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Biomedical subjects

E Parisio

Publications and source records attributed to E Parisio.

At least 19 recordsLinked to original sources

Abdominal placement of tube thoracostomy due to lack of recognition of paralysis of hemidiaphragm.

Tube thoracostomy is an invasive procedure that carries a risk of complications. We report a patient with liver cirrhosis, ascites and large left-sided pleural effusion, in whom a trocar type chest tube was inserted at the seventh left intercostal space in the midaxillary line. Chest roentgenogram revealed that the drainage tube was placed into the abdominal cavity because of a misrecognized elevation of the left hemidiaphragm. This case demonstrates that the placement of a tube thoracostomy requires caution in the identification of possible abnormalities which can lead to dangerous complications.

Abdomen↗

False positivity of tumor markers in pleural fluid of traumatic hemothorax.

Various biochemical parameters of pleural fluid have been employed to identify malignant effusions. However, many of them are also elevated in patients with nonmalignant conditions. We report on a patient with traumatic hemothorax, showing high pleural fluid concentrations of ferritin, tissue polypeptide antigen, and cancer antigen 125. This patient's pleural fluid also contained high levels of bilirubin and many macrophages containing phagocytized red blood cells, suggesting a local metabolism of hemoglobin. Our case confirms that some tumoral markers can give false positive results and suggests that their significance must be evaluated differently in bloody pleural effusions as compared with non-bloody pleural effusions.

Adult↗

Terlipressin-induced metabolic acidosis.

Vasopressin and its analogue terlipressin are potent vasoconstrictors which reduce mesenteric blood flow and have been used in the therapy of variceal hemorrhage. This vasoconstrictor effect applies on vascular beds throughout the body. Since in literature vasopressin is rarely described to determine lactic acidosis, we report of a patient in whom a severe metabolic (probably lactic) acidosis appeared, associated with terlipressin administration for bleeding esophageal varices. By exclusion, the temporal sequence with terlipressin therapy, the contemporary increase of arterial blood pressure and autoptic data in the case presented make likely a diagnosis of terlipressin-induced lactic acidosis. Because of the seriousness of metabolic acidosis observed in our patient we suggest a careful monitoring of acid-base parameters in patients under treatment with vasopressin analogues.

Acidosis↗

Malignant pleural effusions: meaning of pleural-fluid pH determination.

In 36 patients with malignant pleural effusions, we determined the pH and the glucose concentration of the pleural fluid. Twenty-one of 36 patients (58.3%) had a low pH (less than 7.30) and 15 had a normal pH (greater than or equal to 7.30; 7.13 +/- 0.12 vs. 7.37 +/- 0.05; p less than 0.0005). The patients with low pH had significantly lower glucose concentrations than those with normal pH (2.7 +/- 1.4 vs. 6.3 +/- 2.9 mmol/l; p less than 0.0005). Twenty-one of 34 patients (61.7%) had a glucose concentration lower than a cut-off value of 4.4 mmol/l; of these, 17 (81%) had a low pH. The mean survival in the low-pH group was 4.8 +/- 4.4 months, whereas the mean survival in the normal-pH group was 5 +/- 8 months (p greater than 0.4). Twelve of 36 patients (33.3%) were treated with intrapleural Corynebacterium parvum (CBP) injections. Fourteen of 21 low-pH patients (66.6%) survived more than 2 months, and 4 of them are still alive. Six of 15 normal-pH patients (40%) survived more than 2 months, and 1 of them is still alive. Three of the 5 living patients were treated with CBP (2 in the low-pH group and 1 in the normal-pH groups). Our results confirm that pH and glucose concentrations in the pleural fluid of patients with malignant effusions are frequently low. However, the survival and the response to CBP pleurodesis in patients with low-pH malignant effusions are the same as those in patients with normal-pH malignant effusions.

Adolescent↗

[EDTA-induced pseudothrombocytopenia].

EDTA-induced pseudothrombocytopenia is a laboratory artifact caused in vitro by platelet aggregation, due to IgG or IgM class antibodies reacting with antigenic binding site of the GP IIb glycoprotein. Pseudothrombocytopenia is rarely found (about 1% of platelets counts), but must be considered in the differential diagnosis of thrombocytopenia, since it could lead to useless investigations and therapies. We report three patients with pseudothrombocytopenia, one of whom underwent bone marrow biopsy and danazol treatment, before establishing the correct diagnosis. The absence of hemorrhagic manifestations with persisting low platelets counts led to a re-examination of peripheral blood smear and to the diagnosis of pseudothrombocytopenia. Therefore a morphological platelets evaluation and their count on citrate-anticoagulated blood must be performed in every patient under assessment for thrombocytopenia.

Aged↗

Antithyroid antibodies during amiodarone treatment.

In 44 euthyroid and goitre-free patients, 23 treated with amiodarone (group A) and 21 treated with other antiarrhythmic drugs (group B), antimicrosomal antibodies and antithyroglobulin antibodies were determined before the beginning of treatment and after 7, 15, 30, 60, and 180 days. In group A, none of the patients had antithyroid antibodies before treatment. 1 of 15 patients (6.7%) had antimicrosomal antibodies (titre 1:100) on day 7 only, and 1 of 18 (5.5%) had antithyroglobulin antibodies (titre 1:80) on day 180. In group B. 1 of 21 patients (4.8%) had antimicrosomal antibodies (IgG class) at titre 1:400 before the beginning of treatment, which was negative on day 180, and 2 of 17 (11.8%) had antimicrosomal antibodies (titre 1:100) on day 60 only. None of these patients showed clinical and/or laboratory signs of hyper- or hypothyroidism. These data indicated that antithyroid antibodies rarely appear in amiodarone-treated patients and do not differ significantly from patients treated with other antiarrhythmic drugs. The role of autoimmunity and the meaning of antithyroid antibodies in the pathogenesis of amiodarone-induced thyroid dysfunction (mainly of hypothyroidism) in patients without pre-existent thyroid diseases is still unclear.

Aged↗

[Transitory efficacy of potassium perchlorate in hypothyroidism caused by amiodarone].

We report a case of a patient with hypothyroidism due to amiodarone. The short-term administration (1 g/die for 10 days) of potassium perchlorate (KClO4) led to normalization of serum thyroid hormone concentrations and marked reduction of thyrotropic hormone. The reduction of KClO4 (400 mg/die) and its following withdrawal led to reappearance of hypothyroidism signs. No side-effects or toxic reactions occurred during KClO4 therapy. This anion competitively inhibits thyroid iodide transport, reducing intrathyroidal iodide content and removing thyroid hormone synthesis inhibition. We suggest KClO4 therapy when amiodarone-associated hypothyroidism impairs a pre-existent cardiac disease and when a quick restoration of euthyroidism is necessary. Nevertheless, we emphasize that its effect can be transitory in cases of short-term treatment or low doses.

Aged↗

Angiotensin-converting enzyme as a possible marker for lung toxicity in amiodarone-treated patients.

Since it has been observed that in vitro amiodarone induces morphological alterations in endothelial cells similar to those observed in patients with lung toxicity and that the angiotensin-converting enzyme (ACE) seems to be a marker for perturbation of the alveolar-capillary membrane, serum ACE concentrations have been determined in 44 patients, 23 treated with amiodarone (group A) and 21 treated with other anti-arrhythmic drugs (group B), before the beginning of treatment and after 7, 15, 30, 60 and 180 days. Serum ACE concentrations in group A were lower than the basal values (15.8 +/- 5.9 mU/ml) on day 7 (12.7 +/- 4.5 mU/ml) and were higher on day 60 (17.9 +/- 3.8 mU/ml), then returned to basal values by day 180 (15.9 +/- 5.5 mU/ml), but none of the differences were statistically significant. In group B, serum ACE concentrations were significantly higher than basal values (15.2 +/- 4.0 versus 14.2 +/- 3.5 mU/ml, p less than 0.05) only on day 15. In group A serum ACE concentrations were significantly higher than in group B only on day 60 (17.9 +/- 3.8 versus 14.7 +/- 4.5 mU/ml, p less than 0.025). During the period of the study none of the patients showed any clinical or radiological signs of lung toxicity or reduction of lung diffusion capacity for carbon monoxide (DLCO). Serum ACE levels were normal even in three patients who developed pulmonary fibrosis and in four whose DLCO was reduced by more than 20% from the basal values after the study was completed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Hospital pseudo-infections caused by Mycobacterium gordonae].

Sputum specimens from 15 patients with respiratory disease were reported to have positive cultures for Mycobacterium gordonae, an organism generally considered to be non-pathogenic for man. None showed typical radiological changes for mycobacteriosis. Mycobacterium gordonae was also isolated from some components of the aerosol therapy instrument. Because aerosol therapy was used for 4 patients only, we were not able to establish whether the Mycobacterium gordonae was only a colonizer. We suggest that its isolation in culture must be evaluated in an adequate clinical context before concluding that it is pathogenic.

Aged↗

[Anatomical study of the fibrosing action of Corynebacterium parvum in malignant pleural effusion].

Intrapleural injection of Corynebacterium parvum (CBP) has recently been used for the treatment of recurrent neoplastic pleural effusions and its mechanism of action has been suggested to be either a local fibrosis-stimulating effect or immunostimulation. The case is reported of a patient with pleuritis secondary to metastases of mammary carcinoma, treated with CBP plus methylprednisolone, who died five days after the treatment because of an acute myocardial infarction. The pathologic examination showed fibrinous pleuritis with an interconnecting network between the visceral and parietal pleura.

Breast Neoplasms↗

[Is malignant mesothelioma of the pleura only an occupational disease?].

Ten cases of pleural malignant mesothelioma identified histologically at the Department of General Medicine in May 1983-June 1987, are examined in this paper. Occupational risk factors and clinical features are discussed. Only one patient (10%) was subjected to occupational risk of asbestos exposure (as a smith) while the other nine patients showed a negative anamnesis for direct or indirect asbestos exposure. However, one of these patients was a tram-driver. The patients' mean age was 69 years old. 7 patients were males. 7 patients were born in an industrialized urban environment, 3 were born in an agricultural environment: all had been living in Milan for many years. Pleural fluid cytology was only useful in the diagnosis of 2 cases. This study suggests that pleural malignant mesothelioma is a neoplasm which also affects people not exposed to asbestos at work and that its frequency is increasing. The most probable cause is environmental contamination by asbestos of urban industrialized areas. Thus, it is necessary to eliminate this mineral from all manufacturing processes in which asbestos is not indispensable.

Aged↗

Primary hypothyroidism due to leukemic infiltration of the thyroid gland.

We describe a patient with acute B-lymphocyte lymphoblastic leukemia who developed laboratory changes (not detectable free thyroxine, TSH 66 microIU/ml) suggesting severe primary hypothyroidism. Histological examination at autopsy showed massive leukemic infiltration of the thyroid gland: the progressive reduction of thyroid hormone levels with concomitant increase in TSH levels observed over a three-month period from the onset of the hemopathy suggests a cause-effect relationship between leukemic infiltration of the thyroid gland and hypothyroidism.

Acute Disease↗

[Hypertrophic cardiomyopathy mimicking clinical picture of Budd-Chiari syndrome].

A case of a patient with clinical picture of hepatosplenomegaly, portal hypertension, dilatation of hepatic veins and inferior vena cava, without venous thrombosis or other causes of obstruction of right-sided heart, is described. This picture is compatible with the Budd-Chiari syndrome. Echocardiography has shown a hypertrophic cardiomyopathy causing relevant dilatation of both atria and it has allowed us to exclude the presence of a constrictive pericarditis. The hypertrophic cardiomyopathy is first considered as a cardiac cause of cirrhosis mimicking the Budd-Chiari syndrome.

Aged↗

[Excess mineralocorticoid syndrome secondary to nasal sprays containing 9 alpha-fluoroprednisolone].

Two patients with signs of hypermineralcorticism and suppressed plasma aldosterone levels are reported. For both patients the use of a nasal spray containing 9 alpha-fluoroprednisolone had been ascertained, the withdrawal of which was followed by the normalization of the clinical picture as well as by the normal reactivity of the renin-aldosterone system. The endocrine studies excluded the presence of enzymatic defects or the hypersecretion of minor mineralocorticoids. The tests with angiotensin II and ACTH did not result in an increase in aldosterone, which instead increased in a significant way after metoclopramide, even with still suppressed basal values. Since the PRA was normal at the time of the metoclopramide test, a persisting inhibition of the factors directly controlling aldosterone secretion by 9 alpha-fluoroprednisolone could be possibly envisaged. An interesting findings was the onset of severe hypokalemia, conditioning rhabdomyolysis with myoglobinuria in patient 1, after a treatment of few weeks only. Since the factitious use of mineral corticoids is not taken into account, the need of an accurate collection of case history in the differential diagnosis of hyporeninemic hypoaldosteronism with hypokalemia is stressed.

Aldosterone↗

Serum free thyroid hormones in different degrees of hypothyroidism and in euthyroid autoimmune thyroiditis.

Serum total and free T4 and T3, thyroxine-binding globulin (TBG) and TSH, basal and 20, 30 and 60 min after TRH (200 micrograms, iv), were evaluated in 125 hypothyroid patients (38 with severe, 23 with mild, and 64 with subclinical hypothyroidism), in 35 euthyroid subjects with autoimmune thyroiditis, and in 51 healthy controls. T4/TBG and T3/TBG ratios were also calculated. A significant decrease in all indices of thyroid function except for T3 occurred simultaneously with a significant increase in basal and TRH-stimulated TSH levels from healthy subjects to subclinical hypothyroids, from subclinical to mild and from mild to severe hypothyroids; euthyroid patients with autoimmune thyroiditis did not differ from healthy subjects. All severe hypothyroid patients had low T4 as well as free T4 (FT4), free T3 (FT3), T4/TBG and T3/TBG ratios, but among mild and subclinical hypothyroids direct determination of FT4 and FT3 proved to be a better index of thyroid function than determination of T4 and T3 even after correction for TBG levels. FT4 was the most commonly abnormal index (19 of 23 subjects with mild and 14 of 64 with subclinical disease). Regression analysis showed that FT4, T4/TBG ratio, T4, and FT3 had a significant inverse correlation with TSH in hypothyroid patients. Discriminant analysis showed that among the thyroid parameters, FT4 is the variable which discriminates best between control subjects and the 3 groups of hypothyroid patients. These data extend previous reports and in a large series of patients confirm the biological meaning and the clinical value of direct measurement of serum free thyroid hormones in hypothyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗