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Clinical Features of Pulmonary Tumor Thrombotic Microangiopathy: Analysis of 149 Cases in Literature
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A3794 - Clinical Features of Pulmonary Tumor Thrombotic Microangiopathy: Analysis of 149 Cases in Literature
Author Block: R. Godbole1, N. Kamangar2; 1Pulmonary, UC Irvine, Orange, CA, United States, 2Pulmonary, Olive View - UCLA Medical Center, Sylmar, CA, United States.
Rationale: Pulmonary tumor thrombotic microangiopathy (PTTM) is a disease process in which cancer cells embolize to the pulmonary vasculature and fibrocellular intimal thickening occurs causing severe pulmonary hypertension, right heart failure, and death. Analysis of published literature reveals clinical features of PTTM that may enable an earlier diagnosis.
Methods: We conducted a systematic Pubmed search with the term “pulmonary tumor thrombotic microangiopathy” in mid-2017. A total of 188 English language publications were reviewed, of which 70 actually pertained to PTTM and were included in this analysis.
Results: A total of 149 cases of PTTM are reported in literature, 84 men and 65 women, with an average age of 57 years. Fifty-seven out of 66 cases (86.4%) reported a cough and 92 out of 98 cases (93.9%) reported dyspnea. Eighty seven out of 93 patients (93.5%) were hypoxemic. Thirty-one out of 33 patients (93.9%) had an elevated D-dimer, 29 out of 33 patients (87.9%) had an anemia, 16 out of 17 patients (94.1%) had an elevated lactate dehydrogenase, and 28 out of 36 patients (77.8%) had thrombocytopenia. Thirty five out of 50 patients (70.0%) noted an abnormal chest roentgenogram. On computed tomography of the chest, 16 out of 18 patients (88.9%) noted septal thickening, 14 out of 16 (87.5%) noted lymphadenopathy, 20 out of 24 (83.3%) noted nodules, and 20 out of 24 (83.3%) noted ground glass opacities. Fifty-one out of 57 patients (89.4%) had echocardiographic evidence of pulmonary hypertension with an average right ventricular systolic pressure of 70 mmHg. All cases noted the presence of diffuse tumor emboli with fibrocellular intimal proliferation in the pulmonary arterioles. Eighty-nine of 149 patients (59.7%) had gastric adenocarcinoma. In 51 out of 77 cases (66.2%), the primary malignancy was diagnosed an average of 3.5 years prior to the development of PTTM. Lung tissue was examined antemortem in only 13 out of 149 patients (8.7%). From the onset of symptoms, the average time to death was 10 weeks.
Conclusion: Clinical features across 149 cases included in this analysis may help identify PTTM early. More nuanced details, such as the progression of symptoms and laboratory abnormalities, the distribution and appearance of radiographic findings (for example, diffuse versus localized and smooth versus nodular septal thickening), and the presence of pulmonary venular involvement on lung histology ought to be reported to enhance our understanding of this disease process.
Author Block: R. Godbole1, N. Kamangar2; 1Pulmonary, UC Irvine, Orange, CA, United States, 2Pulmonary, Olive View - UCLA Medical Center, Sylmar, CA, United States.
Rationale: Pulmonary tumor thrombotic microangiopathy (PTTM) is a disease process in which cancer cells embolize to the pulmonary vasculature and fibrocellular intimal thickening occurs causing severe pulmonary hypertension, right heart failure, and death. Analysis of published literature reveals clinical features of PTTM that may enable an earlier diagnosis.
Methods: We conducted a systematic Pubmed search with the term “pulmonary tumor thrombotic microangiopathy” in mid-2017. A total of 188 English language publications were reviewed, of which 70 actually pertained to PTTM and were included in this analysis.
Results: A total of 149 cases of PTTM are reported in literature, 84 men and 65 women, with an average age of 57 years. Fifty-seven out of 66 cases (86.4%) reported a cough and 92 out of 98 cases (93.9%) reported dyspnea. Eighty seven out of 93 patients (93.5%) were hypoxemic. Thirty-one out of 33 patients (93.9%) had an elevated D-dimer, 29 out of 33 patients (87.9%) had an anemia, 16 out of 17 patients (94.1%) had an elevated lactate dehydrogenase, and 28 out of 36 patients (77.8%) had thrombocytopenia. Thirty five out of 50 patients (70.0%) noted an abnormal chest roentgenogram. On computed tomography of the chest, 16 out of 18 patients (88.9%) noted septal thickening, 14 out of 16 (87.5%) noted lymphadenopathy, 20 out of 24 (83.3%) noted nodules, and 20 out of 24 (83.3%) noted ground glass opacities. Fifty-one out of 57 patients (89.4%) had echocardiographic evidence of pulmonary hypertension with an average right ventricular systolic pressure of 70 mmHg. All cases noted the presence of diffuse tumor emboli with fibrocellular intimal proliferation in the pulmonary arterioles. Eighty-nine of 149 patients (59.7%) had gastric adenocarcinoma. In 51 out of 77 cases (66.2%), the primary malignancy was diagnosed an average of 3.5 years prior to the development of PTTM. Lung tissue was examined antemortem in only 13 out of 149 patients (8.7%). From the onset of symptoms, the average time to death was 10 weeks.
Conclusion: Clinical features across 149 cases included in this analysis may help identify PTTM early. More nuanced details, such as the progression of symptoms and laboratory abnormalities, the distribution and appearance of radiographic findings (for example, diffuse versus localized and smooth versus nodular septal thickening), and the presence of pulmonary venular involvement on lung histology ought to be reported to enhance our understanding of this disease process.
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