[Evaluation and usefulness of hypercoagulability markers in medical pathology].
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Biomedical subjects
Publications and source records attributed to R Cornudella.
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It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.
PURPOSE: To compare systemic anticoagulation with antiaggregation in patients with coronary stent, with regard to subacute occlusion, mean hospital staying and haemorrhagic complications. PATIENTS AND METHODS: Seventy-five patients with coronary stent were treated with one of two different antithrombotic protocols. A group comprised of 34 patients (group A) received sodium heparin and acenocoumarin, plus acetylsalicylic acid (325 mg) and dipyridamole (225 mg). The remaining 41 patients (group B) were given antiplatelet agents, namely ticlopidine (125-250 mg) and aspirin (125 mg). RESULTS: One case of group A (2.9%) showed thrombosis due to stent occlusion. No thrombotic complications were seen in the patients with antiplatelet drugs. Haemorrhagic complications were present in 11 group A patients (32.3%), and blood transfusion was necessary in 3 of them. Hemorrhage was present in 9 cases of group B (21.8%), and none of them needed blood transfusion. The mean number of days to achieve INR > 2 was 3.06 (1-11) in group and 2.02 (1-5) in group B. CONCLUSIONS: Antiplatelet regimes appear as a good choice in coronary stent, in spite of the fact that the primary indication seems that of group A.
BACKGROUND: Gastrointestinal bleeding is related to non-steroidal anti-inflammatory drug (NSAID) use, especially aspirin, but only a small subset of users bleed. AIM: To look for risk factors or mechanisms whereby aspirin may promote gastrointestinal bleeding. PATIENTS: Sixty one patients with previous aspirin related upper gastrointestinal bleeding and 61 matched controls. METHODS: Patients and controls were given 375 mg of aspirin and sequential skin bleeding time and blood aspirin levels were measured. Additional studies included platelet lumiaggregation, von Willebrand factor, Factor VIII, and coagulation studies. RESULTS: Baseline skin bleeding time was similar in bleeders and controls, but bleeders had a more prolonged skin bleeding time after aspirin use. Hyper-response was more frequent in bleeders (30% v 9.3%; p < 0.01) and was associated with more than one previous separate bleeding event and a lower packed cell volume during the preceding bleeding episode. No differences were found in other factors studied. Logistic regression analysis identified prolonged skin bleeding time after aspirin use as an independent factor contributing to aspirin related gastrointestinal bleeding (RR = 5.4; 95% CI: 1.8 to 17.1). CONCLUSIONS: 30% of patients with a history of aspirin related gastrointestinal bleeding have an exaggerated prolongation of skin bleeding time in response to aspirin, which may be a risk factor for bleeding. This intrinsic defect or to subclinical von Willebrand disease or different aspirin metabolism.
There is a well known relationship between factor XII deficiency and arterial and venous thrombosis. A new case of moderate factor XII deficiency associated to spontaneous deep vein thrombosis and treated with Urokinase is reported. The patient had a partial response to the treatment with Urokinase, with normal study of the fibrinolytic system. The deficiency was found in five relatives within the three generations studied. The genetic transmission had an autosomic dominant pattern. We feel that there is no relationship between the family history or the degree of factor XII deficiency and the risk of developing deep venous thrombosis.
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PURPOSE: To evaluate the fibrinolytic system function in survivors of acute myocardial infarction (AMI) and to appreciate the differences between patients with history of diabetes and/or dyslipaemia and those without such history. PATIENTS AND METHODS: A series comprised of 101 patients (83 men and 18 women) surviving six months after AMI and with mean age of 61.7 +/- 8.5 years was studied. Previous history of type II diabetes mellitus was present in 22 cases, while 42 others had some type of dyslipaemia (16, hypertriglyceridaemia; 15, hypercholesterolaemia; 11 both). Of the patients with diabetes mellitus, 14 had also dyslipaemia (5, hypertriglyceridaemia; 6, hypercholesterolaemia; 3, both conditions). The rates of plasminogen-activator inhibitor (PAI-1), fibrinogen, plasminogen, and alpha-2-antiplasmin, along with the venous occlusion test to determine tissular plasminogen activator (t-PA), both functional and antigenic, before and after venous occlusion, were tested in all cases. The studies were performed at the moment of AMI and 6 months later. RESULTS: PAI-1 concentration during AMI in the patients with some concurrent lipid anomaly showed significant differences with respect to the patients without any such associated disease (p < 0.001). The patients with history of dyslipaemia had significant increase of PAI-1 (p < 0.001) with respect to those without such history. Those patients with associated diabetes showed significantly increased PAI-1 concentration with regard to those without it, both in the acute phase and 6 months later (p < 0.05); significant increase was also found when comparing the patients with diabetes and dyslipaemia with those ones with only diabetes or dyslipaemia (p < 0.05). A significant increase of PAI-1 level (p < 0.001) was found in the 6-month study in the dyslipaemia patients with respect to non-dyslipaemic, and similar findings appeared with respect to diabetics and non-diabetics (p < 0.05). The 14 patients with both disorders showed increased values when compared with those having only one associated impairment (p < 0.05). When comparing the PAI-1 rates at AMI and 6 months later in the patients with dyslipaemia or diabetes, statistically significant decrease could be noted (p < 0.05 and p < 0.01, respectively). Before venous occlusion, t-PA was significantly increased in diabetic or dyslipaemic patients (p < 0.05) and in the patients with both conditions (p < 0.01). CONCLUSIONS: Patients with AMI and abnormalities of the lipidic or glycaemic metabolism have fibrinolytic dysfunction on the basis of an increase of the main inhibitor of the fibrinolytic system and a decreased release of tissular plasminogen activator. Those patients with both metabolic abnormalities have a deeper fibrinolytic hypofunction, with higher PAI-1 concentration.
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PURPOSE: To evaluate the main components of the fibrinolytic system in patients suffering of acute myocardial infarction (AMI), both in the acute phase and once this has been overcome. PATIENTS AND METHODS: Components of the fibrinolytic system (i.e., PAI-1, t-PA, fibrinogen, plasminogen, and alpha 2-antiplasmin) were determined in 100 patients with AMI. The studies were performed at AMI and 6 months later, and the findings were compared with those of a control group of 30 people matched with regard to age and sex with the patient group. The statistical analysis of the results was made with the BMPD pack, using Student's t test for comparing quantitative variables and the matched test for paired samples. RESULTS: At the acute phase the patients showed significant increase of PAI-1 (p < 0.001) and fibrinogen (p < 0.05) concentrations. Plasminogen and alpha 2-antiplasmin rates were lower than in the control group (p < 0.01 and p < 0.005, respectively). In the 6-month study after AMI, significant increase of PAI-1 was found with respect to the control group (p < 0.001). There were also significant differences in the initial PAI-1 rates and the 6-month test (p < 0.05), whereas the increased fibrinogen rates persisted (p < 0.01). Increased antigenic t-PA was found in the patient group before venous occlusion (p < 0.001). Thus, 54 patients (54%) had hypofibrinolysis, due to increased PAI-1 in 41 cases (41%), impaired t-PA release in 13 cases (13%) and both causes in 12 cases (12%). CONCLUSIONS: Fibrinolytic hypofunction was found in this study during the acute phase of myocardial infarction, which was still present six months later, and was due to increased PAI-1 rates in the majority of the cases.
During the period 1986-1990, 10 cases of human disease caused by Mycobacterium bovis were diagnosed in our hospital. The incidence, in relation to the cases of disease from Mycobacterium tuberculosis diagnosed in the same period, was 0.9%. The patients had an average age of 32 years (range 5-68 years). Pulmonary disease was observed in 5 patients (50%), lymphadenitis in 2, pleural effusion in 2 and peritoneal in 1. The most significant of the epidemiological features was that 2 patients were veterinary students. There was 1 death from ovarian neoplasia with abdominal dissemination. The other cases responded favourably to treatment with standard chemotherapy of 6-12 months achieving cure, without relapse, of all the patients.
One hundred and thirty six patients presenting pleural effusion and whose diagnosis was obtained by clinical, biochemical, bacteriological, cytological and histological methods have been studied and classified into seven groups: 20 transudates, 29 inflammatory, 25 tuberculosis, 25 non adenocarcinoid neoplasias, 24 adenocarcinomas, 10 mesotheliomas and 3 miscellaneous. Carcinoembryonic antigen was determined in all of them, evaluating as positives those values above 10 ng/ml, value which we consider discriminatory in our series and which agrees with the literature, finding positive values in 21 out of 24 adenocarcinomas and 3 out of 25 non adenocarcinomas. All benign pleural effusions and mesotheliomas had values lower than 10 ng/ml. The specificity to determine adenocarcinomas in neoplastic effusions was 91.48% and the sensibility was 87.5%. We consider that the CEA determination is useful to differentiate adenocarcinomas from other neoplasias and that a positive value rules out mesothelioma.
Sixty five patients with AIDS and clinical and/or radiological evidence of pulmonary infection underwent 78 bronchofibroscopies (BF) with protected brushing and bronchoalveolar washing-out. Out of the 78 BF, bacterial infection was diagnosed in 30 cases and associated opportunistic infection in 12 cases. The 18 cases of exclusively bacterial infection accounted for 23% of the total and most of them were due by H. influenzae and pneumococcus. Just in one patient, the thoracic radiography showed a localized infiltration. Given the high incidence of bacterial infections observed, along with the relevance of myxoid infections (opportunistic and pyogenic bacteria) and the low specificity of the thoracic radiography, bronchoalveolar washing-out and protected brushing in the same BF is a recommended practice.
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With the aim of testing a method that allows increasing concentrations of oxygen to be administered to patients with severe hypoxemia and hypercapnia while avoiding the risk of increasing respiratory acidosis, we studied 17 male patients with advanced chronic obstructive pulmonary disease (COPD) and severe hypercapnic respiratory failure. During 6 h and on one day only, all patients were given intermittent negative pressure ventilation (INPV) together with oxygenation starting at a concentration of 24 percent and increasing to 30 percent. Using this procedure, it was possible to raise arterial PaO2 to safe levels (from 47.2 +/- 3 mm Hg to 61.5 +/- 6 mm Hg, p less than 0.001) without increasing hypercapnia, and a significant drop in PaCO2 levels (from 74.4 +/- 9 mm Hg to 65.6 +/- 12 mm Hg, p less than 0.005) was even observed. One hour after INPV ended, the mean values of PaO2, PaCO2, oxygen saturation, and pH were also significantly better than prestudy values. We conclude that INPV and oxygen therapy with increasing oxygen flow could constitute an alternative option to intubation and mechanical ventilation in cases of severe hypercapnic respiratory failure due to advanced COPD.
Three cases of multiple simultaneous primary lung carcinomas are presented, in which diagnosis was established by post-surgery pathological exam. In all three cases, chest X-ray showed pulmonary masses suggestive or clinical malignancy, and pre-surgery pathological diagnosis or squamous lung carcinoma. During thoracotomy or in the resected segment, a second lesion we confirmed which made resection necessary being this second lesion classified as lung adenocarcinoma.
The clinical characteristics, radiologic findings, and therapeutic response in 35 cases of pulmonary disease induced by opportunistic environmental mycobacteria collected during a period of 4 years are reported. These cases included 21 infections by Mycobacterium kansasii, 10 by M. xenopi, and 4 by M. avium. The cases reported constituted the 6% of all mycobacterial infections of the lung observed in our institution. The mean age of the patients was 56 years and 83% of them were male. The presence of previous pulmonary involvement was rather frequent, specially the existence of chronic limitation of the air flow (CLAF) (91%) and previous tuberculosis (29%). The clinical symptoms were almost nonspecific and they could frequently be misinterpreted as an intercurrent infection in cases of CLAF. The radiologic findings could not be distinguished from an infection by M. tuberculosis. The clinical course with pharmacologic first line therapy (93% of cases) was satisfactory in 28 patients in whom follow-up controls are available.
We report the case of a young woman presenting productive cough and arthralgia in the left ankle. Chest radiography revealed multiple bilateral pulmonary nodules and abdominal echography and computerized axial tomography demonstrated various hepatic nodules. Definitive diagnosis of an intravascular bronchoalveolar tumor was reached by an open pulmonary biopsy. Liver involvement was confirmed by laparoscopy and biopsy.
The interrelationship between factor XII deficiency (Hageman trait) and thrombosis is well known. A case of moderate factor XII deficiency (activity, 30%) associated to deep vein thrombosis, which occurred in the popliteal region of the left lower limb after abdominal surgery, is reported. The deficit was found in 4 family members of the three generations studied, and all of them showed a close interrelationship between factor XII activity and kallikrein levels. Prolonged APTT was found in 3 of the 4 affected subjects. A multiallelic model is suggested to explain the genetic transmission of this impairment.