Our data suggest that acute DMSA scintigraphy has limited overall ability in identifying VUR and should not be endorsed as replacement for voiding cystourethrography in the evaluation of young children with a first febrile UTI.

We investigated erythropoietin (Epo) response in a cohort of diabetic patients with various types of anemia to approach the pathogenesis of some cases of "unexplained" anemia encountered among diabetics. Serum Epo levels were determined totally in 747 evaluable subjects with normal renal and hepatic function, of whom 694 had anemia. Among anemic patients, 237 were diabetics, while among the 53 nonanemic persons, there were also 21 diabetics. Diabetic and nondiabetic subjects were uniformly balanced in relation to their demographic features and were categorized according to the etiology of their anemia. Hemoglobin (Hb) did not differ between diabetic and nondiabetic subjects in all the etiological groups and in the whole population. Diabetic patients had significantly lower serum Epo levels as compared to nondiabetics (36.5+/-61 vs 69.4+/-191 IU/ml, p<0.0001), and this was true for all etiologic groups of anemia with the exception of patients with myeloproliferative disorders and those with megaloblastic anemia. The natural logarithmic (ln)-EpoxHb component was used as an index of response to anemia and was found to be significantly decreased in almost all subgroups of diabetic patients. Serum Epo levels were also negatively correlated with the percentage of glycosylated Hb, HbA1(C) (r=-0.446), and the correlation was stronger with the ln of serum Epo (r=-0.638, p<0.001). Inappropriately low serum Epo level is a uniform feature in patients with type II diabetes mellitus and may represent a constitutive blunted response to anemia or an altered metabolic rate of Epo, probably as a result of abnormal glycosylation of the cytokine.

Parathyroid scintigraphy and high-resolution ultrasonography are frequently used as preoperative localization procedures in primary hyperparathyroidism. However, when thyroid disease coexists, their diagnostic accuracy is probably abated. DESIGN: 56 patients with primary hyperparathyroidism were prospectively evaluated with parathyroid scintigraphy (with either thallium or technetium-99m agents or both) and 44 of them were also evaluated with ultrasonography. RESULTS: 33 patients (59%) had coexistent thyroid disease. Upon operation, 48 patients were found to have a solitary parathyroid adenoma and were all cured. One patient had a carcinoma and 7 had multiglandular parathyroid disease. Regarding solitary lesions, the sensitivity of parathyroid scintigraphy with Tc-agents was 97% and thallium 78%, while that of ultrasonography was 74%. The false positive rate was 2.6%, 18% and 22%, respectively. Concomitant thyroid disease had a non-significant effect on the results of parathyroid scintigraphy and ultrasonography. The efficiency of both modalities in diagnosing multiglandular disease was low (only 3/7 patients, 43%). CONCLUSIONS: Parathyroid scintigraphy, in conjunction with Sestamibi or Tetrofosmin, constitutes the most sensitive localizing technique as regards solitary lesions. Ultrasonography is also useful in confirming scintigraphic findings, offers more precise anatomic information, and is valuable in the evaluation of concomitant thyroid disease. The complementary use of parathyroid scintigraphy and ultrasonography is beneficial and efficacious in areas with high prevalence of thyroid disease. The value of these modalities is considerably lower in multiglandular disease.

No abstract

The purposes of this study were to assess the occurrence of euthyroid sick syndrome in patients with acute myocardial infarction (AMI) or unstable angina (UA), and the relationship with beta-blocker or thrombolytic therapy. Plasma triiodothyronine (T3), reverse T3 (rT3), free T3 (FT3), thyroxine (T4), free T4 (FT4), thyroid-stimulating hormone (TSH), thyroxine-binding globulin (TBG), and albumin (ALB) levels were determined in 95 patients (59 males, 36 females, aged 58.4+/-9) with AMI and 19 patients (13 males, 6 females aged 54.7+/-12.3) with UA for 5 consecutive days from the onset of the acute syndrome and 1 month later. Patients were divided according to beta-blocker therapy and thrombolytic therapy. There was a significant T3 decrease and rT3 increase in all patients during the first 5 days following admission (p < 0.05). FT3 and FT4 remained unchanged during the study. In patients with complicated infarctions, the rT3 increase and the T3 decrease were significantly greater compared to those with uncomplicated infarctions (p<0.03). TSH, T4, TBG, and ALB were significantly (p<0.05) decreased only in complicated infarctions. No differences were observed between patients with or without thrombolysis or patients with or without beta-blocker treatment. The apparent decrease in T3, the increase in rT3 levels and the decreased TSH and T4 levels, show clearly that the euthyroid sick syndrome (low T3) occurs not only in AMI but also in UA. In addition, these hormonal changes are not affected by beta-blocker therapy and thrombolysis does not influence the occurrence of the syndrome. The degree of T3 decrease is proportional to the severity of cardiac damage and may have a possible prognostic value.

Clinical improvement of this patient, correspondent to previous studies, suggests that continuous bilateral GPi DBS may provide a promising treatment option for TD. Furthermore, this report could imply, as no previous such comparison study exists, a possible correlation between brain functional imaging findings and the movement disorder's response to DBS.

OBJECTIVE: The aim of the study was to evaluate the IGF-I generation test (IGF-I gen) as a possible indirect test of Growth Hormone (GH) secretory status. METHODS: Sixty-five GH deficient (GHD 1 and 2) and 86 control children were studied. Children in the GHD-1 subgroup (n=33) had low GH values (<10μg/L) after clonidine and levo-dopa while those in the GHD-2 subgroup (n=32) had normal GH values after pharmacologic provocation but low 24-hour GH secretory rates compared to 187 Normal Statured (NS) children. Of the 86 controls, who underwent IGF-I gen, 50 were NS and 36 Short-Statured (SS). Serum IGF-I was measured prior to and daily during hGH administration (hGH 0.033 mg/kg/day x 4 days). RESULTS: The prepubertal and pubertal GHD-1 and GHD-2 children had low baseline IGF-I values but their peak IGF-I values during the IGF-I gen reached those of the controls. The percent increase of IGF-I during the test was greater in the GHD groups than in the controls; in the prepubertal groups: 516±58% in the GHD-1, 433±50 % in the GHD-2, 106±12 % in the NS, and 102±18 % in the SS (p=0.001); in the pubertal groups: 191±28 % in the GHD-1, 141±20 % in the GHD-2, 48±8 % in the NS, and 61±17 % in the SS (p=0.003). CONCLUSIONS: The IGF-I response during the IGF-I gen seems to reflect the GH status in children.

The absence of a correlation between erythropoietin and birth weight or length and the negative correlations between alpha-fetoprotein and these anthropometric parameters suggest that the intra-uterine growth retardation caused by maternal smoking is not due to tissue hypoxia, but that both growth retardation and elevated alpha-fetoprotein result from the direct or indirect toxic effect of a factor(s) present in tobacco smoke.