Article, Dermatology

Bone pain as an atypical early manifestation of acute myocardial infarction

clindamycin, and in the subsequent 12 months, the infection has not recurred.

This case illustrates the potential hazards of rifampin therapy for suspected or diagnosed CA-MRSA skin infec- tion. Our case is limited in that we cannot distinguish whether the adverse event was due to TMP-SMX or rifampin. Nevertheless, rifampin has a significant side effect rate, including serious adverse events [4,5]. These adverse events result in unnecessary morbidity and health care cost, as illustrated in this case.

The concerning aspect of this case is that there are no data to support the use of rifampin for skin and soft tissue infections. In a systematic review of the literature of adjunctive rifampin therapy for S aureus infection, some animal models of skin infections showed decreases S aureus colony counts with adjunctive rifampin compared to antibiotic monotherapy, but others showed no extra activity of rifampin [6]. Antibiotics used in the animal investigation varied considerably, and the clinical relevance of some of these models is unclear (eg, antibiotics were sometimes given only one hour after experimental inoculation). Clinical trials to establish the safety and efficacy of adjunctive rifampin therapy for skin infections have not been performed [6]. Furthermore, cure rates in clinical trials of complicated skin infections show cure rates that are in the 80% to 90% range, regardless of the antibiotic used [7-10]. We are unaware that any well-conducted clinical trial has ever shown one antibiotic to be more effective than another, suggesting there may be a ceiling effect in which cure rates exceeding the 80% to 90% range may not be achievable. Hence, it is unlikely that rifampin can improve the efficacy of other antibiotics for the treatment of skin infection and is likely only to contribute to adverse effects and Drug interactions.

In summary, we strongly believe the use of rifampin for the treatment of known or suspected CA-MRSA skin and soft tissue infections is not warranted and places patients at risk for significant morbidity. Although rifampin may have a role as adjunctive therapy in selected S aureus infections (eg, device-associated infections and osteomye- litis) [6], we believe practice guidelines should be explicit in discouraging use of adjunctive rifampin for the treat- ment of known or suspected CA-MRSA skin and soft tissue infections.

Loren G. Miller MD Division of Infectious Diseases Harbor-UCLA Medical Center Torrance, CA 90509, USA

E-mail address: [email protected]

Helen Boucher MD

Division of Infectious Diseases

Tufts Medical Center Boston, MA, USA

doi:10.1016/j.ajem.2009.01.014

References

  1. Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant

S. aureus infections among patients in the emergency department. N Engl J Med 2006;355:666-74.

  1. Miller LG, Quan C, Shay A, et al. A prospective investigation of outcomes after hospital discharge for endemic, community-acquired methicillin-resistant and -susceptible Staphylococcus aureus skin infection. Clin Infect Dis 2007;44:483-92.
  2. Iyer S, Jones DH. Community-acquired methicillin-resistant Staphy- lococcus aureus skin infection: a retrospective analysis of clinical presentation and treatment of a local outbreak. J Am Acad Dermatol 2004;50:854-8.
  3. Grosset J, Leventis S. Adverse effects of rifampin. Rev Infect Dis 1983;5(Suppl 3):S440-50.
  4. Martinez E, Collazos J, Mayo J. hypersensitivity reactions to rifampin. Pathogenetic mechanisms, clinical manifestations, management stra- tegies, and review of the anaphylactic-like reactions. Medicine (Baltimore) 1999;78:361-9.
  5. Perlroth J, Kuo M, Tan J, Bayer AS, Miller LG. Adjunctive rifampin for the treatment of Staphylococcus aureus infections: a systematic review of the literature. Arch Intern Med 2008;168:805-19.
  6. Tack KJ, Littlejohn TW, Mailloux G, Wolf MM, Keyserling CH. Cefdinir versus cephalexin for the treatment of skin and skin-structure infections. The Cefdinir Adult Skin Infection Study Group. Clin Ther 1998;20:244-56.
  7. Wible K, Tregnaghi M, Bruss J, Fleishaker D, Naberhuis-Stehouwer S, Hilty M. Linezolid versus cefadroxil in the treatment of skin and skin structure infections in children. Pediatr Infect Dis J 2003;22: 315-23.
  8. Parish LC, Routh HB, Miskin B, et al. Moxifloxacin versus cephalexin in the treatment of uncomplicated skin infections. Int J Clin Pract 2000; 54:497-503.
  9. Amaya-Tapia G, Aguirre-Avalos G, Andrade-Villanueva J, et al. Once- daily azithromycin in the treatment of adult skin and skin-structure infections. J Antimicrob Chemother 1993;31(Suppl E):129-35.

Bone pain as an atypical early manifestation of acute myocardial infarction

To the Editor,

Leone at al [1] have found a surge of serum level of endogenous granulocyte colony-stimulating factor (G-CSF) is in proportion to the circulation of CD34+ progenitor cells after acute myocardial infarction. This observation sup- ported the notion that the myocardial regeneration com- menced as early as the beginning of cardiomyocyte death in the form of motivating CD34+ progenitor cells from bone marrow in response to a variety of cytokines and G-CSF [2]. With clinical experience of the use of G-CSF administration, the side effect of severe bone pain is frequently encountered accounting for 1% to 5% of all cases. The mechanisms include a rising pressure within bone marrow by increased granulocytes, edema within bone marrow by histamine release, and elevated level of bradykinin [3]. Recently, we observed an 83-year-old man with type 2 diabetes who presented sudden onset of severe

diffuse bone pain for 3 hours before arriving at the emergency department. On admission, he was free of chest pain, and blood pressure was 136/70 mm Hg, pulse rate was 66 beats per minute, and body temperature was

36.2?C. A routine 12-lead electrocardiography was obtained, and it revealed ST-segment elevation of leads II, III, and aVF with reciprocal ST-segment depression of leads I and aVL. The laboratory findings demonstrated a raised leukocyte count of 16 800/uL and positive cardiac troponin-I. Under the impression of acute Inferior wall myocardial infarction, emergent coronary angiography with primary percutaneous coronary angioplasty to the infarct-related right coronary artery was carried out. As soon as the forward flow of right coronary artery was restored, the symptom of severe bone pain was resolved. To our knowledge, patients with unrecognized acute myocar- dial infarction usually presenting with atypical symptoms instead of chest pain have poor prognosis and outcomes [4]. Risk factors including elderly persons, female sex, type 2 diabetes, and inferior wall myocardial infarction have been reported with a higher incidence of atypical manifestations during myocardial infarction. Although severe bone pain due to an increase of endogenous G-CSF response after acute coronary syndromes has rarely been emphasized before, the preliminary data in our hospital revealed about 6% of patients diagnosed as acute myocardial infarction presenting concomitant bone pain with or without angina pectoris on admission. Herein, we stress that the presence of unexplainable bone pain in a patient with high risk of cardiovascular event should be considered as an atypical early presentation of acute myocardial infarction.

Gen-Min Lin MD Department of Internal Medicine Tri-Service General Hospital National Defense Medical Center Neihu 114, Taipei, Taiwan Department of Internal Medicine

Hualien Armed Forces General Hospital

Hualien, Taiwan E-mail address: [email protected]

Chih-Lu Han PhD Department of Internal Medicine Tri-Service General Hospital National Defense Medical Center Neihu 114, Taipei, Taiwan

doi:10.1016/j.ajem.2009.01.017

References

  1. Leone AM, Rutella S, Bonanno G, et al. Endogenous G-CSF and CD34+ cell mobilization after acute myocardial infarction. Int J Cardiol 2006;111:202-8.
  2. Han CL, Campbell GR, Campbell JH. Circulating bone marrow cells can contribute to neointimal formation. J Vasc Res 2001;38:113-9.
  3. Ogata S, Ito K, Kadoike K, et al. The incidence of bone pain with granulocyte colony stimulating factor (G-CSF) administration and the effect of hydroxyzine. ASCO Annual Meeting Proceedings. J Clin Oncol 2005;23(Suppl 1):8242.
  4. Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA 2000;283:3223-9.

Purple urine bag syndrome, not always a benign process

To the Editor,

The subject of the case report presented by Su et al [1] is quite interesting as authors described a patient that was sent to the emergency department in critical condition upon arrival, and purple urine bag syndrome (PUBS) was also found at that time. Finally, the patient died of Aspiration pneumonia and septic shock in the intensive care unit. The case report described the first case of PUBS that occurred involving a patient in critical condition. The authors claimed that PUBS was not the leading cause of mortality in this case. We realize that urinary tract infection is an important factor contributing the development of PUBS [2]. Fourier’s gang- rene is a Urologic emergency with high mortality [3]. One of the major sources of Fourier’s gangrene is urinary tract infection. We came across 2 patients who had PUBS and pyuria. Both of them progressed to Fourier’s gangrene days later. This is the first report of PUBS-associated Fourier’s gangrene.

1. Case 1

A 50-year-old patient had respiratory failure and required ventilator dependence for 5 months. In addition, he had diabetes mellitus, a previous cerebral vascular accident, and congestive heart failure. He also had urinary catheterization for 3 months. He had purple urine bag syndrome since May 20, 2008, and his urine data yielded alkaline urine (pH 8.5) and a urine white blood cell count of 15 to 20 per high-power field (HPF). Blood examination revealed WBC of 10 200/uL, hemoglobin of 8.9 g/dL, and platelet of 141 000/uL. His urine culture grew Escherichia coli and Acinetobacter baumanii. We did not prescribe any antibiotics for him because he was asymptomatic with the exception of purple urine. However, he had abrupt hypotension and hypothermia 1 week later. A detailed physical examination disclosed his edematous necrotic scrotum with a foul odor. Fourier’s gangrene was impressed. Meropenen was imme- diately administered, and repeated extensive debridement was performed. The pus culture yielded Morganella