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  • 1
    ISSN: 1432-1998
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A detailed radiologic and anatomic study of one horseshoe lung syndrome has already been published from this centre. A further case of horseshoe lung, which was also diagnosed prospectively by radiology, is described. Alongside, this is a set of a group of three conditions: we describe a right accessory lung with a peculiar feeding arterial branch originating from the left basal pulmonary artery. The bronchogram and oesophagogram of this case were normal. The other is a case of bridging bronchus where the left lower lobe bronchus originates from the right main stem bronchus. This was discovered at post mortem bronchogram performed on a 19 weeks foetus. Finally, in the dog, we found that the pulmonary angiogram and bronchogram display close similarity to human horseshoe lung though the dog has two separate lungs. The common denominator of all above cases is the presence of a pulmonary arterial branch or bronchus crossing the midline from the ipsi to the contralateral side. Therefore, it may be concluded “in contradiction to the common belief” that pulmonary angiography or bronchography alone is not sufficient for the diagnosis of horseshoe lung. When only one of these investigations is savailable, computerized tomography is necessary to show the isthmic lung tissue before the diagnosis of horseshoe lung is confirmed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 150 (1991), S. 374-378 
    ISSN: 1432-1076
    Keywords: Nephrotic syndrome ; AT III ; Fibrinogen ; Platelet aggregation ; Reptilase time
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Blood coagulation and platelet aggregation were assessed in children, with nephrotic syndrome who were divided into the following groups: (1) relapse without treatment; (2) relapse on steroids; (3) early remission; (4) late remission and (5) steroid resistant. The renal histological findings were also recorded. Plasma antithrombin III (ATIII) levels were markedly reduced in groups 1 and 2, below normal in group 3 and were normal in groups 4 and 5. There was significant urinary loss of AT III in groups 1 and 2 as well as in group 5. Plasma fibrinogen fluctuations exhibited the expected negative correlations with plasma AT III. Reptilase time showed significant prolongation in groups 1, 2 and 3, and was near normal in groups 4 and 5. Platelet aggregation in response to arachidonic acid exhibited aggregation followed by disaggregation in groups 1, 2, 4 and 5, and was normal in group 3. Hyperaggregation in response to decreasing doses of ADP was noted in all patient groups as well as controls with no relationship to serum albumin levels. Aggregation responses to collagen and ristocetin were normal. It is concluded that: 1. The fluctuations in AT III levels in childhood nephrotic syndrome are determined by the response to steroids and not by the renal histology per se. 2. An acquired fibrin polymerization defect (dysfibrinogenaemia) and an abnormality of the prostaglandin pathway of platelet activation, both reversible, are yet other haemostatic abnormalities in childhood nephrosis. 3. The discrepancies in the literature on haemostatic parameters, specially AT III in childhood nephrosis, would not have arisen if their fluctuation in relation to steroid therapy as well as the renal histological features of nephrotic syndrome had been documented simultaneously.
    Type of Medium: Electronic Resource
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