Angiogenesis is important in a large number of normal and pathological processes including tumour growth and development, inflammation and in wound healing. We investigated whether neovascularization exists in hyperplastic, metaplastic and potentially preneoplastic lesions of the bronchial mucosa as prestages for lung cancer. Biopsy specimens from 86 patients were investigated light microscopically. Formalin-fixed and paraffin-embedded specimens of regular bronchial mucosa including epithelium, basement membrane zone and tunica propria (n = 12) without inflammation were compared with specimens with inflammatory reaction (n = 9), basal cell- and goblet cell hyperplasia (n = 24), squamous cell metaplasia (n = 9), squamous cell metaplasia with different degrees of dysplasia (n = 11), specimens of micropapillomatosis (n = 9) and 13 cases with carcinoma in situ. The grade of neovascularization was assessed by the microvessel density, which was obtained by an immunohistochemical staining of endothelial cells using factor VIII-related antigen and determined by an automatic image-analysing-system. Microvessels were counted in selected areas of highest neovascularization on a x 100 field 0.4 mm underneath the basement membrane zone in the tunica propria. Microvessel count, minimal and maximal diameter of the vessels were chosen as morphological variables. A significantly increased microvessel count with 33 vessels/0.6 mm2 was found in specimens with inflammation of the tunica mucosa (regular bronchial mucosa: 20 vessels/0.6 mm2). Microvessel diameter (surface of cut section) increased in specimens of bronchial mucosa with inflammation to 11.3 x 10(-4) mm2 (regular bronchial mucosa: 9.04 x 10(-4) mm2). Microvessel count increased in cases of squamous cell metaplasia (33 vessels/0.6 mm2) squamous cell metaplasia with different degrees of dysplasia (50 vessels/0.6 mm2) and carcinoma in situ with 61 vessels/0.6 mm2. With increasing dysplasia, increasing neo-vascularization was found in close vicinity to the basement membrane zone. Simultaneously, interepithelial sprouts of endothelial cells were seen. Qualitative and quantitative differences were thus found in potentially preneoplastic lesions.

Idiopathic pulmonary fibrosis (IPF) is a disease with progressive and devastating deterioration of lung function and a fatal prognosis, despite aggressive therapeutic attempts, which, in the majority of cases are futile.Recently, a preliminary study of long-term treatment with interferon (IFN)‐γ1band low-dose prednisolone in patients with IPF suggested that IFN‐γ1btreatment may improve lung function parameters of patients with IPF. Ever since, specialists in respiratory medicine who treat patients with IPF, are called by patients demanding treatment with IFN‐γ1b. Therefore, the authors here present another prospective investigation of IFN‐γ1bin five patients with IPF.According to the previously published design, patients received 200 µg IFN‐γ1bsubcutaneously three-times per week and 10 mg prednisolone orally for 12 months. Two patients stopped IFN‐γ1btreatment after 4 months due to side-effects and further lung function deterioration and one patient died 3 months after commencement of therapy. In total, pulmonary function improved in only one patient during IFN‐γ1btreatment, while four patients deteriorated.To conclude, this small series of idiopathic pulmonary fibrosis cases treated with interferon‐γ1band corticosteroids does not support previous data that this treatment improves pulmonary function or alters the natural course of idiopathic pulmonary fibrosis. Furthermore, in the authors' experience, side-effects of interferon‐γ1btreatment can significantly reduce patients' quality of life.

Ten cases of fatal thromboembolism after central venous catheterisation were found among the autopsies of one year. The immediate causes of death were protracted pulmonary embolism (n = 8), cerebral embolism with defect of ventricular septum (n = 1), and central regulatory disturbance following complete thrombotic occlusion of the jugular veins (n = 1). The sources of the fatal embolisms were found in thrombi in the superior vena cava, the innominate veins or subclavian veins. The relation of these thrombi to catheter-dependent lesions in the venous walls was beyond doubt. The catheters had been left in position for periods of 2 to 56 days. In 40 further autopsies with different causes of death, catheter-dependent mural lesions of varying extent were found in the venous system near the heart. Local thrombi were identified after catheterisation of not more than 24 hours. Macroscopic and microscopic appearance of these thrombi was characterised by a groove-like structure corresponding to the apposition of thrombi around the plastic catheter.

We describe a 10 year old boy with organising pneumonia associated with acute Mycoplasma pneumoniae infection. The diagnosis of organising pneumonia was made by open lung biopsy and the M pneumoniae infection was proven serologically. Antibiotic and long term corticosteroid treatment resulted in steadily improving pulmonary function monitored by spirometry. The introduction of antiinflammatory treatment with NSAIDs/immunosuppressive agents in order to spare steroids was well tolerated and resulted in further improvement of the pulmonary function. To our knowledge this is the first documented case of Mycoplasma pneumoniae associated organising pneumonia to be reported in a child.O rganising pneumonia, also described as bronchiolitis obliterans organising pneumonia (BOOP) is a rare disorder, usually occurring in patients over 50 years of age (range 20-80 years), with an equal sex distribution. There are only a few cases reported in adolescents. This rare disorder can be divided into cryptogenic (idiopathic) organising pneumonia (COP) of unknown cause, and secondary organising pneumonia associated with many recognised conditions, for example, infections, drug reactions, malignancy, radiation therapy, or autoimmune diseases. The pathological pattern is not specific for any disorder or cause, but reflects one special type of inflammatory process resulting from lung injury.1 It is characterised by patchy inflammatory changes of the bronchoalveolar lumen and wall, with some associated peribronchial scarring. The characteristic histological feature is the presence of buds of granulation tissue in the distal airspaces and interstitial mononuclear cell infiltrate.Various infectious agents have been described as rare causes of organising pneumonia.2 To our knowledge the association of Mycoplasma pneumoniae infection and development of organising pneumonia in children has not been reported to date. CASE REPORTA 10 year old boy presented with a six week history of dyspnoea on even mild exertion, fatigue, weight loss, and dry cough. These symptoms showed steady worsening that prompted hospital admission. The patient had an uneventful medical history apart from known hay fever. There were no cardiovascular, autoimmune, or pulmonary diseases in the past or in the family history.Physical examination revealed tachypnoea, dyspnoea with reduction of the oxygen saturation below 80% after mild exercise, and fine diffuse crackles on lung auscultation. Spirometry revealed a severe restrictive ventilation defect with the forced vital capacity (FVC) impaired to 25% of reference values ( fig 1). Chest roentgenogram and high resolution computed tomography (HR-CT) scan images showed notable alveolar and interstitial opacities with bilateral infiltration of the lung parenchyma (fig 2). Laboratory studies showed normal full blood count, negative C reactive protein, and slightly raised erythrocyte sedimentation rate (20/40 mm). Serological assays revealed raised M pneumoniae antibody titres (IgM 18 U/ml, IgG 80 U/ml, ELISA) indicating a recen...

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