Extrapulmonary Pneumocystis jirovecii infection in an advanced HIV-infected patient: A case report and literature review.

BACKGROUND: Pneumocystis jirovecii infection is the most common opportunistic infection that causes pneumonia in human immunodeficiency virus (HIV)-infected patients; however, extrapulmonary P. jirovecii infection is extremely rare after the use of antiretroviral therapy. Here, we present the second reported case of paraspinal mass caused by P. jirovecii infection in an advanced HIV-infected patient. CASE PRESENTATION: A 45-year-old woman presented with dyspnea on exertion, and significant weight loss within the preceding 4 months. Initial complete blood count (CBC) findings revealed pancytopenia with a hemoglobin (Hb) level of 8.9 g/dL, a white blood cell (WBC) count of 2180 cells/mm3 with 68% neutrophils, and a platelet count of 106,000 cells/mm3. Anti-HIV was positive with an absolute cluster of differentiation 4 (CD4) count of 16 cells/ mm3. A computed tomography scan of the chest revealed an enhancing soft tissue mass-like lesion at the right paravertebral region (T5-T10 level) and a thick-walled cavity lesion at the left lower lung. A CT-guided biopsy of the paravertebral mass was performed and histopathology revealed granulomatous inflammation consisting of dense aggregates of epithelioid cells and macrophages, and scattered foci of pink foamy to granular materials amidst the granulomatous inflammation. Gomori methenamine silver (GMS) staining revealed thin cystic-like structures (ascus) that were observed to be morphologically consistent with P. jirovecii. Molecular identification and DNA sequencing from the paraspinal mass was 100% identical to P. Jirovecii. The patient was successfully treated with oral trimethoprim-sulfamethoxazole for 3 weeks and antiretroviral therapy (ART) with tenofovir (TDF), lamivudine (3TC), and dolutegravir (DTG). A follow-up CT scan of the chest at 2 months after treatment showed a decrease in sizes of both the paravertebral mass and the cavitary lung lesion. CONCLUSIONS: Extrapulmonary pneumocystosis (EPCP) has become an extremely rare condition in HIV-infected patients after the widespread use of ART. EPCP should be considered in ART-naive HIV-infected patients suspected of having or diagnosed with Pneumocystis jirovecii pneumonia who present with atypical symptoms and/or signs. Histopathologic examination with GMS staining of affected tissue is necessary for the diagnosis of EPCP.

Endotyping of Chronic Rhinosinusitis With and Without Polyp Using Transcription Factor Analysis.

Inflammation of the nose and paranasal sinus or rhinosinusitis (RS) is a significant global health problem that is both very common and very costly to treat. Previous reports reveal variability in histology and mechanism of inflammation in patients with chronic rhinosinusitis with and without polyp (CRScNP and CRSsNP, respectively). There are various methods and hypothesis that try to explain this variability. Accordingly, the aim of this study was to investigate the incidence of each type of sinonasal inflammation among patients diagnosed with CRScNP or CRSsNP using transcription factor analysis (TFA). This study included mucosa specimens from nose/paranasal sinuses from patients with chronic rhinitis (CR), CRSsNP, or CRScNP that were obtained at the Department of Otorhinolaryngology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand during the June 2009 to May 2012 study period. TFA was employed to measure the following transcription factors: T-box transcription factor (T-bet) for Th1, GATA binding protein 3 (GATA-3) for Th2, retinoic acid-related orphan receptor C (RORC) for Th17, and forkhead box P3 (FOXP3) for Treg. Forty-one subjects (22 males, 19 females) were enrolled, with a mean age of 45.93 ± 13 years. Twenty-six patients were diagnosed with CRScNP, 7 with CRSsNP, and 8 with CR (controls). The majority of CRScNP specimens (76.9%) had eosinophil count greater than 100 cells/high-power field (HPF). Mean eosinophil count was 930.08 ± 1,399 cells/HPF (range: 17-5,570). Th2 transcription factor (GATA-3) was statistically significantly higher in the CRScNP group than in the CRS and control groups (p < 0.001); whereas, Treg transcription factor (FOXP3) was statistically significantly lower in the CRScNP group than in the CRSsNP and control groups (p < 0.001). The transcription factors for Th1 and Th17 (T-bet and RORC, respectively) were not significantly different among the three groups. The result of transcription factor analysis revealed hyperfunction of Th2 in patients with CRScNP, which might result in hypereosinophilic infliltration in the polyps. One explanation for this finding is the decreased activity of Treg. Although environment-host interaction is the most probable hypothesis, the etiology of aberrant adaptive immunity needs to be elucidated.

Autologous Fibrin-Base Scaffold for Chondrocytes and Bone Marrow Mesenchymal Stem Cells Implantation: The Development and Comparison to Conventional Fibrin Glue.

Objective: The authors developed the autologous fibrin-base scaffold for chondrocytes and bone marrow mesenchymal stem cells (BM-MSCs) implantation and evaluated cells viability in autologous fibrin-base scaffold comparing to commercial fibrin glue. Material and Method: The chondrocytes and BM-MSCs were seeded into autologous fibrin-base scaffold and commercial fibrin glue. The cell viability and proliferation were evaluated at 1 and 7 days. The histology were evaluated with hematoxylineosin (H&E) staining and cartilaginous matrices formation with Alcian blue, Saffanin-0, Toluidine blue, and Collagen type II staining at 6 weeks. The fixation of the scaffolds was observed. Results: The chondrocytes and BM-MSCs could not survive in commercial fibrin glue. The chondrocytes and BM-MSCs in autologous fibrin-base scaffold could proliferate and synthesize the cartilaginous matrices on Alcian blue, Saffanin-0, Toluidine blue, and Collagen type II staining at 6 weeks. The fixation strength is excellent. Conclusion: The developed autologous fibrin-base scaffold can be used as the scaffold for chondrocytes and BM-MSCs implantation with potential to implant chondrocytes and BM-MSCs arthroscopically.

Inflammatory patterns in upper airway disease in the same geographical area may change over time.

BACKGROUND: Inflammatory patterns of nasal polyps (NPs) may vary. Changes over time have not been investigated so far. This study was designed to evaluate the inflammatory patterns of NPs in Thailand at two time points 12 years apart, explore differences in Staphylococcus aureus (SA) mucosal carriage rates over time, and the latter's relationship with the inflammatory patterns. METHODS: Formalin-fixed nasal tissue was obtained from 89 (47 in 1999 and 42 in 2011) patients suffering from chronic rhinosinusitis with NPs (CRSwNPs). Tissues were evaluated for eosinophils, neutrophils, IgE(+) cells, IgE and macrophage mannose receptors, interleukin (IL)-5 and IL-17 cytokine profile, and the presence of SA, using automated immunohistochemistry and peptide nucleic acid-fluorescence in situ hybridization. RESULTS: We found a significant increase in the absolute values of eosinophils and IgE(+) cells in the 2011 CRSwNP tissue series compared with 1999 and a significant but smaller increase in neutrophils. Semiquantitative evaluation revealed significantly higher mean values of positive cells for all studied inflammatory markers in the 2011 group of patients, except for the high-affinity IgE receptor. This "eosinophilic shift" of inflammation was accompanied by higher SA carriage, as well as higher frequencies of SA invasion (54.8% versus 10.6%; p < 0.001) in the 2011 compared with 1999 subjects. Patients with asthma were more likely to have higher SA carriage rates compared with nonasthmatic patients. CONCLUSION: There was a shift from predominantly neutrophilic to eosinophilic CRSwNPs in Thai patients within 12 years, with an increase in various inflammatory markers including IgE, which is associated with an increase in intramucosal presence of SA.