[A rare complication of chronic pancreatitis: pancreatico-pleural fistula]. / Une complication rare d'une pancréatite chronique: la fistule pancréatico-pleurale.

Pleural effusion is a rare complication of chronic pancreatitis. We report a case observed in a 39-year-old patient hospitalized for dyspnea and pain in the lower left thorax. Chest x-ray revealed left pleural effusion. The exudative pleural fluid contained a very high amylase level. CT-scan revealed a pseudo-cyst of the tail of the pancreas extending into contact with the diaphragm and the chronic pancreatitis lesions. Medical treatment associating thoracic drainage, somatostatin analog, and antibiotics was unsuccessful. Thoracoscopic pleural decortication was performed. The patient then developed pneumonia involving the left base. A new antibiotic regimen was delivered and the pseudocyst was drained percutaneously under CT guidance. The clinical course was favorable at six months with partial involution of the pseudocyst and regression of the pulmonary images.

[Multifocal epithelioid haemangioendothelioma: a difficult diagnosis]. / Hémangioendothéliome épithélioïde multifocal de diagnostic difficile.

INTRODUCTION: Epithelioid haemangioendothelioma is a rare vascular tumour of slow growth and unfavourable outlook, with occasional spontaneous and complete remissions. CASE REPORT: We report the case of a 69 year old woman admitted to hospital on account of haemoptysis. The clinical and radiological findings were compatible with diffuse pulmonary haemorrhage of unknown aetiology. Lung biopsy revealed a picture of pulmonary haemorrhage without vascular changes or tumour cells. Further progress was characterised by recurrent haemoptysis and the development of a haemothorax, liver nodules and skin lesions, biopsy of which confirmed the diagnosis of epithelioid haemangioendothelioma. The patient died several weeks later. CONCLUSION: The pulmonary localisation of epithelioid haemangioendothelioma is non specific, represented mainly by parenchymatous nodules with or without accompanying haemoptysis. Haemothorax is a more uncommon presentation of this disorder and a pleural localisation is often associated with a multifocal and aggressive form. The pathological diagnosis is most often made by surgical lung biopsy. Nevertheless in certain cases it can be difficult to make and this case report shows that, in the presence of a haemothorax, the search for extrapulmonary deposits accessible for biopsy may prove useful.

[Allergic bronchopulmonary aspergillosis]. / Aspergillose bronchopulmonaire allergique.

Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic bronchopulmonary inflammation due to an immune response of the lower respiratory tract against Aspergillus fumigatus. The major clinical features of ABPA include asthma, recurrent pulmonary infiltrates, immediate wheal and flare skin reactivity to A. fumigatus, elevated total serum IgE levels, detectable serum precipitating antibodies to A. fumigatus, peripheral blood eosinophilia, elevated levels of Aspergillus-specific serum IgE and central bronchiectasis with normal distal structures. The diagnosis of ABPA should be considered in asthmatics of all ages. Evolution of the disease comprises five stages from the acute to the fibrotic stage including pulmonary fibrosis and respiratory insufficiency. The goals of ABPA treatment are to control patient's asthma and prevent exacerbations of ABPA. During the acute stage, prednisone should be administered. Antifungals agents (itraconazole) may be useful to prevent exacerbations of the disease.

Effects of itraconazole therapy in allergic bronchopulmonary aspergillosis.

STUDY OBJECTIVES: Allergic bronchopulmonary aspergillosis (ABPA) is the result of an immune reaction to antigens of Aspergillus fumigatus, which colonizes the bronchial lumen of affected individuals. Presently, the recommended treatment of ABPA, mainly for acute episodes of exacerbations, is administration of glucocorticoids. We initiated this study to analyze the effects of itraconazole on the clinical, biological, and functional parameters in patients with ABPA. PATIENTS: in this report, we describe the follow-up of 14 asthmatic patients who presented with ABPA. During the 2-year reference period (a 2-year period before the introduction of itraconazole), 14 patients were treated with inhaled corticosteroids and 12 of the 14 received oral glucocorticoids. During the itraconazole treatment period, the patients were treated with oral itraconazole, 200 mg/d, for at least 12 months. RESULTS: During the 2-year reference period, no significant clinical, immunologic, and functional improvement was observed on a long-term basis. During the itraconazole treatment period, a clinical improvement was observed. Blood eosinophilia, serum total IgE levels, and serum precipitating antibodies against A fumigatus antigen significantly decreased. No decrease of specific IgE against A fumigatus spp was observed. All patients experienced a partial improvement in pulmonary function tests: FEV(1) significantly increased from 1,433 +/- 185 to 1,785 +/- 246 mL/s (p < 0.01). All patients successfully lowered oral glucocorticoid dose when receiving itraconazole. In 7 of 14 patients receiving itraconazole, the removal of oral glucocorticoids was possible. CONCLUSION: These results demonstrate the efficacy of itraconazole in ABPA in reducing or eliminating the need for glucocorticoid therapy, along with clinical, biological, and functional improvement.

Eosinophilic airway inflammation in nasal polyposis.

BACKGROUND: Asthma and asymptomatic bronchial hyperresponsiveness (BHR) are frequent findings in patients with nasal polyposis (NP). OBJECTIVE: To elucidate mechanisms responsible for the development of BHR, we initiated a prospective study of bronchial inflammation as assessed by bronchial lavage (BL) and bronchial biopsy specimens in 35 patients with noninfectious NP. METHODS: BHR was determined with methacholine provocation testing. Differential cell count, ECP, and histamine and tryptase levels were determined in BLs. Pathologic examination of bronchial biopsy specimens was performed with May-Grünwald-Giemsa stain to assess the number of lymphocytes. Indirect immunoenzymatic methods were used to identify eosinophils and mast cells. RESULTS: Fourteen patients did not exhibit BHR (group A); 7 patients had asymptomatic BHR (group B); and 14 patients had BHR associated with asthma (group C). Patients of group C tended to have a longer duration of nasal symptoms than those of groups A and B. FEV1 (L) was significantly lower in group C than in groups A and B. The number and percentage of eosinophils were significantly higher in BLs in groups B and C than in group A (P <. 05). Patients of groups B and C had a significantly higher number of eosinophils in bronchial submucosa (14.0 +/- 1.5/mm2 and 19.0 +/- 1. 9/mm2, respectively) than patients of group A (0.1 +/- 0.1/mm2). The number of lymphocytes was also higher in groups B and C than in group A. FEV1 (percent of predicted value) and eosinophil number within bronchial mucosa correlated negatively. CONCLUSION: Our results demonstrate that patients with NP and asymptomatic BHR had an eosinophilic bronchial inflammation similar to that observed in asthmatic patients with NP, whereas patients with NP without BHR do not feature eosinophilic lower airways inflammation. The clinical relevance of these results requires careful follow-up to determine whether eosinophilic inflammation in these patients precedes and is responsible for the development of obvious asthma.

Ultrasound characterization and quantification of carotid atherosclerosis lesions.

The development of ultrasonography in vascular applications has entailed research of ultrasound parameters leading to precise the diagnosis and quantification of carotid lesions in routine. The use of recent colour Doppler imaging techniques (velocity or power encoding) is recommended as they allow a better definition of the lesions and recesses. At present, features of plaque that could be related to increased incidence of stroke are: echogenicity, with a more frequent observation of anechoic or hypoechoic lesions in the case of clinical signs; texture, with frequent haemorrhage; surface contour, with a high rate of ulcerations which were accompanied by stroke; plaque motion, with a significant alteration in plaque motility in symptomatic patients; progression or regression in size, with a faster progression of anechoic and hypoechoic plaques; an increase in plaque volume is associated with a greater risk of stroke; a significant relationship between the presence of "ulcers" and embolic activity. The quantification of stenosis degree could be made using velocity criteria and/or morphological criteria. Velocity criteria could be obtained at the site of the stenosis (direct criteria) or downstream the carotid stenosis using Duplex systems. Morphological criteria could be obtained using B-mode imaging or colour Doppler but this quantification remains difficult in case of diffuse carotid stenoses or very severe stenoses.

Transforming growth factor-beta1 in sarcoidosis.

Transforming growth factor-beta (TGF-beta) is a cytokine that promotes extracellular matrix accumulation and inhibits matrix degradation. Although the natural course of sarcoidosis is usually favourable, granuloma healing in the lung may result in pulmonary fibrosis and respiratory impairment in some patients. In this study TGF-beta1 was evaluated in bronchoalveolar lavage (BAL) fluid and culture supernatants of alveolar macrophages (AM) from 73 patients with biopsy-proven sarcoidosis. Disease activity was defined when patients recently developed or increased symptoms (cough, dyspnoea, systemic symptoms) and/or demonstrated increasing opacities on chest radiography. Pulmonary function tests were performed in all patients including forced expiratory volume in one second (FEV1), forced vital capacity (FVC), total lung capacity (TLC) and the diffusing capacity of the lung for carbon monoxide (DL,CO). Fourteen patients with idiopathic pulmonary fibrosis (IPF) and 14 healthy subjects were investigated as a control group. Immunohistochemistry was used to evaluate the cell distribution of TGF-beta1 on lung specimens. TGF-beta1 levels in BAL and in AM supernatants were not different between sarcoidosis and healthy subjects, whereas they were markedly increased in IPF. However, the TGF-beta1 level was significantly increased in BAL fluid but not in AM supernatants from sarcoidosis with altered lung function, compared with patients with normal lung function. The TGF-beta1 level in BAL was increased in active sarcoidosis but this increased level was mainly related to the higher level observed in patients with altered lung function. TGF-beta1 levels in BAL correlated significantly with the lymphocyte percentage. TGF-beta1 staining assessed by immunohistochemistry was intense in epithelioid histiocytes comprising non-necrotizing granuloma and in bronchiolar epithelial cells, in hyperplastic type II pneumocytes and occasionally in AM. This study supports the hypothesis that overproduction of transforming growth factor-beta1 is associated with functional impairment in patients with pulmonary sarcoidosis.

Respiratory involvement in relapsing polychondritis. Clinical, functional, endoscopic, and radiographic evaluations.

Although respiratory involvement occurs in 50% of patients with relapsing polychondritis (RP) and augurs a poor prognosis, few previous studies have provided complete descriptions of respiratory tract involvement. For this reason, we investigated the respective role of clinical, functional, endoscopic, and radiographic (computed tomography [CT]) examinations in 9 consecutive patients with RP and lower respiratory tract localization. All exhibited cough, dyspnea, and wheezing. Eight had a nonreversible obstructive pattern with a marked decrease of the maximal flow ratio at 75% and 25% of vital capacity. Rotman functional criteria were evaluated to differentiate upper from lower respiratory tract involvement; they were consistent with the results of other examinations in 4/9 cases. Endoscopic examination showed moderate to severe inflammation in 8/9 patients; tracheal stenosis was present in 6/9 patients, bronchial stenosis in 4/9 patients, and tracheal collapse in 7 cases. CT showed tracheal stenosis in 8/9 patients (diffuse, 7; localized, 1) and bronchial stenosis in 6/9 patients. Tracheobronchial wall thickening and/or calcifications were observed in 7 cases. Clinical symptoms are of poor specificity for defining respiratory involvement precisely, although degree of dyspnea is correlated to the decrease in forced expiratory volume in 1 second (FEV1). Functional criteria were helpful in evaluating the obstructive ventilatory defect but did not differentiate, in most cases, the respective part of lower and upper respiratory involvement when using Rotman criteria. Compared to CT findings, endoscopic examination failed to identify tracheal and bronchial stenosis and tracheal wall alterations at an early stage of the disease. In our series CT appears to be a reliable method to identify tracheal and bronchial involvement and can be repeated safely during the course of the disease.

Increased interleukin-6 production during the acute phase of the syndrome of episodic angioedema and hypereosinophilia.

BACKGROUND: The Gleich syndrome is rare and associates recurrent angioedema, urticaria, fever, weight gain and blood hypereosinophilia, underlying systemic and local inflammation. The pathogenesis of those symptoms remains unclear. OBJECTIVE: We wanted to address the possible implication of Interleukin-6 (IL-6) in the development of those clinical features, and to identify the cells involved in its production. METHODS: A 26-year-old man suffering of this disease was referred in hospital. During an acute attack with weight gain, fever and a diffuse oedema, a marked increase in eosinophils count (42700/mm3 was observed. Serum ECP was elevated at 47 microg/L (normal less than 16). Corticosteroid therapy administrated on the 7th day was followed by a rapid remission. Blood samples were collected (before, during the attack and under corticosteroid therapy) for measurements of serum IL-6 (ELISA, Immunotech, Marseille, France) and plasma histamine (RIA, Immunotech, Marseille, France). Blood monocytes and eosinophils were isolated and a skin biopsy was performed during the attack. RESULTS: The plasma histamine level was within normal range. The level of IL-6 in sera peaked to 74 pg/mL, concomitant with the peak of eosinophilia at the acute phase phase of the attack. Under corticosteroids, we observed a drop in the IL-6 serum level to 29 pg/mL, concomitant with the clinical remission. During the attack, an increase in IL-6 production was observed in 24 h blood monocyte supernatants (11.10(3) pg/mL compared with 2.4+/-0.8.10(3) pg/mL for BM from controls) as well as in skin endothelial cells but not in the blood and skin eosinophils. In vitro, when endothelial cells were incubated in eosinophils supernatants of the patient, liberation of IL-6 was observed (3.3 10(3) pg/mL compared with controls: 2.1 10(3) pg/mL) CONCLUSION: Serum IL-6 elevation may be related to an increased production by blood monocytes and endothelial cells, possibly stimulated by eosinophil mediator during the acute phase of the disease, and might participate in the inflammatory reaction of this syndrome.

[Management of hemoptysis in invasive pulmonary aspergillosis]. / Prise en charge des hémoptysies au cours de l'aspergillose pulmonaire invasive.

Invasive pulmonary aspergillosis is an opportunistic infection occurring in a background of severe immune depression. The majority of cases occur in patients who have malignant hematologic disease, particularly during chemotherapy induction or consolidations phases for acute non-lymphocytic leukemia. The principal risk factors are profound (PN < 500 per mm3) and prolonged (very high risk beyond 20 days) neutropenia, perturbed phagocyte function and cellular immune deficiency (AIDS, immunosuppressive treatment in organ and bone marrow recipients). Clinically, invasive pulmonary aspergillosis presents as acute non-specific pneumonia with cough, chest pain and fever. The severe infection rapidly becomes life-threatening. The development of massive hemoptysis is a major risk. We report four cases of invasive pulmonary aspergillosis in patients who had hemoptysis. All four patients developed non-specific pneumonia resistant to broad-spectrum antibiotics during post-chemotherapy aplasia. Computed tomography of the thorax and bronchoscopy with bronchoalveolar lavage was performed due to the occurrence of hemoptysis. In the first two cases, the patients were recovering from aplasia. The thoracic CT scan showed evidence of a cavitating mass with peripheral vessels. Bronchoscopy findings suggested mucosal lesions. The patients were managed surgically. Pathology confirmed the diagnosis of invasive pulmonary aspergillosis with the presence of ischemic necrosis of the pulmonary parenchyma harboring numerous aspergillus filaments. Outcome was favorable and chemotherapy was re-initiated in one case. These two patient died from their hematological disease a few months later. The other two patients remained in aplasia. A CT of the thorax showed multifocal infiltration with vascular contact. Bronchoscopy was again suggestive. One patient developed massive hemoptysis with respiratory distress. Embolization was performed but the patient died two days after onset of hemoptysis. In the last case, embolization was successful and outcome was favorable enabling a bone marrow allograft; the patient died a few months later from the hematological disease. The potential gravity of hemoptysis in the course of invasive pulmonary aspergillosis should lead to early treatment with emergency CT scan and, if possible, bronchoscopy with bronchoalveolar lavage to establish the therapeutic strategy based on surgical excision or embolization of the pulmonary or bronchial arteries.

CD8 lymphocytosis in primary cytomegalovirus (CMV) infection of allograft recipients: expansion of an uncommon CD8+ CD57- subset and its progressive replacement by CD8+ CD57+ T cells.

Allograft recipients undergoing cytomegalovirus infection present increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction revealed selective imbalances of peripheral blood CD8+ T cell subsets. Initially, CMV viraemia is associated with elevated CD8+bright T cell numbers and T cell activation. Activation markers fall to normal when viral cultures become negative (before the end of the first month). During the second to sixth month, most (12/16) patients keep up high CD8+ T cell counts (1050-2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCR alpha beta+, but were not stained by anti-CD28, CD11b, CD16, CD56, and CD57 antibody. Unexpectedly, CD8+CD57+ T cells, a hallmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively thereafter. They become the predominant CD8+ T cell subset after 6 months of infection and their persistence for several (up to 4) years is strongly correlated (r = 0.87) with expansion of CD8+ cells. By analysis with MoAbs, there was no bias towards the use of particular TCR-V beta gene families at any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8+CD57- subset and its progressive replacement by CD8+CD57+ T cells that are chronically elicited by CMV.

Successive emergence of two CD8 subsets in primary CMV infection of allograft recipients.

Allograft recipients with cytomegalovirus (CMV) infection develop increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and 5 liver allograft recipients with primary CMV infection but no other aetiological factor to explain graft dysfunction revealed selective imbalances in peripheral blood CD8+ T cell subsets. Initially, CMV viraemia was associated with elevated CD8+bright T cell numbers and T cell activation. Activation markers fell to normal when viral cultures became negative (before the end of the 1st month). During the 2nd-6th months, most (12/16) patients continued to have high CD8+ T cell counts (1050-2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCRalphabeta+ but were not stained by anti-CD28, CD11b, CD16, CD56 and CD57 antibody. Unexpectedly, CD8+ CD57+ T cells, a hallmark of CMV infection, did not appear until the 2nd-6th months of primary CMV infection, and their numbers increased progressively thereafter. They became the predominant CD8+ T cell subset after about 6 months of infection and their persistence for several (up to 4) years was strongly correlated (r = 0.87) with expansion of CD8+ cells. Persistence of CD8 lymphocytosis was, thus, directly related to the rate of expansion of an uncommon CD8+ CD57- subset and its progressive replacement by CD8+ CD57+ T cells that were chronically elicited by CMV.

[Echotomography and spectral analysis of the Doppler signal in the assessment of carotid lesions]. / L'échotomographie et l'analyse spectrale du signal Doppler dans le bilan des lésions carotidiennes.

Real-time echography and C.W. Doppler examination with spectrum analysis are the two methods most widely used for the study of the circulation. Echography allows the detection and the localization of the atheromatous defects whereas Doppler examination provides information on the blood flow. With the help of the frequency analysis of the Doppler signal it is possible to study much more accurately the local haemodynamic conditions. Spectrum analysis is one of the possible display mode for the Doppler signal. It provides in comparison with the zero crossing mode, much more haemodynamic parameters on the blood flow, such as velocity spectrum, density of red cells on each velocity... In this study, we tried to demonstrate that a relationship exists between the amplitude of the spectrum disturbances, recorded just after a stenosis and the degree of this stenosis. For that we propose a classification of the spectrum disturbances in five grades, each of them being related to an interval of possible values for the stenosis degree (grade I----stenosis less than 40% in area, grade II----40-60% stenosis, grade III----60-75% stenosis (extended defects) grade IV----70-90% (extended defects) and 60-90% short stenosis. Grade V: stenosis greater than 90%. The results provided by this classification were compared to those obtained by measurements of the stenosis degree on the piece of endarterectomy (72 cases). The results were in agreement in 94% of the cases.(ABSTRACT TRUNCATED AT 250 WORDS)