INTRODUCTION: Kaposi's sarcoma of Lung is a complication of Herpes virus 8 which predominantly is thought to occur in HIV infected male homosexual population with extensive muco-cutaneous involvement. We present a case where Kaposi's sarcoma of Lung occurred in an HIV infected woman without any muco-cutaneous involvement.
CASE PRESENTATION: A 28-year-old woman with AIDS was admitted to the hospital with two weeks history of progressively worsening right sided chest pain, cough and dyspnea. Patient had been hospitalized and treated for pneumonia twice in the past eight months with her chest radiographs demonstrating right middle lobe pneumonia. The patient was well-developed and well-nourished. Her temperature was 38o C, respiratory rate was 18 breaths/min, and blood pressure and heart rate were normal. Oxygen saturation was 93% on 2L/min by nasal cannula. Chest auscultation revealed coarse crackles in right axilla. Rest of her examination was unremarkable. WBC count was 5000/mcL with a differential of 46% neutrophils, 30% lymphocytes, 9% monocytes and 15% eosinophils. CD4 cell count was 216. Blood and sputum cultures showed no growth. Chest CT scan demonstrated a ‘crazy paving’ pattern in the RML. At bronchoscopy, there were no oral or tracheobronchical mucosal lesions, no endobronchial masses. The patient was evaluated for non resolving consolidation. Our differential diagnosis included organizing pneumonia, tuberculosis, fungal pneumonia, viral infection and neoplasm. Patient underwent VATS with biopsy of RML which was consistent with KS. Since the patient showed marked clinical and radiographic improvement following treatment with HAART decision to with hold cytotoxic therapy was made. The patient has returned to work. She has gained weight and her respiratory symptoms have resolved.
DISCUSSIONS: Pulmonary Kaposi's sarcoma affects 15 to 20% of HIV infected individuals. KS is more prevalent in homosexual males. Involvement of Lungs is thought to be multicentric in the backdrop of extensive mucocutaneous disease. Spindle cells are the hallmark of KS. Endothelial cells, extravasated erythrocytes, hemosiderin laden macrophages, granulation tissue, vascular slits and vascular processes complete the histological picture. Necrosis is not a feature of KS and might be caused by concurrent infection. Involvement of pleura may lead to pleural effusions which are usually exudative and hemorrhagic. Concurrent opportunistic infection occurs in 75% of patients with pulmonary KS. KS may present as reticulonodular infiltrates, diffuse interstitial infiltrates with linear or septal infiltration and focal airspace consolidation. Crazy paving as a feature of KS has not been reported earlier. KS is identified as red or purple appearing lesion at airway bifurcations in most of patients on Bronchoscopy. Absence of endobronchial lesions in patients with parenchyma KS is rare. Because of patchy nature of KS, transbronchial biopsy has a low diagnostic yield (26 to 60%) and the risk of bleeding is thought to be about 30%. Video assisted thoracoscopy and open lung biopsy have relatively high yield. Treatment for KS is not curative. Liposomal daunarubicin has become standard of care. Radiation therapy is reserved for patients in whom disease progresses despite chemotherapy. HAART therapy causes regression in size of KS lesions. HAART effectively prevents progression of KS lesions and allow discontinuation of maintenance chemotherapy.
CONCLUSION: 1.KS should be considered in AIDS patient with non-resolving pneumonia even in absence of mucocutaneous involvement. 2.KS should be included in the differential diagnosis of crazy paving pattern on CT scan of chest.3.Liposomal anthracyclines are effective for palliation and well directed HAART plays a role in containing the disease.
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