A patient with multiple myeloma and respiratory insufficiency due to accumulation of paraprotein in the alveolar space

Meijer, W. G.; Kooy, Marinus van Marwijk; Laddé, Ben E.

doi:10.1111/j.1365-2141.1994.tb08338.x

Cited by 10 publications

(4 citation statements)

References 8 publications

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“…Different studies reported high serum levels of LDH, CRP, IL-6, and the high fever in the course of multiple myeloma have been indicated poor prognostic rate with terminal stage (Barlogie et al, 1989;Murakami et al, 2000). Direct myeloma cell infiltration and amyloid deposit in lungs tissues associates with terminal stages of multiple myeloma (Suchman et al, 1981;Meijer et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Liver Involvement in Multiple Myeloma: A Hospital Based Retrospective Study

Poudel¹,

Mittal²,

Shrestha³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

Liver Involvement in Multiple Myeloma: A Hospital Based Retrospective Study

Poudel¹,

Mittal²,

Shrestha³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Most of the initial reports have been of patients with chronic myeloid leukemia (CML) [2,3,5,13,47] but the disease has been also reported in acute leukemia [3,8], myeloma [28], Waldenstr6m disease, and lymphoma [3] ( Table 2).…”

Section: Secondary Alveolar Proteinosis: Which Underlying Conditions?mentioning

confidence: 99%

Secondary alveolar proteinosis in cancer patients

Ladeb

Fleury‐Feith²,

Escudier³

et al. 1996

Support Care Cancer

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Pulmonary alveolar proteinosis (AP) is a rare cause of progressive respiratory failure in the normal host. It was first described by Rosen and coworkers in 1958 on the morphological basis of the accumulation of a PAS-positive material in the alveolar space. A couple of years later, AP was found to be unexpectedly associated with malignant diseases, especially with acute or chronic myeloid leukemias. These forms were called secondary AP in opposition to the primary forms observed in normal hosts. Probably because of its morphological definition and late diagnosis by means of histology or autopsy material, secondary AP has been considered to be life-threatening for a long time. However, recent observations show that AP can be diagnosed early in the course of the disease, especially through bronchoalveolar lavage, as long as the pathologist is aware of this possibility. Another point is that secondary AP can be reversible, both clinically and morphologically. This article summarizes the clinical features, morphological findings, and the main malignant diseases associated with secondary AP. We also comment on the hypotheses proposed in the literature to explain the association of AP, malignant disease, and immunosuppression. Alveolar macrophage is likely a key factor in the occurrence of secondary AP.

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“…[2][3][4][5] One patient with respiratory failure and infiltration of lung tissue with plasma cells had been diagnosed with multiple myeloma 5 years earlier and developed respiratory failure following radiation therapy for an orbital plasmacytoma. 3 Two other patients without acute lung injury had bilateral lung densities on radiographic imaging and pathological evidence of neoplastic plasma cell infiltration of the lungs.…”

Section: Discussionmentioning

confidence: 99%

Acute respiratory distress syndrome due to pulmonary involvement by neoplastic plasma cells in multiple myeloma

Marmor

Farber²,

Gottlieb³

2006

Thorax

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Pulmonary involvement with multiple myeloma occurs infrequently and may be difficult to distinguish from more common primary lung tumours, metastatic disease, or other pleural and parenchymal abnormalities. A patient who developed acute respiratory distress syndrome (ARDS) was subsequently found to have multiple myeloma with involvement of lung parenchyma by neoplastic plasma cells. Only one other report of ARDS in association with multiple myeloma was found, and there are no previous reports where the appearance of ARDS antedated a diagnosis of multiple myeloma. In patients with ARDS, parenchymal involvement from multiple myeloma should be included in the differential diagnosis.A 65 year old woman was admitted to hospital complaining of dull pleuritic retrosternal chest pain of 5 days' duration. It had been somewhat relieved with non-steroidal anti-inflammatory drugs. She also complained of a cough and worsening dyspnoea upon exertion. A 2 month history of nausea was accompanied by a weight loss of 11 lb. Past medical history included non-insulin dependent diabetes, hypertension, asthma, and obesity.On physical examination the patient initially appeared comfortable at rest but was dyspnoeic with limited activity. Her temperature was 101.7˚F, heart rate 96 beats/min, respiratory rate 20 breaths/min, blood pressure 117/ 72 mm Hg. The only significant physical finding was bilateral basilar crackles. Laboratory data revealed a white blood cell count of 10 400/mm 3 and haemoglobin of 9.7 g/dl. The serum sodium was 131 mEq/l, total calcium 8.5 mg/dl, and creatinine 1.0 mg/dl. Urinalysis revealed trace protein. The chest radiograph showed bilateral multifocal areas of nodular consolidation (fig 1), and the ECG showed normal sinus rhythm with diffuse non-specific T wave abnormalities. Serum troponin levels were normal. Oxygen saturation was 88% on room air and 94% on 5 l oxygen via nasal cannulae.The patient's respiratory status steadily declined over the ensuing days, despite treatment with antibiotics for presumed pneumonia. Four days after admission she was in acute respiratory distress with tachypnoea and the use of accessory muscles. Arterial blood gas showed pH 7.46, PaCO 2 5.2 kPa, and PaO 2 4.5 kPa on 50% FiO 2 non-rebreather mask. She required intubation and mechanical ventilation with a low tidal volume high positive end expiratory pressure protocol. Bronchoalveolar lavage yielded fluid that contained 40% macrophages, 25% neutrophils, and 35% lymphocytes. No malignant cells and no pathogens were identified. All blood, sputum, and urine cultures were negative. A chest CT scan showed diffuse, patchy, multifocal air space consolidation bilaterally with a nodular character, small bilateral pleural effusions, mediastinal lymphadenopathy, and a questionable lytic lesion of the T9 vertebra.

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A patient with multiple myeloma and respiratory insufficiency due to accumulation of paraprotein in the alveolar space

Cited by 10 publications

References 8 publications

Liver Involvement in Multiple Myeloma: A Hospital Based Retrospective Study

Liver Involvement in Multiple Myeloma: A Hospital Based Retrospective Study

Secondary alveolar proteinosis in cancer patients

Acute respiratory distress syndrome due to pulmonary involvement by neoplastic plasma cells in multiple myeloma

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