Lymphangioleiomyomatosis, chylous ascites, and diet.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J L Alvarez-Sala.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The bronchoalveolar lavage (BAL) is considered a basic technique as a diagnostic aid in Pneumology. However, one of the main problems faced by the clinician is the lack of standardization of the technique. This has been resolved through the drafting of international standards. The other problem is the lack of what might be called a "reference" BAL. In order to establish a reference BAL, we analyzed 203 BAL divided in two groups: a control group and a pathologic group, make up by extrinsic asthma, intrinsic asthma, pulmonary infections, diffuse interstitial pneumopathies, bronchopulmonary tumors and chronic bronchitis. We have studied both the cytologic and the biochemical component of the BAL. Among the biochemical markers, we have considered; carcinoembrionary antigen (CEA), tissular polypeptidic antigen (TPA), neuronal specific enolase (NSE), ferritin (FER), calcitonin (CT), ACTH, histamin (HIS) and prostaglandin (PGE2). In order to establish the reference values, we have used the modified Baye's theorema. The BAL that we obtained was the following: volume 20 ml, cells 35 x 10(5) cells/ml, macrophages 77%, lymphocytes 22%, neutrophils 4%, eosinophils 2%, CEA 14 ng/mg, TPA 84 U/g PT, NSE 5 ng/mg PT, FER 42 ng/mg PT, CT 15 pg/mg PT, ACTH 51 pg/mg PT, HIS 1.22 ng/mg PT, PGE2 35 pg/mg PT.
Few important side-effects of nasal continuous positive airway pressure (nCPAP) have been reported. No increase of intraocular pressure (IOP) complicating this treatment has previously been described. The goal of our study was to analyse the influence of nCPAP on IOP. We evaluated 18 patients previously diagnosed as having glaucoma and 22 normal subjects. nCPAP was used during wakefulness, at +12 cmH2O for 15 min. The results showed that nCPAP significantly increases IOP in patients with glaucoma (before nCPAP 20.3 +/- 6.3 mmHg) (mean +/- SEM); after nCPAP 22.3 +/- 5.7 mmHg. We believe that nCPAP might be relatively contraindicated in difficult to manage glaucoma patients, if these results are corroborated.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare disease, whose origin seems to lie in a acquired defect in the membrane of the pluri-potential hematopoietic cell. Chronic or intermittent acute hemolytic syndrome is the most frequent clinical manifestation, although in the literature there are also some references to the leukocytic and immunologic disorders of this disease. In this paper, we present the case of a 63-year-old patient with NPH who developed severe neutropenia and sustained febrile syndrome. In the past four years, she had suffered frequent episodes of fever and leukopenia, which apparently disappeared spontaneously. In the physical exploration, we observed hepatosplenomegaly. The hemogram showed mild iron deficiency anemia (hemoglobin 10.8 g/dl), severe neutropenia (neutrophil 0.3 x 10(9)/l) and significant reticulocytosis (610 x 10(9)/l). Iron deposits were greatly reduced in the marrow. Simultaneously to a new febrile episode and isolation of Escherichia coli in the urine, there was a severe anemization (hemoglobin 5 g/dl) and a significant thrombopenia (platelets 30 x 10(9)) resulting in a positive hemosiderinuria and sucrose test. The study of the leukocytic function showed a defect in the neutrophil chemotaxis, although a normal phagocytic capacity and microbicidal activity. In the following nine months, the patient had several severe infections, with intense but transitory pancytopenia, which always improved when treating the infection with antibiotics. The patient died due to a septic shock twelve months after the diagnosis. Recurrent febrile episodes and severe neutropenia are very rare in the PNH (less than 4% of the cases). The cause of these disorders is still unknown.(ABSTRACT TRUNCATED AT 250 WORDS)
In patients with chronic renal failure, renal transplantation improves anemia and the production of erythropoietin. In patients undergoing hemodialysis the administration of recombinant human erythropoietin improves anemia with a decrease in bodily iron stores. Therefore, one would expect a similar decrease after kidney transplantation. We followed the ferric parameters to determine the incidence of iron deficiency anemia in 24 consecutive renal transplant patients for an interval long enough to achieve steady state values of hemoglobin (5.1 +/- 0.8 months). Hematological parameters and serum levels of iron, ferritin and erythropoietin were measured. The patients were divided into 2 groups according to the decrease in serum ferritin: group 1--16 with a decrease in respect to basal values (114 +/- 56 ng./ml.) and group 2--those without modifications (720 +/- 320 ng./ml.). Except for the similar values, group 1 showed greater improvement in anemia (red blood cells 4.3 x 10(6) +/- 1.1 x 10(6) versus 3.7 x 10(6) +/- 1.5 x 10(6)/ml., p < 0.01) and hematocrit index (38.5 +/- 5.2 versus 33.0 +/- 5.1%, p < 0.05). Four patients had microcythemia (mean corpuscular volume 76.6 +/- 1.4 fluid) with lower hemoglobin values than the other patients in group 1 (10.77 +/- 0.42 versus 12.79 +/- 0.42 gm./dl., p < 0.05). Among the 16 patients in group 1, 7 of 8 whose basal serum ferritin was less than 150 ng./ml. achieved ferritin levels of less than 30 ng./ml. In conclusion, our data support that renal transplantation produces a rapid decrease in iron stores and in some cases induces iron deficiency anemia. This fact should be evaluated and treated properly.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The appearing of splenic complications in the evolution of acute or chronic pancreatitis is a known fact, even though it is not that frequent. A case of splenic rupture happens during an acute bout of chronic pancreatitis. The possible pathogenic mechanisms implied are analysed as well as the forms of presentation and the approximation to diagnosis. The great difficulty in the diagnosis is determined by the scarce specificity of the clinical and biochemical manifestations. Therefore, it is called the attention upon the eventuality of this complication and the therapeutic attitudes which should be adopted.