Campbell, Lee Ann

Malinverni, Raffaele

Matter, Lukas

Schaad, Heinz J.

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162 Brief Reports CID 1999;28 (January)Two weeks later, he was seen in our lipid clinic. He was thin the dose. It is not yet known if use of ritonavir is safe for patientswith abnormal lipid values at baseline; however, further investiga-(weight, 63 kg) and muscle wasting was noted, but otherwisethe examination ®ndings were unremarkable. The CD4/ lym- tion is warranted.phocyte count was 517/mm3, and the viral load, as determinedby HIV-RNA PCR, was 8,815 copies/mL. Blood glucose, hemo- R. Clark Perry, Herbert E. Cushing, Mark A. Deeg, andglobin Alc, thyroid-stimulating hormone, and serum amino- Melvin J. Prince*transferase levels were normal. The triglyceride level, however, Divisions of Endocrinology and Metabolism and of Infectious Diseases,had again risen to 25.24 mmol/L (2,234 mg/dL). The total cho- Department of Medicine, Indiana University School of Medicine; andEndocrinology Section, Richard Roudebush Veterans Affairs Medicallesterol value was 7.26 mmol/L (281 mg/dL), and that of HDLCenter, Indianapolis, Indianacholesterol was 0.41 mmol/L (16 mg/dL). Gem®brozil therapywas initiated. Antiretroviral therapy was reinstituted with zido-vudine, didanosine, delaviridine, nel®navir, and saquinavir, and Referencesno complications were noted. Currently his cholesterol level is 1. Carpenter CC, Fischl MA, Hammer SM, et al. Antiretroviral therapy for4.91 mmol/L (190 mg/dL), and the triglyceride level is 4.79 HIV infection in 1997: updated recommendations of the Internationalmmol/L (424 mg/dL). AIDS Society±USA Panel. JAMA 1997;277:1962±9.Markowitz et al. [3] demonstrated triglyceride level elevations 2. Danner SA, Carr A, Leonard JM, et al. A short-term study of the safety,pharmacokinetics, and ef®cacy of ritonavir, an inhibitor of HIV-1 prote-in excess of 200% over baseline values in 65% of patients receivingase. N Engl J Med 1995;333:1528±33.ritonavir. These effects on serum lipids appear to be dose-related3. Markowitz M, Saag M, Powderly WG, et al. A preliminary study of rito-and can be seen as early as 1 week after initiation of therapy withnavir, an inhibitor of HIV-1 protease, to treat HIV-1 infection. N Englritonavir [2].J Med 1995;333:1534±9.The mechanisms leading to hyperlipidemia with ritonavir4. Eagling VA, Back DJ, Barry MG. Differential inhibition of cytochromeare not known. Although ritonavir inhibits the CYP3A4 iso-P450 isoforms by the protease inhibitors ritonavir, saquinavir, and indi-form of cytochrome P450 [4], there is no de®nitive evidence navir. Br J Clin Pharmacol 1997;44:190±4.that inhibition of this enzyme leads to hyperlipidemia [5]. Re- 5. Gylling H, Vanhanen H, Miettinen TA. Hypolipidemic effect and mecha-cently, it has been suggested that protease inhibitors may alter nism of ketoconazole without and with cholestyramine in familial hyper-the structure or function of the peroxisome proliferator± acti- cholesterolemia. Metabolism 1991;40:35±41.6. Carr A, Samaras K, Chisholm DJ, Copper DA. Pathogenesis of HIV-1vated receptor type gamma (PPAR-gamma), but this has yetprotease inhibitor±associated peripheral lipodystrophy, hyperlipidaemia,to be studied fully [6].and insulin resistance. Lancet 1998;351:1881±3.HIV infection alone is associated with hypertriglyceridemia,7. Constans J, Pellegrin JL, Peuchant E, et al. Plasma lipids in HIV-infected patients:and the triglyceride level correlates inversely with the CD4/a prospective study in 95 patients. Eur J Clin Invest 1994;24:416±20.lymphocyte count [7]. The degree of hypertriglyceridemia attrib-8. Feingold KR, Krauss RM, Pang M, Doerrler W, Jensen P, Grunfeld C. Theuted to HIV infection, however, is generally less than that de-hypertriglyceridemia of acquired immunode®ciency syndrome is associ-scribed in this case [8]. Furthermore, triglyceride levels tend toated with an increased prevalence of low density lipoprotein subclassbe normal in HIV-infected individuals who have no manifesta- pattern B. J Clin Endocrinol Metab 1993;76:1423±7.tions of AIDS [9]. 9. Grunfeld C, Pang M, Doerrler W, Shigenaga JK, Jensen P, Feingold KR.Clinicians need to be familiar with the association between rito- Lipids, lipoproteins, triglyceride clearance, and cytokines in human im-navir and hyperlipidemia, and serum lipids should be monitored munode®ciency virus infection and the acquired immunode®ciency syn-drome. J Clin Endocrinol Metab 1992;74:1045±52.during the early stages of ritonavir treatment or with escalation ofaortic-valve regurgitation, moderate mitral-valve regurgitation, andMyocardial Infarction, Culture-Negative Endocarditis,a vegetation (5 1 14 mm) on the right coronary lea¯et of theand Chlamydia pneumoniae Infection: A Dilemma?aortic valve. There was no history of fever, weight loss, or shakingchills in the preceding weeks.The role of Chlamydia pneumoniae infection in cardiovascularThe axillary temperature was 36.27C, pulse was 110/min, anddiseases remains unclear. Herein we describe a case in which theblood pressure was 120/70 mm Hg. A 3/6 holosystolic murmurmany aspects of possible involvement are illustrated.and a 2/6 diastolic decrescendo murmur were noted. Skin andA 67-year-old woman previously in good health was admittedmucous membranes as well as funduscopic ®ndings were normal.for pulmonary edema. An electrocardiogram showed typical signsThe C-reactive protein level was 114 mg/L. The leukocyte countof acute myocardial infarction. Echocardiography revealed severewas 13,400/mm3, with a normal differential, and the serum chemis-try was compatible with recent myocardial infarction. Three pairsof aerobic and anaerobic cultures of blood drawn before adminis-Reprints or correspondence: Dr. H. J. Schaad, Department of Medicine, tration of antibiotics remained negative. Antibiotic therapy withUniversity Hospital, 3010 Bern-Inselspital, Switzerland (heinz.schaad@ high-dose intravenous ¯ucloxacillin, later replaced by penicillininsel.ch).and gentamicin, was initiated. Body temperature was 377C, ex-Clinical Infectious Diseases 1999;28:162±3 cept for two spikes to 38.47C on days 14 and 16. Doxycycline andq 1999 by the Infectious Diseases Society of America. All rights reserved.1058±4838/99/2801±0040$03.00 rifampicin were added on day 14./ 9c5e$$ja47 12-30-98 16:18:33 cidas UC: CID163CID 1999;28 (January) Brief ReportsTable 1. Serological evaluation of a 67-year-old woman presenting and IgA after surgery and adequate antibiotic treatment. Evaluationwith acute pulmonary edema. for IgM was always negative, suggesting either reinfection or reac-tivation of C. pneumoniae infection. In contrast to the patientTiter described by Marrie et al. [2], our patient had no fevers, sweats,chills, or productive cough. That patient had declining IgM titersTest (method) for: Antibody Day 10 Day 21during the observation period, suggesting primary infection. Inanother report, an increase in IgG titers from 1:64 to 1:512, fol-Chlamydia (CF) 1:30 1:15lowed by a decrease to 1:32 without IgM response, suggestedC. pneumoniae (MIF)* Ig Positive NDreinfection [3]. The third case also involved increasing IgG againstIgG 1:160 1:80C. pneumoniae, without IgM [4].IgM 1:20 1:20IgA 1:1280 1:320 In none of the previously published cases was PCR examinationC. psittaci (MIF) Ig Positive ND of the valve performed. Immunohistochemistry proved to be nega-IgG 1:64 1:80 tive when performed, as it was in our case. In a recent report,IgM 1:20 ND nonrheumatic stenotic aortic valves without evidence of endocardi-IgA 1:20 ND tis were frequently positive for C. pneumoniae, either by immuno-C. trachomatis (MIF) Ig Equivocal NDstaining or PCR [5]. These ®ndings question the relevance of theIgG ND 1:80positive PCR in our case. Although it is conceivable that ourpatient did have C. pneumoniae endocarditis with concurrent myo-NOTE. CF  complement ®xation; MIF  microimmuno¯uorescence;ND  not determined. Slides from MRL Diagnostics, Cypress, CA. cardial infarction, an etiologic role for this pathogen in any of* Results con®rmed by S.-P. Wang (Department of Pathobiology, University these events is not proven.of Washington, Seattle). This case report suggests that C. pneumoniae infection, with itstropism for the human vascular system, may be simultaneouslyactivated in various parts of the system, such as coronary arteriesand heart valves, producing complex diseases [6]. As evidence ofOn day 15, pain and swelling of the right knee were noted.Cultures of joint ¯uid remained sterile. On day 18, the results of the widespread presence of C. pneumoniae in the cardiovascularsystem increases, clinicians are likely to face more diagnostic di-various serological examinations were reported and revealed apositive reaction for C. pneumoniae (see table 1), while antibodies lemmas, as in our case.to Brucella, Coxiella burnetii, Legionella, Bartonella, and Trepo-nema were undetectable. On day 19, the aortic valve was replaced. Heinz J. Schaad, Raffaele Malinverni, Lee Ann Campbell,The right coronary lea¯et was partially destroyed and contained a and Lukas Mattergrayish vegetation with a diameter of4 mm. Aerobic and anaero- University Hospital (Department of Medicine and MedizinischePoliklinik) and the Institute for Medical Microbiology, University ofbic cultures of valve tissue remained negative. PCR for C. pneu-Berne, Berne, Switzerland; and Department of Pathobiology, Universitymoniae (performed at the Department of Pathobiology, Universityof Washington, Seattle, Washington, USAof Washington, Seattle [1]) was positive in a specimen from theleft aortic lea¯et but negative in material from the right lea¯et.ReferencesThe postoperative course was complicated by severe bleedingin the operative area, necessitating repeated surgery with mass 1. Campbell LA, Perez-Melgosa M, Hamilton DJ, Kuo CC, Grayston JT.transfusions. The patient died 15 days later, following progressive Detection of Chlamydia pneumoniae by polymerase chain reaction. Jmultiorgan failure due to invasive candidiasis. Necropsy was not Clin Microbiol 1992;30:434±9.2. Marrie TJ, Harczy M, Mann OE, et al. Culture-negative endocarditis proba-permitted by the patient's relatives.bly due to Chlamydia pneumoniae. Clin Infect Dis 1990;161:127±9.A MEDLINE search revealed only three reports of possible and3. Dumont D, Mathieu D, Alemanni M, Eb F, Manigand G. Endocarditeprobable endocarditis due to C. pneumoniae [2±4]. There wasd'Osler probablement due aÁ Chlamydia pneumoniae (souche TWAR).evidence of myocardial infarction in our patient, possibly due toPresse Med 1990;19:1054.a thromboembolic event. In fact, coronary angiography showed4. Norton R, Schepetiuk S, Tuck WK. Chlamydia pneumoniae pneumonianormal coronary arteries except for a complete obstruction of thewith endocarditis. Lancet 1995;345:1376±7.®rst marginal vessel. The recently diagnosed aortic insuf®ciency 5. Juvonen J, Laurila A, Juvonen T, et al. Detection of Chlamydia pneumoniaewith a large vegetation and observations during surgery were com- in human nonrheumatic stenotic aortic valves. J Am Coll Cardiol 1997;patible with infective endocarditis. 29:1054±9.Microbiological evaluation revealed an evolving antibody re- 6. Danesh J, Collins R, Peto R. Chronic infections and coronary heart disease:is there a link? Lancet 1997;350:430±6.sponse to C. pneumoniae, with rapidly decreasing titers of IgG/ 9c5e$$ja47 12-30-98 16:18:33 cidas UC: CID

Myocardial Infarction, Culture-Negative Endocarditis, and Chlamydia pneumoniae Infection: A Dilemma?

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