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Biomedical subjects

M Lazzarin

Publications and source records attributed to M Lazzarin.

At least 19 recordsLinked to original sources
PubMed1996

[Altered thyroid in dialysed uremic patients].

Thyroid abnormalities were studied in 40 uremic patients half of whom were receiving hemodialysis and half peritoneal dialysis. The following parameters were examined in all patients: total and free thyroxinemia, free and total triiodothyroninemia, basal thyreotropinemia and levels 20 mins after releasing hormone (TRH) stimulation, reverse T3, thyroglobulinemia, antithyroglobulin , antimicrosomial and antithyroperoxidase antibodies; a thyroid echography was also performed. Numerous alterations were found in thyroid parameters, with a greater frequency in hemodialysed patients (65%) than those undergoing peritoneal dialysis (52.5%). Among the parameters examined it is worth noting that total thyroxinemia was significantly reduced compared to controls, and FT3 was very significantly reduced. Among those patients undergoing peritoneal dialysis thyreotropinemia was increased in 6 cases (15%), whereas among hemodialysed patients it was reduced in 2 cases (5%). Ten patients (25%) in all appeared to be free of thyroid alterations and 30 (75%) showed one or more alteration of the parameters examined. Of the latter, 1 case of toxic multinodular goiter, 1 case of Plummer's adenoma in a pretoxic phase, 1 case of hypothyroidism, 15 cases of "sick euthyroid of syndrome", 3 cases with high antibody levels and 2 cases of single node goitre were diagnosed. The study confirmed the high incidence of thyroid alterations in uremic patients and, surprisingly, allowed the authors to diagnose a case of toxic multinodular goitre and a case of Plummer's adenoma at a pretoxic phase. The authors discuss the rarity of thyroid hyperfunction in uremia and suggest the need to consider patients with chronic renal insufficiency as being at risk of hypo-, normo- and hyperfunctioning thyreopathy, and to use a routine thyreotropinemia assay in all uremic patients.

Adolescent↗
PubMed1996

[Rhabdomyolysis and acute renal failure caused by haloperidol-decanoate (neuroleptic malignant syndrome)].

A case of rhabomyolysis with attendant severe acute renal failure, arisen in a 59-year-old male treated with haloperidol-decanoate, is presented. The patient has been affected by paranoia schizophrenia since childhood, and he was treated with electroshock and successively with neuroleptics p.o. Four years before our observation, a therapy with haloperidol decanoate (50 mg i.m. monthly) was started. After some time, catatonic like episodes appeared, which got more and more frequent, until they appeared weekly. In occasion of the last of them, he was admitted to our hospital. At the objective examination he presented psychomotory arrest, perspiration, mytacism, severe muscle rigidity, moderate oedems to lower limbs. Laboratory findings showed a pattern consistent with rabdomyolysis and severe renal failure. After that haloperidol decanoate was stopped and rehydration and intensive diuretic therapy was started, the clinical and laboratory pattern went normal, persisting however a light creatinine increase. Probably the rhabdomyolysis was induced by the haloperidol decanoate, and renal failure by secondary severe hyvolemia. This case comes into the so-called neuroleptic malignant syndrome which can rarely arise in patients treated with antipsycotic agents and which causes high mortality, particularly when there are rhabdomyolysis and acute renal failure.

Acute Kidney Injury↗
PubMed1993

[The pharmacological therapy of Basedow's disease].

Symptomatic and anti-thyroid drugs are discussed under the profile of the way of action, of the pharmacologic characters, of attack and maintenance doses and of unwanted effects. The time of treatment and the criteria (still not satisfactory) to decide the moment suitable to stop it are also considered. To the light of latest acquisitions some particular aspects of therapy about thyrotoxic storm, treatment during pregnancy, pharmacologic preparation to surgery, treatment of ophthalmopathy are discussed. To conclude, present medical therapy (or, alternatively, surgical and radioisotopic) allow satisfactorily to control the disease; it's possible, in the shown cases, to advise a prolonged pharmacologic treatment with antithyroid drugs.

Antithyroid Agents↗
PubMed1983

A family with heterozygous factor X Friuli defect outside Friuli.

Three members of the same family were found to have a clotting defect consistent with the diagnosis of heterozygous factor X Friuli disorder. The main features of the defect were a mild prolongation of prothrombin time and partial thromboplastin time, but a normal Stypven-Cephalin clotting time. Factor X activity was 40-50% of normal using tissue thromboplastin, but was perfectly normal using Russell's viper venom and cephalin. Using chromogenic substrate S-2222 the level was 30% of normal. Immunologically, factor X was normal. Bleeding manifestations were mild if any. The hereditary pattern was autosomal. The family comes from an area far away from Friuli and represents the first example of factor X Friuli discovered outside the Friuli.

Adult↗
PubMed1977

[Effects of clonidine on various blood-coagulation parameters in hypertension].

The effect of oral clonidine on prothrombin time, partial thromboplastin time, blood fibrinogen, fibrinolytic activity and platelet count was investigated in 25 hypertensive and 7 normal subjects. High plasma fibrinogen levels were present in 80% of the hypertensive patients and prolonged lysis time in 28%; the means values were 487 +/- 135 mg % and 223 +/- 62 min., respectively. The other coagulation tests were normal. 0,300-0,450 mg/day clonidine per os for 15 days both decreased fibginogen levels (mean 406 +/- 149; p less than 0.05) and shortened lysis time (mean 153 +/- 78 min; p less than 0.005). No changes were noted in the normal subjects. The pathophysiological mechanism of these findings is discussed and their possible implications for the treatment of hypertension are emphasised.

Blood Coagulation↗