Miliary tuberculosis with acute respiratory failure and histiocytic hemophagocytosis. Successful treatment with extracorporeal lung support and epipodophyllotoxin VP 16‐213

B, Monier; Fauroux, Brigitte; Chevalier, Jean-Yves; Leverger, Guy; Nathanson, M; Costil, J; Tournier, G

doi:10.1111/j.1651-2227.1992.tb12347.x

Cited by 27 publications

(11 citation statements)

References 6 publications

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“…Three (11.1%) of ourp atients hadh aemophagocytosis, whichi sa nother rare haematologic manifestation of TB (25,(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43). The mechanisms of TB that cause haemophagocytosis are unknown.…”

Section: Discussionmentioning

confidence: 90%

Mycobacterium tuberculosis inducing disseminated intravascular coagulation

Wang

Hsueh²,

Lee³

et al. 2005

Thromb Haemost

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Disseminated intravascular coagulation (DIC) can develop infrequently in patients with tuberculosis and has a very high mortality rate. We conducted a retrospective study to evaluate the incidence of tuberculosis-induced DIC and to investigate the clinical manifestation, outcome, and prognostic factors of such patients. From January 2002 to December 2003, all culture-proven tuberculosis patients who developed DIC before starting anti-tuberculosis treatments were selected for this study. Patients who had other clinical conditions or were infected by other pathogens that may have been responsible for their DIC were excluded. Survival analysis was performed for each variable with possible prognostic significance. Our results showed that 27 (3.2%) out of the 833 patients with culture-proven tuberculosis had tuberculosis-induced DIC with a mortality rate of 63.0%. The most common clinical manifestations were fever (63.0%) and multiple patches of pulmonary consolidation (59.3%). Seven (25.9%) patients had disseminated tuberculosis. Twelve (44.4%) developed acute respiratory distress syndrome and three (11.1%) were associated with hemophagocytosis. Twenty-four (88.9%) patients had findings that were unusual for an acute bacterial infection, such as positive acid-fast smear, miliary pulmonary lesions, lymphocytotic exudative pleural effusion, and mediastinal lymphadenopathy. Early anti-tuberculosis treatment significantly improved survival. In conclusion, tuberculosis can cause DIC. Patients with non-miliary, non-disseminated tuberculosis could also develop the rare clinical manifestation. Since the prognosis was very poor in patients not treated at an early stage, a high index of suspicion is required, especially in those with clinical findings suggestive of tuberculosis.

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Section: Discussionmentioning

confidence: 90%

Mycobacterium tuberculosis inducing disseminated intravascular coagulation

Wang

Hsueh²,

Lee³

et al. 2005

Thromb Haemost

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“…Oyama et al [17] presented data indicating that there is an alteration in T cell function in HS with uncontrolled T cells producing large amounts of interfer on (IFN)-y and other lymphokines. Elevated levels of IFN-y, soluble interleukin (IL)-2 receptor (sIL-2R), solu ble CD8, and macrophage-colony stimulating factor (M-CSF) have been found in patients with HS [18][19][20][21], The elevated levels of sIL-2R and sCD8 in active HS, and the normal levels observed in remission, indicate that an acti vation of T cells, especially CD8-positive T cells, contrib utes to the development of HS [21], Uncontrolled IFN-y and M-CSF can lead macrophages to a haemophagocytosing and tumour-necrosis-factor-a-and IL-6-secreting state [17,21], Successful treatment of the syndrome with cyclosporin A or VP-16 (etoposide) and méthylpredniso lone would favour this suggestion [10,17,22].…”

Section: Discussionmentioning

confidence: 99%

Tuberculosis-Associated Haemophagocytic Syndrome: A Report of Two Cases and a Review of the Literature

Ündar¹,

Karpuzoğlu²,

Karadogan³

et al. 1996

Acta Haematol

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The haemophagocytic syndrome (HS) is an uncommon reactive proliferation of mature histiocytes, and is more frequently but not exclusively associated with infections in individuals with pre-existing immunologic abnormalities. As far as we know, only 13 cases of tuberculosis-associated HS have previously been reported. We present here two cases of disseminated tuberculosis-associated HS. Both of the cases recovered with antituberculosis therapy. High-dose methylprednisolone and intravenous immunoglobulin were added in one case because of the extremely severe clinical presentation. This therapy seemed to contribute to the favourable outcome of the patient. The similarities in HLA phenotypes of this patient and others reported in the literature may provide evidence for an underlying immune dysregulation in some cases of infection-associated HS.

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“…The mortality of ARDS patients with PTB requiring MV is relatively high compared with that of patients with ARDS from other causes [9] . Five patients with acute respiratory failure due to PTB were recently reported to be successfully rescued by ECMO [10] , [11] , [12] , [13] , [14] , [15] ( Table 1 ). Given the high mortality rate of ARDS patients with PTB, ECMO could be an important treatment option.…”

Section: Discussionmentioning

confidence: 99%

Acute respiratory distress syndrome due to severe pulmonary tuberculosis treated with extracorporeal membrane oxygenation: A case report and review of the literature

Omote

Kondoh

Taniguchi

et al. 2016

Respiratory Medicine Case Reports

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Mortality in patients with pulmonary tuberculosis remains high, especially in those who develop acute respiratory distress syndrome (ARDS). We report on a-48-year-old man with ARDS due to severe pulmonary tuberculosis who was rescued by extracorporeal membrane oxygenation (ECMO). He was initially hospitalized in the intensive care unit and noninvasive positive-pressure ventilation started. He was also administered anti-tuberculosis drugs and received systemic corticosteroid therapy. Six days later, further deterioration of gas exchange prompted the decision to intubate. However, he experienced progressive deterioration of arterial oxygenation despite conventional ventilatory support. We therefore decided to administer ECMO on day 9. After initiation of these treatments and ECMO support, pulmonary infiltrate and oxygenation status gradually improved and ECMO was discontinued on day 52. The patient was finally discharged from our hospital without severe disability. ECMO should be considered one of the treatment options for the management of ARDS due to severe pulmonary tuberculosis.

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Miliary tuberculosis with acute respiratory failure and histiocytic hemophagocytosis. Successful treatment with extracorporeal lung support and epipodophyllotoxin VP 16‐213

Cited by 27 publications

References 6 publications

Mycobacterium tuberculosis inducing disseminated intravascular coagulation

Mycobacterium tuberculosis inducing disseminated intravascular coagulation

Tuberculosis-Associated Haemophagocytic Syndrome: A Report of Two Cases and a Review of the Literature

Acute respiratory distress syndrome due to severe pulmonary tuberculosis treated with extracorporeal membrane oxygenation: A case report and review of the literature

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