A case of Simmonds' disease following chronic sclerosing hypophysitis is described in a moderately confused, 54-years-old woman in an extremely advanced cachexia. The patient died four days later in cardio-respiratory failure. The anterior lobe of the hypophysis showed dense, interlacing bands of fibrosis delineating small areas of atrophic pituitary cells. More than four-fifths of the anterior hypophyseal lobe was replaced by fibrosis or dense scarring. A scarce lymphocytic infiltrate between the fibrous bands was noted. The liver showed advanced fatty changes. An interesting finding was the presence of a chronic lymphocytic infiltrate in the adrenals. The association of chronic adrenalitis and sclerosing hypophysitis could be interpreted as an autoimmune endocrinopathy.

Autoimmune Diseases↗

PubMedDate not supplied

[The late results of respiratory kinesitherapy in tubercular serofibrinous pleurisy].

The authors have investigated 93 cases with sero-fibrinous pleurisy in their antecedents, and that had kinetotherapy during their disease. All the cases were controlled from the viewpoint of the respiratory function, as well as by radiological and electrocardiographic methods. Changes in the ventilatory function were evaluated by increased VEMS in absolute value in contrast with the VEMS value on hospitalization. The general late results of respiratory kinetotherapy were reflected in the fact that 84% of the cases presented either significant increase in the value of VEMS (56%), or had stationary values (28%). The most significant functional increases were noted in the patients who were under the age of 18 years upon release from hospital (median age : 14,8 years), and were mostly due to somatic development, and physical activity. The positive effects of physical activity in the frame of the occupation of the patients were amplified by respiratory kinetotherapy continued at home. Respiratory kinetotherapy demonstrated its efficiency especially in the subjects from lowage groups, and males had better results than females. Advanced age, important pleural sequels, as well as other disturbances, without apparent relation to the pleurisy, had negative effects. In the present conditions of treatment (chemotherapy + corticoid therapy and immediate and long-duration kinetotherapy) sero-fibrinous pleurisy has no significant impact on the socio-professional evolution of the patient.

Adolescent↗

PubMedDate not supplied

[Semiquantitative correlations between angiopneumography and vascular scintigraphy in various pulmonary diseases].

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Adult↗

PubMedDate not supplied

Level of ventricular myosin light chains 1 and 2 determined by ELISA in serum of patients with acute myocardial infarction.

The serum level of human ventricular myosin light chains 1 and 2 was determined by competitive ELISA assay in 56 patients, of whom 26 with acute myocardial infarction (18 with simple AMI and 8 with complex AMI), 10 with unstable angina pectoris and 20 healthy subjects. The serum level of human ventricular myosin light chains 1 and 2 (HVMLC1 and HVMLC2) in healthy subjects was of 6-10 ng/ml. Sensitivity of the assay was 10 ng/ml, and the working range was 10-100 ng/ml. In all AMI patients the HVMLC1 serum level exceeded 2-3 times the reference range within the first 24 hours after the onset of chest pain, the mean (+/- ISD) peak concentration was of 45.7 (+/- 13.6) ng/ml (simple AMI) and 64.22 (+/- 18.5 ng/ml) (severe AMI) 48 hours after infarction and it remained significantly higher than the normal value for another 7-10 days after the onset of infarction. The serum HVMLC2 concentration exceeded 10 ng/ml 48 hours after infarction, with a mean (+/- 1SD) peak concentration of 37.8 (+/- 10.4) ng/ml (simple AMI) and 53.8 (+/- 16.1) ng/ml (complex AMI) 90 hours after the onset of infarction and remained at high values for another 4-7 days. In two of ten patients with unstable angina pectoris LC2 increases above 10 ng/ml. The prolonged release of HVMLC1 and HVMLC2 in serum for 4-7 days after the onset of myocardial infarction may facilitate the retroactive detection of infarction, hence the extension of myocardium necrosis.

Creatine Kinase↗