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S Maître

Publications and source records attributed to S Maître.

8 recordsLinked to original sources
PubMed2003

[Pulmonary hypertension: CT findings in pulmonary veno-occlusive disease].

PURPOSE: To describe the CT findings of pulmonary veno-occlusive disease. MATERIALS AND METHODS: Pre-therapeutic CT of 15 patients suffering from pulmonary veno-occlusive disease were retrospectively reviewed. Pathologic evaluation of pulmonary veno-occlusive disease was obtained after post mortem examination or pulmonary transplantation. CT protocol always included intravenous helical CT and high resolution CT. RESULTS: The most frequent CT-findings in pulmonary veno-occlusive disease were the following: ground glass opacity with poorly defined nodular opacities (73%), septal lines (93%), and adenopathy (80%). Pericardial (60%) and pleural effusions (27%) were also noted. Other parenchymal findings were unusual. CONCLUSION: HRCT must be systematically included in the initial CT evaluation of pulmonary hypertension. Combination of poorly defined nodular opacities, septal lines, and adenopathy are indicative of pulmonary veno-occlusive disease.

Adult↗
PubMed2000

A Light Scattering Study of the Association of Hydrophobically alpha- and alpha,omega-End-capped Poly(ethylene oxide) in Water.

Several hydrophobically alpha- and alpha,omega-end-capped poly(ethylene oxide) polymers were studied by light scattering below and above their critical association concentration, in order to understand their association mechanisms. In the case of monofunctionalized PEO, a one-step closed association model well fits the experimental data, with a limit number of aggregation of about 30, consistent with other experimental data and a theoretical approach. In the case of difunctionalized PEO, a good description of the experimental data is obtained by assuming a two-step association process: at low concentration, the formation of "flower-like" micelles is well described by a closed association model, whereas at higher concentration, the progressive bridging of these "flowers" can be modeled by an open association. Copyright 2000 Academic Press.

Journal Article↗
PubMed2000

Severe pulmonary hypertension in histiocytosis X.

Diminished exercise capacity in advanced pulmonary histiocytosis X does not appear to be related to ventilatory limitation but may be related to pulmonary vascular dysfunction. Pulmonary hemodynamics and respiratory function were studied in 21 consecutive patients with advanced pulmonary histiocytosis X, and compared with parameters of patients with other severe chronic lung diseases (29 patients with chronic obstructive pulmonary disease and 14 patients with idiopathic pulmonary fibrosis). All patients with pulmonary histiocytosis X displayed severe pulmonary hypertension: mean pulmonary arterial pressure, 59 +/- 4 mm Hg; cardiac index, 2.6 +/- 0.8 L/min/m(2); and total vascular pulmonary resistance, 25 +/- 3 IU/m(2) (p < 0.05, as compared with patients with other chronic lung diseases). Pa(O(2)) was similar in the three groups, whereas FEV(1) was lower in patients with other chronic lung diseases (p < 0.05). In contrast to other chronic lung diseases, the degree of pulmonary hypertension was not related to variables of pulmonary function in pulmonary histiocytosis X. Histopathology was available for 12 patients with pulmonary histiocytosis X and revealed proliferative vasculopathy involving muscular arteries and veins, with prominent venular involvement. Two consecutive lung samples (taken before and after the occurrence of pulmonary hypertension) were available for six patients with pulmonary histiocytosis X, and showed that pulmonary vasculopathy worsened, whereas parenchymal and bronchiolar lesions remained relatively unchanged. These results indicate that pulmonary hypertension in pulmonary histiocytosis X might be related to an intrinsic pulmonary vascular disease, in which the pulmonary circulation is involved independent of small airway and lung parenchyma injury.

Adult↗
PubMed1998

Pulmonary edema complicating continuous intravenous prostacyclin in pulmonary capillary hemangiomatosis.

Continuous intravenous epoprostenol (prostacyclin) produces hemodynamic and symptomatic responses and improves survival in patients with severe primary pulmonary hypertension refractory to conventional medical therapy. However, it has been recently shown that short-term infusion of epoprostenol can produce pulmonary edema in pulmonary veno-occlusive disease, presumably because of increased pulmonary perfusion in the presence of downstream vascular obstruction. We describe two additional cases of pulmonary edema complicating continuous intravenous epoprostenol in patients displaying severe pulmonary hypertension and pulmonary capillary hemangiomatosis, a rare condition characterized by the proliferation of thin-walled microvessels in the alveolar walls. This report indicates that epoprostenol therapy should not be used in patients with severe pulmonary hypertension secondary to pulmonary capillary hemangiomatosis.

Adult↗
PubMed1998

High-resolution CT of the chest in four patients with pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease.

OBJECTIVE: Clinical differentiation of isolated pulmonary hypertensive arteriopathy from pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease can be difficult on a clinical basis alone. Differentiation is important because misdiagnosis of pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease may lead to severe vasodilator-induced pulmonary edema. The objective of our study was to determine whether high-resolution CT of the chest could distinguish pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease from isolated pulmonary hypertensive arteriopathy. CONCLUSION: Pulmonary hypertension in patients who also have pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease shows characteristics on high-resolution CT that are not seen in patients with isolated pulmonary hypertensive arteriopathy.

Adult↗
PubMedDate not supplied

[Priapism in the course of generalized atopic dermatitis].

BACKGROUND: Priapism is a pathologically prolonged and painful penile erection, not resulting in ejaculation. Causes include certain oral medication, perineal trauma, thrombo-embolic process or primary priapism. We report a case of priapism secondary to diffuse general atopic dermatitis. CASE REPORT: An 11 year-old child, with atopic dermatitis, presented over the last 36 hours an irreduced painful penile erection. Other than priapism, he presented numerous scratched lesions on the body and the penis having developped over the last 2 months (treated by daily topical corticosteroid application) and consistent with atopic dermatitis exacerbation. Due to the urological emergency, a puncture of the corpora cavernosa was made, followed by an injection of etilephrine in the penis. Complete and definitive detumescence was obtained. Application of betamethasone healed the cutaneous lesions. The child was treated with ciclosporine for his atopic dermatitis with good results at 6 months. DISCUSSION: In our case, hypothesis of myeloid leukemia, sickle-cell disease and essential thrombocythemia were turned down. The young child did not exhibit any recent perineal trauma but the scratched lesions can be considered as microtraumas. The formation of an inflammatory oedema obstructed venous drainage of the penis and provoked priapism. We can not rule out the responsibility of topical corticosteroids in the formation of the priapism in this patient. Indeed, it was the only drug therapy prescribed, and since introduction of ciclosporine, there has been no relapse.

Anesthesia, General↗