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+A 69-year-old woman with a history of hypertension presented with a generalized petechial rash and shortness of breath of 3 days duration.
+The rash was nonpruritic, painless, and started at the thighs, but rapidly disseminated to the rest of the body.
+She had progressive dyspnea on exertion, with a significant decrease in exercise tolerance.
+She denied fever, headache, dizziness, hemoptysis, or bleeding from anywhere.
+There was no history of new drug use, unusual food intake, contact with any sick persons, or recent travel.
+Her only medication was enalapril, which she had been taking for several years.
+The patient denied any use of recreational drugs, tobacco, or alcohol.
+On admission, she was afebrile, normotensive with mild tachypnea (respiratory rate of 22 breaths per minute).
+Physical examination revealed scattered petechial rash, more prominent in lower extremities, nonpalpable and nonblanching.
+Chest auscultation revealed coarse crackles bilaterally.
+Cardiovascular, abdominal, and neurological examinations were normal.
+There was no palpable lymphadenopathy or visceromegaly.
+Laboratory examination revealed thrombocytopenia (platelets 7000/μL), anemia (hemoglobin 10.8 mg/dL and hematocrit 34%), and leukocytosis (white blood cells [WBCs] 11,600/μL).
+The coagulation profile was normal, which excluded disseminated intravascular coagulation.
+Arterial blood gas on ambient air revealed a partial pressure of oxygen (PaO2) of 64 Torr, a partial pressure of carbon dioxide (PaCO2) of 37 Torr (pH 7.45), and an increased alveolar-arterial gradient (44 Torr).
+Diffuse airspace consolidation was found on chest roentgenogram (Fig.1A).
+Computed tomography (CT) of the chest showed diffuse ground glass alveolar opacities and patchy infiltrates (Fig.1B, C).
+She was started on broad-spectrum antibiotics and received intravenous steroids.
+Peripheral smear showed giant platelets and occasional small platelet clumps, with no schistocytes.
+A flexible fiber-optic bronchoscopy (FFB) showed normal mucosa with no endobronchial lesions (Fig.2A).
+Serial aliquots of BAL fluid (BALF) turned more hemorrhagic, confirming the bronchoscopic diagnosis of DAH (Fig.2B).
+Cytology of BALF showed a substantial amount of hemosiderin-laden macrophages, further supporting the diagnosis.
+All BALF cultures and gram stains were negative.
+The patient remained with severe thrombocytopenia and hypoxia despite steroids and platelets transfusion.
+High doses of pulse steroids and intravenous immunoglobulins (IVIGs) were added with clinico-radiological improvement.
+A bone marrow aspirate was morphologically normal.
+Additional laboratory studies failed to reveal an etiology for secondary thrombocytopenia (Table ​1), supporting the diagnosis of ITP.
+Steroids were gradually tapered.
+Repeat chest radiograph showed almost complete resolution of bilateral infiltrates (Fig.3).
+Platelet count returned to normal by week 10 after admission without any additional therapies (Fig.4).