Kaposi sarcoma secondary to pulmonary tuberculosis: a rare case.

Abstract: Kaposi sarcoma commonly occurs in HIV-positive and immunocompromised patients. We describe a case of Kaposi sarcoma that developed in an HIV-negative patient with tuberculosis. The Kaposi sarcoma completely regressed with antituberculous therapy without the institution of chemotherapy. The patient remained disease-free after a follow-up period of 20 months. Patients with Kaposi sarcoma should be monitored for coexisting diseases such as tuberculosis.

Key Words: Kaposi sarcoma, tuberculosis

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Tuberculosis is a common, worldwide health problem. Because of the increasing incidence of diabetes mellitus, chronic renal failure, and immunodeficiency syndrome, tuberculosis rates have been increasing. (1,2) Kaposi sarcoma occurs most frequently in immunocompromised patients. (3) We report the case of an HIV-negative patient who had development of Kaposi sarcoma secondary to tuberculosis.

Case Report

A 54-year-old male with a 20 pack-year smoking history presented with a 2-month history of fever, night sweats, poor appetite, weight loss (8 kg within 3 months), sputum, and cough. His medical history was relevant for chronic obstructive lung disease and sporadically treated diabetes mellitus. He had no history of tuberculosis, alcohol intake, or risk factors for HIV infection. He denied any contact with patients with tuberculosis. The systemic review was otherwise unremarkable. At admission, the patient was in moderate clinical condition. His vital signs revealed a blood pressure of 80/50 mm Hg, heart rate of 104/min, body temperature of 38.2 C, and oxygen saturation of 84%. Chest examination revealed prolonged expiration and rales but was otherwise unremarkable. Chest radiography showed multiple, ill-defined nodular opacities, distributed peripherally in the middle zone. Laboratory data at admission yielded a sedimentation rate of 115 mm/h and C-reactive protein of 145 mg/dL (0 to 6). The remaining biochemical parameters and urinalysis were within normal limits. The patient received 500 mg/d levofloxacin, 60 mg/d hydrocortisone (5 days), 800 [micro]g/d salbutamol, and nasal oxygen therapy on the diagnosis of exacerbation of chronic obstructive lung disease. Even with aggressive treatment, his clinical condition progressively worsened. Sputum revealed three positive acid-fast bacilli stains as well as positive Mycobacterium tuberculosis culture. A daily regimen of 600 mg rifampicin, 300 mg isoniazid, 1,200 mg ethambutol, and 1,500 mg pyrazinamide was initiated. Culture antibiogram revealed that Mycobacterium tuberculosis was resistant to isoniazid, rifampicin, and streptomycin. A daily regimen of 12,000 mg para-aminosalicylic acid, 800 mg ofloxacin, 750 mg cycloserine, 750 mg ethionamide, 150 mg thiacetazone, and 1,000 mg amikacin was administered for 2 years, with the diagnosis of multidrug-resistant tuberculosis. Diabetes mellitus was regulated with insulin therapy. Two weeks after starting antituberculous therapy, multiple indurated, painless, cherry-red, nonpruritic skin lesions occurred on his head, left shoulder, trunk, and abdomen (Fig. 1). Skin biopsy histopathology from the head and trunk was consistent with Kaposi sarcoma (Fig. 2). Herpes simplex, cytomegalovirus, HIV, and hepatitis B were all negative. The treatment regimen was maintained and the patient's skin lesions regressed. Within 8 weeks, the lesions disappeared almost entirely without chemotherapy, radiotherapy, or surgery. The patient remained disease-free after a follow-up period of 20 months.

Discussion

In the present case, delayed diagnosis of pulmonary tuberculosis in an immunocompetent patient caused Kaposi sarcoma. This case revealed that delayed diagnosis of tuberculosis can cause serious and unusual complications. Other complications reported in the literature have included Addison disease, tuberculous meningitis, and inappropriate antidiuretic hormone syndrome. (4-6) Even though our patient had no history of active tuberculosis, previous exposure raises the possibility of subclinical pulmonary involvement.

Diagnosis of tuberculosis is confirmed by the presence of acid-fast bacilli in the sputum or gastric juice and growth of Mycobacterium tuberculosis complex in the laboratory, in addition to clinical manifestations. Conventional culturing, although sensitive, takes a long time, and polymerase chain reaction is now used for early diagnosis. (3) In our patient, acid-fast bacilli was detected in the sputum, and there were manifestations on chest radiography.

The possible cause of Kaposi sarcoma is decreased immune surveillance caused by cellular immune deficiency, usually caused by HIV infection. It has been shown that the occurrence of Kaposi sarcoma in HIV-positive patients is more than 7,000 times higher than that in non-HIV-infected individuals, (5) and it is 300 times more common than in iatrogenically immunosuppressed individuals. (6) As in our case, Kaposi sarcoma occurs most frequently in the head and trunk. Human herpes virus 8, hepatitis B virus, human papilloma virus, and cytomegalovirus may have a role in the pathogenesis of Kaposi sarcoma. (3,7) Epidemiologic data revealed that Kaposi sarcoma is more common in organ-transplanted patients, patients receiving long-term immunosuppressive therapy, and cytotoxic chemotherapy. Even on extended investigation, we were unable to pinpoint how this patient became immunocompromised, other than from his tuberculosis.

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Conclusion

Tuberculosis can cause serious complications such as Kaposi sarcoma, and a high index of suspicion must be maintained when developing the differential diagnosis. We emphasize the importance of obtaining a tissue sample in all patients with a suspicious lesion in any organ, to avoid missing any curable pathologies.

References

1. Oben FT, Wright RDE, Ahaghotu CA. Tuberculous epididymitis with extensive retroperitonealand mediastinal involvement. Urology 2004;64:156-158.

2. Lederman MM. Diseases of the lower respiratory tract. In: Andreoli TE, Carpenter CCJ, Griggs RC, et al (eds). Cecil's Essentials of Medicine. Philadelphia, PA: WB Saunders; 2001:794-795.

3. Chen YJ, Shieh P, Shen L, Orificial tuberculosis and Kaposi sarcoma in an HIV-negative individual. Clin Exp Dermatol 2000;25:393-394.

4. Castro A, Pedreira J, Soriano V, et al. Kaosis sarcoma and disseminated tuberculosis in HIV-negative individual. Lancet 1992;339:868.

5. Emmanoulides C, Miles SA, Mitsuyasu RT. Pathogenesis of AIDS-related Kaposi sarcoma. Oncology (Huntingt) 1996;10:335-341.

6. Beral V, Peterman TA, Berkelman R, Jaffe HW. Kaposi sarcoma among patients with AIDS: sexually transmitted infection? Lancet 1990;335:123-128.

7. Lesher JL. Cytomegalovirus and skin. J Am Acad Dermatol 1988;18:1333-1338.

Zuhal Mujgan Guler, MD, Asiye Kanbay, MD, Bulent Ciftci, MD, Mehmet Kanbay, MD, Aydin Yilmaz, MD, Yetkin Agackiran, MD, and Yurdanur Erdogan, ASSOC. PROF.

From the Department of Pulmonary Medicine and the Department of Pathology, Ataturk Chest Disease and Chest Surgery Hospital, Ankara, Turkey; Department of Pulmonary Medicine, Gazi University School of Medicine, Ankara, Turkey; and Department of Internal Medicine, Fatih University School of Medicine, Ankara, Turkey.

Reprint requests to Mehmet Kanbay, MD, 35. Sokak, 81/5, Bahcelievler, 06490, Ankara, Turkey. Email: [e-mail]

Accepted February 8, 2005.

RELATED ARTICLE: Key Points

* Tuberculosis can be a cause of serious complications such as Kaposi sarcoma and should be taken into account in the differential diagnosis of Kaposi sarcoma.

* Kaposi sarcoma regressed completely with antituberculous therapy without institution of chemotherapy.

* Patients with Kaposi sarcoma should watch for coexisting diseases, such as tuberculosis.