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Biomedical subjects

E Parisio

Publications and source records attributed to E Parisio.

28 records · Page 2Linked to original sources
PubMed1987

Amiodarone lung toxicity: role of pulmonary function tests.

Forty-three patients treated with amiodarone hydrochloride with an average daily dose of 204.7 +/- 79.4 mg/day for a mean period of 37.1 +/- 25.3 months, were studied by clinical examination, chest roentgenograms, pulmonary function tests and blood gas analyses. The habits of cigarette smoking were also recorded and expressed as cigarette pack/years. Pulmonary function tests did not show any differences from control subjects and no correlation was found between exposure to drug and lung function. However, one patient developed abnormalities in the chest X-ray (interstitial type) and a reduction of carbon monoxide diffusion capacity as a possible manifestation of amiodarone lung toxicity. Nine patients (22%) had a 20% decrease from normal in carbon monoxide diffusion capacity and three (7%) had a 15% decrease in total lung capacity. More treated patients had interstitial abnormalities in the chest X-ray (14%) than controls (5.5%). Although pulmonary function test abnormalities could be detected in patients taking amiodarone, they were not usually severe enough to interfere with gas exchange. Our results confirm the rarity of amiodarone lung toxicity when a low dosage is used, and suggest the advisability of periodical monitoring, including clinical examination, chest X-ray and pulmonary function tests in order to detect the earliest signs of amiodarone lung toxicity.

Adult↗
PubMed1986

Amiodarone-induced thyroid dysfunction: diagnostic role of free serum thyroid hormone levels and pathogenetic significance of antithyroid antibodies.

Forty-six patients treated with amiodarone hydrochloride for a mean period of 41 +/- 3.5 months, with an average daily dose of 240 +/- 57 mg/day, have been studied. Thyroid function was assessed clinically and by laboratory tests, which included free-triiodothyronine (free-T3), free-thyroxine (free-T4) and thyrotropin. Antimicrosomal and antithyroglobulin antibodies were also looked for. Three patients (6.5%) were found to be hyperthyroid and two (4.3%) hypothyroid. Of the 41 clinically euthyroid patients, 19 (46.3%) showed one or more abnormalities in the thyroid function tests. In this group, only free-T4 was found significantly increased (p less than 0.05) as compared to both control populations. Antimicrosomal antibodies (titre greater than or equal to 1:1600) were present in 4 of 41 (9.7%) euthyroid patients, but not in hyper- or hypothyroid patients. There were no antithyroglobulin antibodies in any patients. Free hormone measurements have proved to significantly correlate with the clinical picture. Increases in free-T3 and free-T4 are the main features of hyperthyroidism, while a reduction in free-T4 serum level was specific for hypothyroidism. There are probably several mechanisms responsible for hyperthyroidism and some genetically controlled defects in synthesis and release of thyroid hormones might be among these. The presence of antithyroid antibodies could be due to deposits of amiodarone in the thyroid gland, with a consequent release of antigen from the follicle cell, but only in those patients with genetically determined defects in immunological surveillance could an autoimmune thyroiditis, with consequent hypothyroidism, develop.

Adult↗
PubMed1985

[Secondary hypothyroidism with thyrotropic hormone deficiency. Presentation of a case and review of the literature].

A patient with clinical signs of hypothyroidism, low basal serum thyrotropin (TSH) and lack of response to releasing-factor (TRH) is described. The normal secretion of other anterior pituitary hormones both basal and after stimulation tests and the absence of hypophysial sella alterations found with computed axial tomography suggest the presence of a selective idiopathic TSH deficiency. The pituitary origin of this defect has been reported in literature only in five further patients, tested with TRH. The exact pathogenetic mechanism of these cases is still unknown: in the patient observed by the authors unresponsiveness both to TRH and to metoclopramide suggest an absence of TSH-producing pituitary cells or an alteration of the mechanism beyond the receptor and within the cell. However the possibility that such a secretion defect may represent a first sign of a pituitary tumor should not be excluded.

Aged↗
PubMedDate not supplied

Pulmonary asbestosis associated to pleural non-Hodgkin lymphoma.

We describe herein a case report of a patient affected by pulmonary asbestosis who developed a non-Hodgkin lymphoma originating in the pleura. The case is unusual for the uncommon site and because the chronic antigenic stimulation by asbestos bodies may have locally promoted an immunologic derangement.

Aged↗
PubMedDate not supplied

[Still's disease in adults: diagnostic problems].

Still's disease is a seronegative arthritis of children which, in a limited number of cases, can affect adults. The diagnosis of adult-onset Still's disease is characterized by high fever, arthritis and negative serologic tests for rheumatoid factor and antinuclear antibodies and by at least two minor symptoms (leukocytosis, evanescent rash, serositis, hepato- or splenomegaly, and lympho-adenopathy). Since many diseases present analogous manifestations and the adult-onset Still's disease is generally diagnosed by exclusion, we report two patients, aged 26 and 39, with Still's disease, the former with a classic clinical feature, the latter with a clinical feature characterized by severe hepatic abnormalities. The determination of histocompatibility antigens can be useful because some of them (HLA-DR4 in case 1 and HLA-DRw6 in case 2) are frequently associated with the adult-onset Still's disease. The role of anti-inflammatory therapy (acetylsalicylic acid, indomethacin, steroids) must be emphasized, whose efficacy can constitute the pathognomonic element on which the diagnosis of adult-onset Still's disease can be based in a proper clinical pattern.

Adrenal Cortex Hormones↗
PubMedDate not supplied

HIV-related thrombotic thrombocytopenic purpura (TTP) as first clinical manifestation of infection.

A case of thrombotic thrombocytopenic purpura (TTP) in a 40-year-old bisexual man unaware of being HIV positive is reported. The hematologic syndrome represented the first clinical manifestation of this viral infection. The clinical picture, characterized by severe hemolytic microangiopathic anemia, thrombocytopenia, fluctuating neurologic abnormalities and fever, quickly improved after plasma exchange and corticosteroid therapy. Two blood tests showed severe depletion of the CD4+ lymphocyte count and HIV antigenemia was positive. This case represents a clinical epiphenomenon of HIV infection in an advanced phase. According to recent CDC criteria the patient should be considered in AIDS. Antiretroviral treatment was started and after nine months of follow-up there has been no relapse.

Adult↗