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J Tran Van Nhieu

Publications and source records attributed to J Tran Van Nhieu.

9 recordsLinked to original sources
PubMed2003

Severe recurrent cytomegalovirus disease revealed by a colocutaneous fistula in a kidney transplant recipient.

Intestinal disorders are classical complications of cytomegalovirus (CMV) infection in kidney transplant recipients (Helderman JH, Goral S. Gastrointestinal complications of transplant immunosuppression. J Am Soc Nephrol 2002: 13: 277-287). Severe ulcerative colitis that is sometimes lethal has been reported (Foucar E, Mukai K, Foucar K, Sutherland DE, Van Buren CT. Colon ulceration in lethal cytomegalovirus infection. Am J Clin Pathol 1981: 76: 788-801 and Frankel AH, Barker F, Williams G, Benjamin IS, Lechler R, Rees AJ. Neutropenic enterocolitis in a renal transplant patient. Transplantation 1991: 52: 913-914). The immunosuppressive drugs currently used, and notably mycophenolate mofetil (Cellcept), cause significant changes in the incidence, duration, and viral load of CMV infections with severe atypical forms of CMV disease (De Maar EF, Verschuuren EA, Homan vd Heide JJ, et al. Effects of changing immunosuppressive regimen on the incidence, duration and viral load of cytomegalovirus infection in renal transplantation: a single center report. Transpl Infect Dis 2002: 4: 17-24 and Perez Valentin MA, Cofan F, Sole M, et al. Atypical cytomegalovirus in renal transplantation: a new form of presentation. Nefrologia 2002: 22: 381-385). This report describes a patient who suffered from several episodes of colitis due to an unusual and late-appearing CMV infection.

Antigens, Viral↗
PubMed1997

Histopathologic impact of GB virus C infection on chronic hepatitis C.

BACKGROUND & AIMS: Dual infection by hepatitis GB virus type C (GBV-C) and hepatitis C virus (HCV) is common. To assess the histopathologic impact of GBV-C infection on liver lesions, liver biopsy specimens of 105 patients chronically infected with HCV, 17 of whom (15%) were also infected with GBV-C, were reviewed. METHODS: Semiquantitative histopathologic assessment of liver lesions was performed using the Knodell's score and the METAVIR grading system. RESULTS: Hepatitis activity was mild, moderate, or severe in 3 (18%), 11 (64%), and 3 (18%) patients, respectively, infected with GBV-C and HCV vs. 26 (29%), 56 (64%), and 6 (7%) patients, respectively, infected with HCV alone (no significant difference). Cirrhosis was present in 4 (24%) coinfected patients vs. 19 (22%) HCV-positive patients (no significant difference). No significant difference in fibrosis, presence of portal lymphoid aggregates, steatosis, and hemosiderosis was observed between the two groups. There was no significant difference in the evaluation of each item of the Knodell's score. CONCLUSIONS: This detailed histopathologic evaluation of GBV-C infection in chronic hepatitis C shows that GBV-C infection does not affect histopathologic severity and characteristics of chronic hepatitis C, thus suggesting a minor role of GBV-C infection in liver disease.

Adult↗
PubMed1996

Secondary alveolar proteinosis in cancer patients.

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.

Biopsy↗
PubMed1993

Expression of tumor necrosis factor-alpha gene in alveolar macrophages from patients with the adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is a complex syndrome in which pathogenesis is multifactorial. TNF-alpha, known to be pivotal in tissue damage, has been shown to have high levels in blood and alveolar fluid in ARDS. The identification of the cells responsible for this production in the alveolar milieu has not yet been reported. In order to evaluate the TNF-alpha gene expression in ARDS we have analyzed by in situ hybridization, using RNA probes, alveolar macrophages (AM) obtained by BAL from seven patients with ARDS, eight patients with miscellaneous respiratory diseases, and three control patients. In freshly collected AM from patients with ARDS, 66 +/- 14.5% cells expressed the TNF-alpha gene without in vitro stimulation. This TNF-alpha expression does not result from the BAL procedure itself since only a few unstimulated control AM contained TNF-alpha mRNA transcripts. TNF-alpha expression in AM is not restricted to patients with ARDS since it has also been observed in miscellaneous respiratory diseases; however, this expression is a constant feature in ARDS. These results demonstrated the major role of AM in the intra-alveolar production of TNF-alpha, and they point out the necessity in ARDS for a specific intra-alveolar therapy.

Adult↗
PubMed1990

Pulmonary alveolar proteinosis associated with Pneumocystis carinii. Ultrastructural identification in bronchoalveolar lavage in AIDS and immunocompromised non-AIDS patients.

Pneumocystis carinii (PC) has been recognized as frequently responsible for most opportunistic pulmonary infections occurring in immunocompromised AIDS and non-AIDS patients. Moreover, these patients can be considered at risk for secondary pulmonary alveolar proteinosis. Therefore, we have investigated the occurrence of associated secondary alveolar proteinosis and PC pneumonitis in AIDS and non-AIDS immunocompromised patients. In a series of 26 bronchoalveolar lavages (BAL) in patients with PC pneumonitis (19 AIDS and seven non-AIDS patients), we observed on light microscopy, in addition to the honeycombed material, areas of an extracellular material that had a different pattern which was suggestive of that described in alveolar proteinosis. A systematic ultrastructural study of these 26 BAL fluid samples demonstrated in each of them an accumulation of phospholipid surfactantlike extracellular material mixed or not with the PC cysts. In nine cases, the observation of lipoproteinaceous material on light microscopy and abundant phospholipid material with myelinlike and myelin tubular laminated structures on electron microscopy was highly suggestive of an associated pulmonary alveolar proteinosis (PAP). Such an accumulation of extracellular material was not observed in the 11 BAL fluid samples collected in immunocompromised patients (seven AIDS and four non-AIDS patients) without PC pneumonitis. These findings demonstrated a particular frequency of associated PAP with PC pneumonitis. These results raise important questions concerning (1) the consequence of such an alveolar accumulation of lipoproteinaceous material on the clinical status and prognosis of the pneumonitis, and (2) the mechanisms responsible for this accumulation.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Hyperintense benign liver lesions on spin-echo T1-weighted MR images: pathologic correlations.

BACKGROUND: To determine the incidence of hyperintensity on T1-weighted spin echo (SE) images in benign liver lesions, value of fat-suppressed magnetic resonance (MR) imaging for the detection of fat within these lesions, and the causes of hyperintensity by correlation to pathologic examinations. METHODS: Five hundred forty-nine patients with 805 benign liver lesions including 585 hemangiomas, 188 focal nodular hyperplasias (FNHs), 14 hepatic adenomas (HAs), 14 focal fatty infiltrations (FFIs), two biliary cystadenomas, and two hemorrhagic cysts were examined by T2-weighted and T1-weighted SE MR imaging. For hyperintense lesions on T1-weighted SE images, fat-suppressed images were obtained by selective presaturation of fat. RESULTS: Thirty-two lesions (four FNHs, 10 HAs, 14 FFIs, two biliary cystadenomas, and two hemorrhagic cysts) appeared hyperintense on T1-weighted SE images; 21 of these became hypointense on the fat-suppressed T1 weighted SE images (one FNH, six HAs, and 14 FFIs) and contained fat at pathological examination. The other 11 lesions remained hyperintense on fat-suppressed T1-weighted SE images and had no fat deposition. Causes of hyperintensity in these cases were sinusoidal dilatation, copper deposition, hemorrhage, and high protein content. CONCLUSION: Among benign liver lesions, hyperintensity on T1-weighted SE images is rare (3.9%). Causes of this hyperintensity are fat deposition, copper accumulation, sinusoidal dilatation, bemorrhage, and high protein content. Fat-suppressed imaging can distinguish fat deposition from other causes of hyperintensity.

Adenoma↗