 60%. Finally, a negative CIE on CSF in no way rules out meningitis caused by the organisms for which the sample was tested. Therefore, it is our feeling that appropriate antibiotic coverage should be instituted based on the Gram smear and clinical presentation. Discontinua¬ tion or modification of such therapy should be based primarily on CSF culture results, not on CIE findings.
John Eckfeldt, MD, PhD Grace Mary Ederer, MPH Rebecca Oetjen University of Minnesota Hospitals
1. Edwards EA, Muehl PM, Peckinpangh RO: Diagnosis of bacterial meningitis by counterelectrophoresis. J Lab Clin Med 80:449-454, 1972. 2. Coonrod JD, Rytel MW: Determination of etiology of bacterial meningitis by counterelectrophoresis. Lancet 1:1154-1157, 1972. 3. Shackelford PG, Campbell J, Feigin RD: Countercurrent immunoelectrophoresis in the evaluation of childhood infections. J Pediatr 85:478-481,1974. 4. Colding H, Lind I: Counterimmunoelectrophoresis in the diagnosis of bacterial meningitis. J Clin Microbiol
Demeclocycline and Renal Insufficiency To the Editor.\p=m-\Demeclocyclinecauses diuresis of ascitic fluid in cirrhotic patients.1 A major side effect, however, is renal insufficiency caused by an uncertain pathophysiologic mecha-
with afflicted by
symptoms of hypovolemia: postural
dizziness, dry mouth, excessive thirst,
and intractable headaches. For two years a diet restricted to 850 ml of fluid and 45 mEq of sodium, together with a regimen of furosemide (80 mg three times a day), hydrochlorothiazide (25 mg twice a day), and spironolactone (25 mg twice a day), had kept the ascites to a barely tolerable limit (abdominal girth of 106.7 cm and large abdominal hernia). She was unable to carry on
routine self-care activities such as putting on stockings and shoes. Results of physical examination showed substantial orthostatic changes in blood even
(decrease of 20 mm Hg systolic and 10 mm Hg diastolic) and heart rate (increase of 15 beats per minute). Also present were poor skin turgor, dry mucus membranes, and soft eyeballs. Following the administration of de¬ meclocycline (300 mg orally three times a day) for ten days, all symptoms of hypovolemia disappeared, and pos¬ tural changes in blood pressure and pressure
pulse were no longer present. Abdom¬ inal girth diminished by 25.4 cm and weight by 8.1 kg. However, her BUN
1. DeTroyer A, Dilloy W, Broeckaert I, et al: Demeclocycline treatment of water retention in cirrhosis. Ann Intern Med 85:336-337, 1976. 2. Wapnick S, Grosberg S, Kinney M, et al: LeVeen continuous peritoneal jugular shunt. JAMA 237:131-133,
rose from 40 mg/dl to nearly 200 mg/dl (simultaneous creatinine lev¬ els, 2.7 and 3.6 mg/dl, respectively), and symptoms of uremia developed. Throughout the trial of demeclocycline, the previous regimen (diuretics and fluid and salt restriction) was contin¬
ued as before. Within two weeks of discontinuance of demeclocycline, she regained the symptoms of hypovolemia, and her girth and weight returned to levels before demeclocycline. Renal function improved (creatinine level, 2.5 mg/dl; BUN level, 63 mg/dl). The original regimen of fluid restric¬ tion and diuretics was never altered during this treatment, and at all times the patient kept compulsive records of fluid intake and output. Later a LeVeen shunt2 relieved all symptoms and removed her ascites without affecting renal function (current cre¬ atinine level, 2.7 mg/dl; BUN level, 40
This case raises several questions about fluid balance. First, the patient's mild renal insufficiency was quantified initially by BUN and creatinine levels whose ratio was 15 mg/dl (40/2.7
mg/dl). Ordinarily, severe hypovolemia (and resulting hypoperfusion) cause a so-called prerenal azotemia character¬ ized by a ratio of BUN to creatinine levels of 25 mg/dl or more. The occurrence of a high BUN-to-creatinine ratio after demeclocycline treatment and correction of hypovo¬ lemia is difficult to explain. Whereas
the rise in BUN level may reflect the well-known anabolic effects of demec¬ locycline3 and other tetracyclines, the rise in the creatinine level probably demonstrated a direct renal toxicity of the drug. Also confusing is the correction of hypovolemia during treatment with a drug that normally causes a partial diabetes insipidus syndrome (and fur¬ ther hypovolemia).4,5 Perhaps demeclo¬ cycline alters one of the factors involved in the pathogenesis of ascites (such as hyperaldosteronism) or inter¬ feres with the mechanism of action of one or more of the diuretics taken by the patient. Alternatively, it may have stabilized the peritoneal membrane to prevent reaccumulation of fluid in the abdomen. Correction of ascites by a drug with an anti-antidiuretic-hormone effect also raises the question of a primary role of the antidiuretic hormone in the formation of ascites. Rich Kirkpatrick, MD Longview, Wash
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K, Becker KL, Shaqhoub RJ, et al: Nephrotoxdemethylchlortetracycline hydrochloride. Arch
Intern Med 120:433-435,1967. 4. Singer I, Rotenberg D: Demeclocycline-induced nephrogenic diabetes insipidus: In-vivo and in-vitro studies. Ann Intern Med 79:679-683, 1973. 5. Castell
DO, Spacks HA: Nephrogenic diabetes inhydrochloride.
sipidus due to demethylchlortetracycline JAMA 193:237-239,1965. ,
US Health Care
To the Editor.\p=m-\The commentary by E. Grey Dimond, "Medicine\p=m-\Where It
Seems To Be: An American Health Care System" (238:1251, 1977), deserves
repeated, careful study. Indeed, the main dilemma today is how we can encourage development of the health care system along lines other than the blind, doctrinaire plunge into centralization, bureaucratic control, and socialism that has proved so fruitless else-
where. Not only the Veterans Administration hospitals but all government medical institutions must be included in the comprehensive development of an overall health care system. In Alaska the Public Health Service and Indian Health Service are a serious obstacle to the development of a first-class health care system for anyone. The PHS and the military each promote a racially or
occupationally monopolistic, expensive, divisive, and resource-wasteful system. Having three separate, individually
inadequate health care systems in this
vast, sparsely-populated state is
incredible absurdity. Our current hope is that health system planning and certificate-of-need laws will be able to encompass all health and medical programs in Alaska, not just those of "private" medicine. Peter S. Rosi, Sitka, Alaska
Direct Current Cardioversion. \p=m-\Inthe Jan 9 issue of The Journal (239:122\x=req-\ 124, 1978), the last sentence of the synopsis-abstract to the ORIGINAL CONTRIBUTION "Direct Current Cardioversion: Effect on Creatine Kinase, Lactic Dehydrogenase, and Myocardial Isoenzymes" should read as follows: "Therefore, new CK-MB or LDH1 elevations associated with arrhythmias must result from myocardial damage unrelated to DC cardioversion." In addition, the values footnoted in the Table are abnormal, not normal, values.