Amiodarone may induce hyper- or hypothyroidism. Patients with beta-Thalassemia Major (beta-Thal) have an increased prevalence of primary hypothyroidism and often require amiodarone for hemosyderotic cardiomyopathy. Aim of this study was to retrospectively evaluate thyroid function in beta-Thal adult patients on long-term amiodarone. The study group consisted of twenty-two (21 males, 1 female; age: 23-36 yr) beta-Thal patients submitted to long-term (3-48 months) amiodarone therapy from January 1991 to July 1996. Controls included 73 beta-Thal patients (23 males and 50 females aged 25-35 yr) not treated with amiodarone. In all cases serum free thyroid hormones, thyrotropin and thyroid autoantibodies were evaluated. A higher prevalence of overt hypothyroidism (5/22 [22.7%]) as compared to controls (3/73 [4.1%], p=0.02) was found in beta-Thal patients < or = 3 months after starting amiodarone, while the prevalence of subclinical hypothyroidism was similar in amiodarone-treated (18.2%) and untreated (15%) beta-Thal patients. Overt hypothyroidism resolved spontaneously after amiodarone withdrawal in 1 case, while the remaining patients were maintained euthyroid on amiodarone by L-thyroxine administration. After 21-47 months of amiodarone therapy, 3 patients (13.6%) developed thyrotoxicosis (2 overt and 1 subclinical), which remitted shortly after amiodarone withdrawal. No case of hyperthyroidism was observed in beta-Thal controls (p=0.012 vs amiodarone-treated patients). In conclusion, amiodarone administration is often associated in adult beta-Thal patients to a rapid progression of the pre-existing subclinical hypothyroidism, but transient thyrotoxicosis may also be observed after a longer period of therapy. These findings should be carefully considered in the management of these patients.
A rare case of amiodarone-iodine-induced thyrotoxicosis (AIIT) associated with nonthyroidal illness is reported. Serum total thyroxine (TT4) and free T4 (FT4) concentrations were elevated and serum TSH was undetectable as frequently observed also in euthyroid amiodarone-treated patients. At variance with common forms of AIIT, serum total triiodothyronine (TT3) was reduced due to low-T3 syndrome. The laboratory diagnosis was made on the basis of elevated free T3 (FT3) levels. Thus, in patients with severe nonthyroidal illness submitted to chronic amiodarone treatment, thyroid status can only be determined by free hormone measurement, particularly FT3 in the case of thyrotoxicosis.
theless, other factors, particularly the adrenergic system, may contribute to myocardial hypertrophy rr), 1. Fifteen patients with essential hypertension, class 1, 11 WHO, nine males and six females, whose mean age was 46 were given atenolol, 100 mg a day, for 1 year.2. After 1 month, compared with control, systolic and diastolic blood pressures, heart rate and cardiac Output were whereas left ventricular end-diastolic dimension and stroke volume were increased and total vascular resistances, wall stress, left ventricular mass and hldialL$he reversibility of hypernnsive left ventricular hypertrophy with treatment is controversial and the influence of the various antihypertensive drugs is still doubtful.The aim of this study was to investigate the influence of atenolol, a selective Badrenergic blocking agent, on hypertensive left ventricular hypertrophy.stolic radius (R) ratio were unchanged.3. After 1 year, compared with control, systolic Methods and diastolic-blood pressures, heart rate and cardiac output were still reduced, total vascular resistance and wall stress were unchanged. Enddiastolic dimension and stroke volume reverted to previous values; left ventricular mass and h/R ratio were significantly decreased. 4. These results show that leR ventricular hypertrophy in essential hypertension can revert after 1 year of treatment with atenolol, at least in relatively young people. Since the left ventricle wall stress was not changed after atenolol, the regression of left ventricle hypertrophy seems prevalently to be related to the decrease of adrenergic activity of the heart. Fifteen patients (nine males and six females), of mean age 46 f. SD 9 years, with essential arterial hypertension, class I, I1 WHO, lasting for 4 f 3.9 (0-12) years were investigated after informed consent.After 15 days of placebo, they received 100 mg of atenolol, once a day, for at least 1 year.Patients were examined at the end of a period of placebo (control) and after 1,2,3,6,9 and 12 months of atenolol treatment. Blood pressure was evaluated by sphygmomanometer measurements and heart rate by the electrocardiogram, after 10 min in a supine position and after 3 min standing. An M-mode echocardiogram was recorded after placebo and after 1 and-12 months of treatment. An Organon Teknika ultrasound unit with transducer of 2-25 MHz, 0 12 mm, focused at 7.5
Chryseomonas luteola is a gram-negative microorganism that has rarely been reported as a human bacterial pathogen. Few cases are described in the literature and these mostly involve patients with health or indwelling disorders. Clinical infections in reported cases showed septicaemia, meningitis, peritonitis, endocarditis and ulcer infections. In the present paper, we describe a clinical case with neonatal onset recently observed in our ward and a review of the literature.
We conducted a 4-yr prospective trial to evaluate the long-term effects of combined deferiprone (DFP)/deferoxamine (DFO) on reversal of cardiac complications in thalassemia major compared to those of DFO alone. Twenty-eight patients (pts) with cardiac disease requiring medication were stratified according to their risk for cardiac death. Fourteen pts were high risk, serum ferritin (SF) > 2500 ug/L on two-thirds of occasions since the onset of cardiac disease. Of those with a SF < 2500 ug/L (low risk), six had progressive decrements of left ventricular ejection fraction (LVEF). Nine high-risk pts and six low-risk pts were placed on DFP/DFO (DFP, 75 mg/kg/d divided t.i.d.; DFO, 40 – 50 mg/kg over 8 – 12 h at night 5 – 7 d/wk. The others infused DFO alone. If SF fell below 500 ug/L, DFO infusions were reduced to 2 d/wk. Cardiac follow-up (including blood work and ECG) was done at 4-m intervals. M-mode and two-dimensional echocardiograms were done at 4- to 6-m intervals. Cardiac T2* was not available at the beginning of the study. All but eight patients (3 death, 1 refusal, 2 claustrophobic, 2 pacemaker) subsequently had at least one T2* assessment. Routine lab tests were done at 1- to 6-m intervals. Blood counts were done at 7- to 10-d intervals for those taking DFP. Mean follow-up was approximately 40 m. Compliance with DFO was significantly better among low-risk pts in both treatment groups (DFP/DFO, 82% vs 61%; DFO alone, 83% vs 52%) as was that with DFP (94% vs 76%). At baseline, no statistically significant differences were observed between the SF levels, LVEFs or left ventricular shortening fractions (LVSFs) of pts on DFP/DFO or DFO alone in either risk group except for the LVEFs of the low-risk group (DFP/DFO, 56.5% +/− 5.5%; DFO alone, 65.4% +/− 5.0%; p = 0.032). In the high-risk group, four cardiac events (3 deaths, 1 worsening of CHF) occurred in the group getting DFO alone vs none in the DFP/DFO-treated group. The latter pts showed a decrease in SF and an increase in both LVEF and LVSF at the end of study (EOS). The three pts who died (at 17 to 35 m) had increased SFs. These pts were not rescued by IV DFO (98 +/− 12 mg/kg/d). The two DFO-treated pts who survived had marginally improved T2*s (1.5 to 3.0 ms and 7.6 to 8.8 ms) over the year prior to EOS. Only one of the seven evaluable pts on DFP/DFO had a T2* < 10 ms, the others averaging 19.4 +/− 6.7 ms. Among the low-risk pts, those on DFP/DFO showed a reduction in SF and an improvement in both LVEF and LVSF. Those on DFO alone had increased SF but essentially no change in LVEFs or LVSFs. Five pts on DFP/DFO had T2* evaluations. In two pts, T2* rose from 9.0 to 37 ms (38 m) and from 9.3 to 11.8 ms (17 m). The remaining three had T2* values > 20 ms at EOS. Similar results were seen in low-risk pts on DFO alone. These finding clearly support the notion that DFP/DFO has a beneficial effect upon the heart, even in well established disease. Moreover, our finding of low T2* values associated with low SF levels indicates the importance of tailoring treatment to each individual.
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