Subacute Cor Pulmonale due to Tumor Embolism

Nakamura, Hiroyuki; Adachi, Hideki; Sudoh, Akihiko; Yagyu, Hisanaga; Kishi, Koji; Oh‐ishi, Shuji; Kusama, Hiroshi; Hashimoto, Takeji; Matsuoka, Takeshi

doi:10.2169/internalmedicine.43.420

Cited by 24 publications

(11 citation statements)

References 10 publications

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“…The vascular involvement of gastric cancer presented here differs from conventional vascular invasion by a malignant neoplasm because its principal change is proliferation of intimal myofibroblasts on pulmonary blood vessels. This type of vascular involvement has been reported under various names, such as subacute cor pulmonale due to pulmonary tumor embolism, 7 hemangiosis carcinomatosa, 8 vascular intimal carcinomatosis, 9 diffuse pulmonary carcinomatous embolization, 10 thrombendarteriitis pulmonalis carcinomatosa, 11 and pulmonary tumor thrombotic microangiopathy 2 . Among these terms, pulmonary tumor thrombotic microangiopathy is widely used correctly to describe this lesion.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary tumor thrombotic microangiopathy resulting from metastatic signet ring cell carcinoma of the stomach

Sakashita¹,

Yokose²,

Fujii

et al. 2007

Pathology International

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Pulmonary tumor thrombotic microangiopathy is an unusual malignancy-related respiratory complication characterized by multiple microthrombi and intimal myofibroblast proliferation. Its clinical manifestation is subacute respiratory failure with pulmonary hypertension. Herein is reported a case of pulmonary tumor thrombotic microangiopathy associated with gastric signet ring cell carcinoma. A 51-year-old woman with gastric cancer died of subacute respiratory failure. Autopsy showed gastric signet ring cell carcinoma with diffuse metastasis of pulmonary lymphatics and pleurae; every organ examined lacked a space-occupying tumor mass. Histologically, proliferated intimal myofibroblasts obliterated most of the pulmonary vascular lumen, and a few stenosed vascular lumina contained cancer cells. In addition, pulmonary vasculature associated with intimal proliferation contained microthrombi. Most cancer cells in the stomach and pulmonary lymphatics were typical signet ring cells, whereas those in vascular lesions were cells of poorly differentiated adenocarcinoma without mucous production. Consistent with a previous report, the latter expressed vascular endothelial growth factor (VEGF) and tissue factor (TF). The proliferated intimal myofibroblasts also expressed type 2A serotonin receptor (5-HT(2A)). These findings suggest that local expression of VEGF, TF, and 5-HT(2A) may be linked to the pathogenesis of this unusual pulmonary complication.

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Section: Discussionmentioning

confidence: 99%

Pulmonary tumor thrombotic microangiopathy resulting from metastatic signet ring cell carcinoma of the stomach

Sakashita¹,

Yokose²,

Fujii

et al. 2007

Pathology International

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“…Macroembolism is a feature of primary tumour sites that are connected by the vena cava to the right ventricle [151]. Tumour emboli possess an unusual level of resistance to recannulation and are therefore more likely to lead to progressive, irreversible obstruction.…”

Section: Pathophysiologymentioning

confidence: 99%

Nonthrombotic pulmonary embolism

Jorens¹,

Marck²,

Snoeckx³

et al. 2009

European Respiratory Journal

161

127

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Nonthrombotic pulmonary embolism (NTPE) is defined as embolisation to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumour), bacteria, fungi, foreign material or gas. The purpose of this article is to describe the clinical signs, pathogenesis, diagnosis and treatment of the different NTPE subtypes.The complex and diverse pathogenesis of different subtypes of emboli is subject to continuing speculation and is certainly far more complex than ''simple'' mechanical obstruction after embolisation of vascular thrombi. Nonthrombotic emboli may also lead to a severe inflammatory reaction both in the systemic and pulmonary circulation, as well as in the lung.NTPE presents a formidable diagnostic challenge, as the condition often presents with very unusual and peculiar clinical signs that are frequently overlooked. They range from very dramatic acute presentations such as acute respiratory distress syndrome to signs observed late in the disease course. Pathological observations play a key role in the exact diagnosis, and sometimes carefully aspirated blood from the pulmonary artery or specific staining of cells recovered from bronchoalveolar lavage fluid may be helpful. Frequently, lung biopsies revealing severe granulomatous reaction or unfortunate post-mortem pathological investigations of pulmonary tissue are necessary to confirm the diagnosis. Here, we also aim to familiarise the reader with the atypical radiological features of NTPE. Thin-section computed tomography of the lungs showing peculiar radiographic findings, such as a feeding vessel, the so-called tree-in-bud pattern or the appearance of micronodules distributed at the termination of bronchovascular bundles, may be observed in certain forms of NTPE.Increased awareness of NTPE as an underestimated cause of acute and chronic embolism, which may result in acute and chronic pulmonary hypertension, is needed. Despite the fact that detailed descriptions of several forms of NTPE have existed for nearly 100 years, well-designed trials have never been performed to evaluate therapy in the different subsets of these patients.

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“…PTTM is detected in 0.9-3.3% autopsies of patients with malignant tumors [1,2] . Although PTTM is relatively well discussed in a number of case reports, the diagnosis of PTTM was made overwhelmingly on autopsy [3][4][5][6][7] , and cases of PTTM with antemortem diagnosis, including our present case, are very rare [8,9] .…”

Section: In View Of These Findings What Is Your Diagnosis?mentioning

confidence: 99%