[Bilateral carpitis in palmo-plantar pustulosis].
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Biomedical subjects
Publications and source records attributed to O Bletry.
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Five patients with eosinophilic lung diseases and blood hypereosinophilia (PIE syndrome) were investigated clinically and by bronchoalveolar lavage (BAL). Comparative studies on blood and alveolar eosinophils were carried out after purification and selection of eosinophil subpopulations according to their density. A predominant 'hypodense' alveolar eosinophil population was found in BAL fluids of active chronic eosinophilic pneumonia (CEP). In addition, supernatants of alveolar macrophages obtained from CEP are able to enhance spontaneously the generation of eosinophil oxygen metabolites. Such eosinophil stimulation emphasizes a probable tissue cell cooperation. In addition, BAL permitted the study of membrane immunological markers on eosinophilic inflammatory cells endowed with migratory properties. An increase in eosinophils carrying surface IgE was demonstrated in alveolar cells from PIE Syndrome particularly with hypodense eosinophils from CEP patients. Although no specific stimulus is known at the present time, this work underlines the potential implication of IgE-mediated hypersensitivity processes in the pathogenesis of eosinophilic lung diseases.
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A randomized study was carried out in 36 patients to determine the diagnostic value of abdominal computerized tomography (CT) in protracted fever of obscure origin and/or unexplained inflammatory syndromes. There were no clinical or biological signs pointing to a diagnosis, and 55% of the patients had already been unsuccessfully explored in other hospital departments. CT was performed initially in group I patients and after some of 56 predetermined conventional examinations (including 20 considered "invasive") carried out in a definite order in group II patients. An early diagnosis could be made within 2 months in 17 patients (47%): 7 in group E and 10 in group II. The underlying disease was diagnosed in 4 cases in group I and 1 case in group II (where 4 other cases could have been diagnosed, had CT been performed earlier); the difference was not significant. Nor was there any difference between the two groups in the number of examinations performed, the cost of investigation and the duration of stay in hospital. However, a number of reasons are in favour of early CT examination in protracted fever: the so-called "invasive" explorations were uncomplicated in group I and complicated in 2 patients of group II; following randomization, a diagnosis was made by CT within less than 3 days in the 4 patients of group I, and there were neither false-positive nor false-negative results of CT. If CT had been performed early in all patients, 9 diagnoses would have been made, representing 25% of the cases or 1/2 of early diagnoses. Abdominal CT proved unable to establish the 10 late diagnoses (i.e. after a mean delay of 18 months).
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Muscle involvement in ankylosing spondylitis has been little studied. The authors report two cases with marked muscular atrophy and functional impotence, which had directed the diagnosis towards a myopathy over a period of several years in the first case, and a suspected primary muscular disease associated with ankylosing spondylitis in the second. Muscle biopsies eliminated the diagnosis of myopathy in both cases, with rapid functional recovery with proper treatment. Following a review of the literature, two hypotheses can be considered to explain the muscular involvement in ankylosing spondylitis: one mechanism which appears well-established is a radiculitis with involvement of the paravertebral muscles: other authors suggest that there is nonspecific, generalized muscular involvement in this disorder.
Aetiological diagnoses obtained by means of an algorithm were retrospectively compared with those made in the Internal Medicine Department of the La Pitié Hospital, Paris, in 22 cases of hypercalcaemia (24 causes detected). These cases covered all the usual causes of the disease. The algorithm produced no erroneous diagnosis. In 2 cases it would not have resulted in a precise diagnosis, but in all other patients the diagnosis obtained by this method was in agreement with the clinical diagnosis. Proposals are put forward for an improved version of the algorithm that would provide more rapid diagnoses and avoid the risk of a "no diagnosis" answer.
Determinations of antinuclear antibodies (ANA) were performed before treatment, then every 3 months for one year, in 45 hypertensive patients treated with acebutolol alone in daily doses equal or superior to 800 mg. Non significant ANA titers (1/10 to 1/40) were detected before treatment in 8.8% of the patients. After one year of treatment, 15.5% of the patients were found to have antinuclear antibodies. In 4 (8.8%) female patients (3 of whom were ANA-negative before treatment) the ANA titers were above 1/40. Treatment was discontinued in one of these due to the occurrence of bronchospasm. No lupus-like syndrome was observed during the course of the study. Prolonged prospective studies with acebutolol alone would be required to determine whether in the long term the incidence of significant ANA titers remains at the 8.8% level or increases.
Sixty-five cases of necrotizing angiitis, including 20 with asthma (group A) and 45 without asthma (group B) were studied retrospectively. All patients were investigated for markers of hepatitis B, at least the HBs antigen. Skin lesions and arthralgias were more common in group B patients. Eosinophilia during angiitis was almost constant in group A and was observed in only 6% of group B patients. Renal involvement, hepatic lesions and arterial hypertension seemed to be more frequent in group B but the difference was not significant. The HBs antigen was present in 1/20 patients of group A and in 17/45 patients of group B (p less than 0.01). The anti-HBs antibody was found with equal frequency in both groups. The clinical and biological differences observed between these two groups of patients strongly suggest that necrotizing vasculitis with and without asthma are two separate nosological entities and in particular, that they have different causes.
Four cases of monoclonal gammopathy associated with polyarteritis nodosa are reported. In view of the chronology of events and course of the disease, the connections between protein peak and polyarteritis nodosa can be considered. Management of polyarteritis nodosa is discussed according to the existence of a peak which may originate in myeloma. The part played by plasma exchanges is debated.
Four cases of periarteritis nodosa (PAN) associated with HB virus are reported in three couples. The spouse also had periarteritis nodosa (cases 1 and 2) or had hepatitis B (spouses of cases 3 and 4). These observations underscore the part played by conjugal transmission of HB virus and the risk of secondary PAN. Such observations are uncommon as the four reported cases occurred among a group of 95 PAN patients. Nevertheless, they are additional evidence in support of the role of HB virus which is associated with PAN in 45% of cases in this series.
The authors report their experience with 45 cases of inferior vena cava thrombosis. Diagnosis was delayed for an average of 55 days. One-third of cases were revealed by an embolic complication. Inflammatory diseases were the most common causes (Behcet disease: seven cases, systemic lupus erythematosus: 5 cases). Malignancies accounted for 20% of cases. Abnormalities of coagulation were uncommon: antithrombin III deficiency in one patient and protein C deficiency in another. Estrogen-progestogen combinations could be incriminated in 4 cases. Outcome was fatal in 20% of cases, usually as a result of the underlying disease. Functional status was good in two-thirds of patients without malignancy followed up for an average of 27 months. In 14 patients a clip was inserted to ensure total (3 cases) or partial (11 cases) interruption of vena cava blood flow because of a free thrombus and/or recurrent pulmonary embolism. Three patients had thrombectomy. After clip insertion two embolisms were recorded, one of which occurred in the immediate post-operative period.
The prognosis of the hypereosinophilic syndrome (HS) depends mainly on the development of endomyocardial fibrosis (EMF). This complication may be overlooked at an early stage, although its presence is an indication for steroid or antimitotic therapy of the HS. Even at an advanced EMF and associated intracardiac thrombi may not be visualised by angiography. This study was undertaken to assess the diagnostic value of 2D echocardiography in 12 patients. The patients were all men (12 of them) aged 22 to 64 years with unexplained eosinophilia 1 500/mm3 for over 6 months, and visceral lesions. The patients were divided into 3 clinical groups. Group A comprised 4 "allergic" patients with chronic asthma and a significant elevation of IgE; Group B comprised 5 "myeloproliferative" patients with splenomegaly and/or hepatomegaly and a significant elevation of serum B12 levels. The 3 remaining patients who could not be allocated to either Group A or B formed the third group (Group C). 2D echocardiography was carried out on average 30 months after diagnosis of the HS and six planes of examination were used systematically (two parasternal, two apical, one extreme apical and one subcostal). Right and left ventriculography was performed in 6 patients (less than one month before or after 2D-echo). Anatomical studies were obtained in 4 cases (2 operations, 3 autopsies). Echocardiographic signs of EMF were observed in 8 cases. Four patients had a restrictive cardiopathy associated to a large LV thrombus in 2 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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Considerable variations in the distribution of eosinophil populations were revealed by density gradient centrifugation of peripheral blood leukocytes from 14 normal subjects and 31 patients with a transient or persistent hypereosinophilia. Such a purification procedure enabled us to collect in healthy controls, eosinophils (77.1 +/- 15.9% SD purity) with an appreciable cell recovery (21.7 +/- 14.0% SD) in the densest gradients ('normodense' cells). A high degree of purity was obtained in the same gradients, with leukocytes from patients with hypereosinophilia (84.4 +/- 11.9% SD pure eosinophils) but the cell recovery was significantly decreased (4.1 +/- 3.4% SD; p less than 0.001). A study of the various fractions found to contain eosinophils showed cells with an altered cellular density ('hypodense' cells) especially in marked hypereosinophilia. Furthermore, studies on leukocytes from patients with a very high hypereosinophilia (differential cell count greater than 70%) led to the recovery of almost pure fractions of eosinophils in the low density gradients. Functional studies were performed on each distinct cell fraction collected. They included investigations of their cytotoxic ability in a heterologous antibody-dependent cell-mediated cytotoxicity assay and their biochemical activity by using a previously described technique evaluating the membrane hexose transport. Variability in the functional potentialities was observed in relation to the cellular density: higher cytotoxic eosinophil abilities were noted in the case of the 'hypodense' cell population. According to biochemical criteria, these latter cells appear to be more activated and capable of responding to stimulation.
Five cases of periarteritis nodosa or Churg and Strauss angeitis are reported. They all had one feature in common, their onset after desensitivity procedures, an injection of gammaglobulin or vaccination. These factors were found either at the onset or before a relapse of the disease. None of the patients had HBS antigen, which supports the hypothesis of a multiple antigenic etiology of periarteritis nodosa, some of which may cause respiratory symptoms, especially asthmatic attacks. The authors emphasise the importance of prohibiting desensitivity procedures and vaccinations in patients with severe asthma.