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(CHEST 2000; 117:250S-251S) Abbreviations: [[Alpha].sub.1]AT = [[Alpha].sub.1]-antitrypsin; ANEC = antineutrophil elastase capacity; ELF = epithelial lining fluid; IL = interleukin; NE = neutrophil elastase Individuals with [[Alpha].sub.1]-antitrypsin ([[Alpha].sub.1]AT) deficiency develop [...]

AbstractBackground: Histiocytoses represent a large, puzzling group of diseases which may involve the skin and other organs. At present, juvenile xanthogranuloma is the disorder most often confused with Langerhans cell histiocytosis. A complex overlap exists between juvenile xanthogranuloma and Langerhans cell histiocytosis, with lesions showing clinical and/or pathological features of both disorders. Observations: We report 2 patients affected by Langerhans cell histiocytosis who, during chemotherapy, presented cutaneous lesions with clinical and histological features of juvenile xanthogranuloma. During the therapy, in both cases, histological examination of new biopsies revealed the presence of Touton giant cells in the dermis with a few histiocytic cells; immunohistochemical staining was negative for CD1a, and no Birbeck granules were seen by ultrastructural examination. Results and Conclusion: A possible explanation for the link between Langerhans cell histiocytosis and juvenile xanthogranuloma regards the lineage development and the relationships of histiocytes. We suggest that chemotherapy can modify the production of cytokines by influencing the conversion or ‘maturation’ of pathological cells into macrophages or xanthomatous cells and fusing them to form multinucleated giant Touton cells. In our opinion, the modification of the cutaneous lesions during chemotherapy in Langerhans cell histiocytosis patients, as observed in our cases, could be a favorable prognostic factor.Copyright © 2004 S. Karger AG, Basel

Abstract Orthotopic liver transplantation (OLT) is used as a definitive treatment for end-stage liver disease and prolonged posttransplant survival has already been reported. The incidence of late mortality and graft morbidity is, however, not well defined and the role of primary viral disease in the long-term follow-up results is not clear. Data of posttransplant follow-up in 213 patients, 156 adults and 57 children, who survived at least 1 year were reviewed in order to define causes of graft dysfunction, graft loss and death. In 98 patients, 103 persistent graft dysfunctions were found. Thirty-four grafts were later lost [28 deaths and 6 successful retransplantations (re-OLT)]. The results were reviewed grouping patients according to their age and viral hepatitis status at the time of the transplantation. HBV-positive patients (51) showed 4 re-OLT (1 HBV), 3 liver-related deaths (2 HBV), 24 graft dysfunctions (8 HBV, 5 HCV), and 85.2 % 6-year survival (based on 100 % survival at 1 year). HCV-positive adults (28) showed 1 re-OLT, 3 HCV-related deaths, 24 graft dysfunctions (19 HCV), and 68.8 % 6-year survival. HBV–HCV-positive patients (14) showed no graft loss and death, 10 graft dysfunctions (7 HCV, 1 HBV, 2 HBV–HCV), and 81.8 % 6-year survival. HBV–HCV-negative adults (63) showed 3 non-hepatitis-related re-OLT, 5 liver-related deaths (2 HCV), 24 graft dysfunctions (6 HCV, 2 HBV), and 83.1 % 6-year survival. HBV–HCV-negative children (49) showed no re-OLT, 1 HCV-related death, 14 graft dysfunctions (3 HCV), and 92.6 % 6-year survival. HCV-positive children (8) showed 1 HCV-related re-OLT, 2 HCV-related deaths, 4 graft dysfunctions (3 HCV), and 81.3 % 6-year survival. The main cause of graft dysfunction was hepatitis (45 HCV and 13 HBV), followed by technical complications (21), rejection (16), recurrent alcoholism (3), HIV infection (1), and unknown causes (4). In this long-term posttransplant follow-up series, viral hepatitis led to graft dysfunction in 58/103 (56.3 %) cases, late graft failure was viral hepatitis-related in 11/20 (55 %) cases, and, as a total, HCV infection was present in 45/58 (77.5 %) cases of viral hepatitis-related graft damage. Looking at the timing of hepatitis-related graft failure, in 70 % of cases death occurred after the 5th post-transplant year. In our experience, the occurrence of hepatitis, particularly HCV induced, was common and led to abnormal graft function, but the 6-year posttransplant survival (based on 100 % survival at 1 year) in patients surviving for at least 1 year did not differ on the basis of the pretransplant viral hepatitis status. This finding may be consistent with the slow progression of the viral damage and longer follow-up results remain to be established. Nevertheless, data from the present study suggest that in long-term liver transplant survivors, the risk of deteriorating liver damage and eventual failure after 5 years remains only in those patients experiencing a viral hepatitis infection.

Between June 1988 and May 1991 88 orthotopic liver transplants and 1 liver and pancreas transplant were performed at the Liver Transplantation Department of the Ospedale Maggiore of Milan. All the patients underwent mycological surveillance and received antifungal prophylaxis with oral amphotericin B (6000 mg/day) or oral or intravenous fluconazole (200 mg/day) from the time of their transplant. The incidence of Candida colonization was 67%. Fluconazole was superior to oral amphotericin B in the treatment of C. albicans colonization (99 vs 15), but less effective in the treatment of colonization by other Candida spp. (03 vs 33). Deep-seated candidiasis developed in 5 patients, caused by C. albicans in 4 cases and C. krusei in 1. C. albicans infection resolved rapidly with fluconazole in 2 subjects, with intravenous amphotericin B alone in 1, and with amphotericin B plus flucytosine in the other. On the contrary, C. krusei infection did not respond to treatment with amphotericin B combined with flucytosine. Aspergillosis was diagnosed in 11 patients, of whom 4 died from invasive aspergillosis, despite 15 and 26 days of amphotericin B treatment in 2. In another patient invasive aspergillosis, diagnosed a few hours before retransplantation, improved with liposomal amphotericin B, but this man died from cytomegalovirus infection one month later. Aspergillosis was eradicated by itraconazole in 4 other patients and by topical amphotericin B in 2 whose infection was localized to surgical wound.

By means of a mathematical score previously generated by discriminant analysis on 90 lung cancer patients, a new and larger group of 261 subjects [209 with non-small-cell lung cancer (NSCLC) and 52 with small-cell lung cancer (SCLC)] was analysed to confirm the ability of the method to distinguish between these two types of cancers. The score, which included the serum neuron-specific enolase (NSE) and CYFRA-21.1 levels, permitted correct classification of 93% of the patients. When the misclassifications were analysed in detail, the most frequent errors were associated with limited disease SCLC with low NSE levels and with advanced NSCLC with high NSE levels. This demonstrates the importance of the marker in correctly categorizing patients.

We present a patient with left atrial myxoma embolizing to the ascending aorta. The features have not been reported previously and were diagnosed with transesophageal echocardiography. (J Am Soc Echocardiogr 1997;10:381-3.)

Endogenous PCR inhibitors hamper DNA amplification of Mycobacterium tuberculosis DNA in sputum samples. Use of an anion binding resin (GeneReleaser [GR]) improved PCR sensitivity from 77% (27 of 35 culture-positive samples) with phenol-chloroform extraction (P-C) alone to 91% (GR without P-C; P > 0.05) and 100% (P-C and GR combined; P < 0.05).