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In 12 patients with arterial hypertension (stages I and II according to WHO), adrenergic stimulation was induced by the immersion of a hand in ice water for 2 min. Blood samples were withdrawn before, at the end of, and 15 min after the cold application: the experiment was repeated 2 h after the ingestion of 200 mg acebutolol, a selective betablocking agent. The following assays were performed: serum nonesterified fatty acid (NEFA), plasma beta-thromboglobulin (BTG) and PF4 with specific radioimmunoassays; thromboxane B (TXB) in plasma was also estimated with radioimmunoassay, platelet sensitivity to exogenous prostacyclin; furthermore, the thrombin-induced thromboxane production before and after acebutolol ingestion as well as serum TXB-levels were measured. The blood pressure and the heart rate were also monitored. After cold stimulation, a significant increase of NEFA, BTG, and plasma TXB was observed, which was still discernible 15 min after the application of cold. After acebutolol, the cold treatment led to a lower increase of blood pressure with a reduction of the heart rate, as well as to a diminished release of BTG, PF4 and TXB no changes in the reduced platelet sensitivity to prostacyclin were noticed. [ABSTRACT FROM PUBLISHER]

Relapses of hyperthyroidism after treatment with radioiodine for uni- or multi-nodular goiter may be accompanied by the appearance of TSAb. However, this phenomenon has only emerged from one retrospective study on Northern European patients, in which it was not possible to determine whether TSAb also appeared in treated patients who did not relapse. The present study aimed to assess the appearance, immunogenic nature and clinical characteristics of hyperthyroidism relapse after treatment with 131I for nodular toxic goiter in patients from the Mediterranean area. A retrospective study was performed on 76 consecutive patients, born and resident in Sicily and aged 56-80 yr at diagnosis, who were treated with radioiodine. Serum aliquots obtained from the patients before 131I treatment and during a follow-up of 36-144 months were assayed for TSAb and TPOAb. The clinical charts of the patients were also re-examined. Twenty-six out of 76 patients (36.8%) had a hyperthyroidism relapse after a first treatment with 131I. Eight of the 26 (30.7%) also relapsed after the second treatment. Three out of 26 (11.5%) relapsed after a third treatment. The 50 patients who required only one treatment and the 18 who relapsed only once were all TSAb-negative at baseline, while 3/8 (37.5%) who relapsed also after the second treatment were already TSAb-positive at baseline. TSAb became positive in 3/18 patients (16.7%) who relapsed once, and in 4/8 (50.0%) of those who relapsed after a second treatment. One of these 7 TSAb-positive relapsers was also already TPOAb-positive at baseline and another became TPOAb-positive after treatment. The presence of circulating TSAb in 3/76 (3.9%) patients before treatment for toxic goiter more probably points to a diagnosis of Marine-Lenhart's syndrome. In contrast, the de novo appearance of TSAb in the presence of hyperthyroidism relapse in 4/76 (5.3%) patients suggests the development of a Graves'-like disease after radioiodine treatment. This occurrence does not seem to have precise ethnic grounds, since the incidence we observed in Mediterranean patients was similar to that previously reported in Northern European patients.

Objectives: This study aimed at investigating the respective impacts of virus-related chronic hepatitis (CH) and liver cirrhosis (LC) on glycemic homeostasis, with reference to grading and/or staging of liver disease and to contribution of the two main responsible viruses., Material and Methods: The glycometabolic features of 82 patients with CH (B-related 16, and C-related 66) and 145 with LC (B-related 24, and C-related 121) were evaluated., Results: Impaired glucose tolerance (IGT) was detected in 9 (11.0%) and diabetes mellitus (DM) in 6 (7.3%) of the CH patients [(P<0.05 vs controls, in both cases; respective odds ratios (95% CI): 2.6 (1.1-6.3), and 4.0 (1.2-13.2)]. IGT was detected in 86 (59.3%) and DM in 34 (23.4%) of the LC patients [(P=0.000 vs controls, in both cases; respective odds ratios: 10.0 (7.0-14.4), and 5.5 (3.5-8.5)]. The odds ratios for the prevalence of IGT and DM in the LC patients were 11.8 (5.2-27.5) and 3.9 (1.5-10.8), compared with the CH patients. In the CH patients, glycometabolic failure was significantly related to age (P=0.026), but not to grading and staging, and in the LC patients to Pugh-Child score (P=0.037). IGT was found in 17/40 (42.5%) HBV-related patients and in 13/40 (32.5) matched HCV-related patients. DM was found in 9/40 (22.5%) HBV-related patients and in 10/40 (25.0%) HCV-related matched patients, without significant difference in the respective proportions., Conclusion: The prevalence of DM associated to virus-related CH is on average four times higher than in the general population, independently of the histopathological picture of disease. Virus-related LC further increases the prevalence of both IGT and DM, independently of sex and age, but in relationship with the severity of disease. HBV and HCV infections do not appear to have a different impact on glycemic homeostasis.

Thyroid function and presence of thyroid autoantibodies were assessed in a group of 75 consecutive female patients with mood disturbances and in a group of 38 healthy women of similar age recruited as controls. Nine patients suffered from major (endogenous) depression and 66 from minor (neurotic) depression. The individual patients had normal values of circulating thyroid hormones. Nevertheless, endogenously depressed patients had total serum triiodothyronine (M +/- SE = 1.49 +/- 0.09 nmol/l) and both total (83.9 +/- 4.3 nmol/l) and free serum thyroxine (13.9 +/- 1.1 pmol/l) lower than in the group of minor depressed and in the group of controls (p < 0.01, in both comparison). The median value of serum thyrotropin was 5.22 mU/l in the major depressed patients versus 1.72 mU/l in the minor depressed and 1.69 mU/l in the controls. Thyroid function test results in the minor depressed group did not significantly differ from those in the controls. Five of the 9 endogenously depressed patients were subclinically hypothyroid, while none of the 66 patients with minor depressive disorder showed thyroid dysfunction. Antibodies against thyroglobulin and/or thyroid peroxidase were positive in all the 5 endogenously depressed women with subclinical hypothyroidism, revealing a symptomless autoimmune thyroiditis, which was also confirmed by ultrasonography in all cases and histopathologically demonstrated in one case. None of the endogenously depressed women without thyroid dysfunction and none of the 66 minor depressives were seropositive for thyroid autoantibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l. The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay from midnight (0 degrees) of the highest level in the rhythm) was -9.9 degrees. In contrast, severely ill patients showed only slight and anticipated elevations of serum TSH levels (mesor 0.93 mU/l, amplitude 0.22 mU/l, acrophase +82.4 degrees). Moreover, whereas the episodic TSH secretion in healthy individuals consisted of 5-8 pulses/24 h, mainly clustered around midnight, only one pulse of reduced amplitude was detected in two of the eight severely ill patients and no pulses in the other six. Since earlier studies have indicated that the loss of TSH pulsatility is associated with the relative insensitivity of the thyrotrophs to low thyroid hormone levels and our analytical procedures have demonstrated that 24 h pulsatile pattern of TSH closely overlapped with baseline TSH secretion, it seems reasonable to assume that low-thyroid-hormone state, deficient pulsatile TSH secretion and altered nyctohemeral TSH periodicity do not coincide by chance, but that there is a causal relationship between such abnormalities in severely ill patients.

Indobufen is a reversible inhibitor of platelet prostaglandin G/H-synthase. To verify the dose dependence of the antiplatelet effect of indobufen on ex vivo and in vivo indexes of thromboxane (TX) biosynthesis and TXA2-dependent platelet function, we studied nine patients with non-insulin-dependent diabetes mellitus (NIDDM). This was a randomized, double-blind, crossover study in which each patient was treated with three different daily regimens (50 mg BID, 100 mg BID, and 200 mg BID) of indobufen for 1 week, with a 7-day washout period between treatments. Urinary 11-dehydro-TXB2 excretion averaged 58.2 +/- 21.8 ng/h at baseline. TX metabolite excretion was reduced dose dependently by indobufen: by 67% at 50 mg BID, 72% at 100 mg BID, and 81% at 200 mg BID. Platelet cyclooxygenase activity, ATP release, collagen-induced platelet aggregation, and bleeding time also were modified dose dependently by indobufen. Biochemical demonstration of suppressed platelet TXA2 in vivo was accompanied by evidence of inhibited platelet function as assessed ex vivo. Under pathophysiological conditions, such as NIDDM, which are associated with enhanced TXA2 synthesis, more than 95% suppression of platelet cyclooxygenase activity may be necessary to produce virtually maximal inhibition of platelet TXA2 biosynthesis in vivo.

To evaluate the 24-h pattern of serum thyrotropin (TSH) in critically ill patients, we measured serum concentrations of TSH in blood samples collected every 2 h for 24 h from nine patients (six with malignancy, two with liver cirrhosis, one with chronic renal failure), who had subnormal levels of both triiodothyronine (T3) and thyroxine (T4), in the absence of history, symptoms or signs of thyroid disease. Analysis of the data, performed using a second-order inferential statistical methodology for rhythmometry (cosinor method), demonstrated that critically ill patients still had daily oscillations of serum TSH which significantly adapted to the function approximating the circadian rhythms (R2 = 74.3%). However, the mean level (mesor) in the rhythm of the patients was found to be significantly lower than that of healthy subjects (0.96 vs 2.18 mU/l); the amplitude of rhythmical daily variations also was lower in patients than in healthy subjects (0.23 vs 0.56 mU/l), even though the amplitude/mesor ratio was similar (23% vs 26%). Lastly, the highest level in the TSH rhythm of the patients was found to be in the late afternoon, in contrast to healthy subjects, who had a TSH surge after midnight. Although these alterations are consistent with the existence of a dysregulation at suprahypophyseal level in critically ill patients, it remains to be established whether the state of low T3 and T4 may be ascribed to anomalous circadian rhythm of TSH.

Patients with severe non-thyroidal illness (NTI) often evidence concomitant anomalies in thyroid function (TF). In order to shed light on the implications of these anomalies and/or changes and disease course, we monitored TF changes in a selected cohort of 45 patients with serious NTI (21 with liver cirrhosis, 15 with renal failure and 9 with malignancy) from April 1985 to October 1989. TF test results on admission were as follows: all patients had normal thyroid stimulating hormone (TSH) levels; 16 patients had no TF abnormalities; 28 had decreased serum triiodothyronine (T3) and increased serum reverse triiodothyronine (rT3) levels, (8 of them had low serum free T3 values as well); 1 patient had subnormal level of both T3 and thyroxine (T4). Fifteen (53.5%) of the 28 subjects with initial low T3 sustained a subsequent decline in total and free serum T4 to subnormal levels; in 13 of these patients the drop occurred shortly before death. Patients in critical condition with below normal serum T4 also had decreased serum TSH concentrations: the so-called "low T3 and low T4 syndrome" might thus result from decreased TSH concentrations: due to failure of the usual feedback mechanism. Eighteen patients (40%) had died by the end of the study period. The mortality rate was 89% in patients with initial T3 level less than 0.40 nmol/L. This finding leads us to the hypothesis that initial low T3 levels in NTI patients are indicative of a poor prognosis.

The effects of a TRH-T (protireline tartrate) treatment at a dose of 2 mg/day for 3 weeks on the serum levels of the pituitary-thyroid axis hormones, have been studied in a randomized group of 10 elderly euthyroid hospitalized patients with cerebrovascular disease. At the end of the treatment an 8.3% mean increase of serum T3 level and a 12.5% mean increase of serum FT3 level (p less than 0.02 in both cases) have been observed. At the same time a 34% mean decrease of the basal TSH (p less than 0.05) and a 26% mean decrease of the delta-TSH after TRH-test (p less than 0.025) have been noted. However, the hormone concentrations changes never exceeded the normal values. In a randomized group of 9 hospitalized untreated patients with cerebrovascular disease used as controls (matched for age and sex), no significant changes of studied hormones have been recorded. In the treated patients, one week after the withdrawal of therapy serum levels of thyroid hormones and TSH went back to the levels observed before treatment. TRH-T seems to cause these modest hormone changes by decreasing the number of TRH receptors and the activity of TSH secreting cells. Nevertheless, the presence of the normal feedback in the pituitary-thyroid axis, allows a good tolerance to such a treatment.

Thyroid hormone picture of 28 patients (15 males and 13 females), mean age 56.6 yr (range 45-65 yr), with seriously decompensated type II diabetes mellitus has been studied. In each patient the study was repeated after 3 months of treatment of diabetes. The patients showed significantly lower serum T3 levels and significantly higher serum rT3 levels (P less than 0.001), in comparison with a group of 16 normoglicemic subjects. After 3 months of strict control of diabetes T3 and FT3 significantly increased (P less than 0.01), whereas significant variations of rT3 were not found. Among the whole group of diabetics 5 patients had low levels of serum T4 (P less than 0.01 vs. controls), high levels of serum TSH (P less than 0.001 vs. controls) and an exaggerated responsiveness to exogenous TRH (P less than 0.001 vs. controls). After the 3 months of treatment these patients showed a significant decrease of rT3 (P less than 0.02) and of delta-TSH (P less than 0.01). In the whole group of diabetics significant statistical correlations between glycometabolic and thyroid parameters were not found. The study, on the whole, showed in patients with seriously decompensated type II diabetes, a hormone picture like the low-T3 syndrome, in some cases, however, pituitary TSH secretion suggested the existence of incipient failure of thyroid hormones. A connection between alterations in thyroid hormone picture and glycometabolic imbalance, even statistically labile, is however indicated by improvement of thyroid function when diabetes is carefully controlled.

This work was performed in order to analyze thyroid hormone picture of alcoholic patients with reference to hepatic damage. Forty consecutive patients of male sex, aged 28-64 years, were investigated. They consumed more of 50 g ethanol/day for at least 2 years. According to investigations on hepatic condition, 2 cases had normal liver, 22 cases had steatosis and 16 had cirrhosis. None of patients disclosed a clinical and/or hormonal behaviour pointing to alterations of thyroid function. In alcoholics serum T3 levels resulted significantly lower compared to a control group of 40 healthy males (P less than 0.001), independently of degree of hepatic damage. Instead, serum T4 levels did not result significantly different in the comparison between alcoholics and controls. Serum FT3 and FT4 levels resulted significantly higher (P less than 0.001) only in alcoholics with liver cirrhosis. In comparison with normals, serum rT3 was significantly lower in alcoholics without liver cirrhosis (P less than 0.001), but significantly higher in alcoholics with liver cirrhosis (P less than 0.005). Serum TBG behaved in the same manner. According to euthyroidism in our alcoholic patients basal and TRH-stimulated TSH were normal, however significantly lower when compared to controls (P less than 0.005). On the whole these results suggest the existence of an autonomous ethanol-dependent mechanism that determine decreased serum T3 levels in the alcoholics, in absence of serum T4 variations. In the alcoholic with liver cirrhosis, an increased conversion of T4 in rT3, correlated to hepatic damage, joins to previous mechanism. The tendency to low secretion of pituitary TSH might be dependent of action of alcohol on neuromodulation of TRH secretion.

In order to investigate the nature of impaired glucose tolerance (IGT) in 3 young patients with Graves' disease we have studied their insulin secretion fasting and in response to oral glucose by means of measurement of serum C-peptide. Fasting levels of serum C-peptide of these patients were beyond the range of 15 age-matched normal subjects; the C-peptide/glucose ratio was also significantly higher (p less than 0.001) in the patients than in the controls. Following glucose ingestion serum levels of C-peptide resulted high in the range of normals, with a mean C-peptide/glucose ratio greater than in the controls, but without reaching of statistical significance. To investigate whether the anomaly in fasting insulin secretion of these patients had any correlation with their hyperthyroidism, afterwards we surveyed fasting concentrations of serum C-peptide in parallel with progressive variations of serum free thyroxine and triiodothyronine (FT4 and FT3) and thyrotrophin (TSH) during antithyrotoxic treatment with methimazole. The data of 23 tests on serum FT3 and FT4 levels, carried out during 16-18 months, resulted in significant correlation with contemporaneous measurements of fasting serum C-peptide (p less than 0.001). No significant correlation was found between serum TSH and fasting C-peptide levels. The results suggest that IGT of the patients in this study is not dependent on lacking insulin secretion, but on mild insulin resistance. Such glucose metabolic anomaly appears to be in clear correlation with the degree of hyperthyroidism, even if its pathogenesis remains to be further investigated.

We have attempted to determine if mild hyperglucagonemia induced by exogenous glucagon infusion induces changes of serum thyroid hormone levels. Eleven healthy subjects, overnight fasting, received glucagon infusion (2 mg/90 min i.v.), whereas 5 healthy subjects (control group) received normal saline infusion. In the subjects infused with exogenous glucagon plasma glucagon concentrations increased from 130 +/- 24 pg/ml to 550 +/- 68 pg/ml at the end of infusion. At the same time no significant changes in serum T3, rT3 and T4 levels were found. A significant increase in serum rT3 levels was found 270 min after glucagon infusion withdrawal, whereas serum T4 levels remained unaltered during the whole period. Normal saline infusion failed to induce any variation in control group, however a late (at 6th hour) mild increase of serum rT3 in these subjects resulted comparable to the same increase of glucagon infused subjects. The results from this study suggest that mild increase in plasma glucagonemia, as found in patients with severe illness, does not induce a short-time significant lowering of serum T3 and a simultaneous rise of serum rT3 in normal subjects.

Several studies have demonstrated that a consistent part of patients with severe depression shows anomalous responses of neuroendocrine axes. In the last years, altered TSH responsiveness to exogenous TRH have been reported also in patients with panic disorders. Because of these suggestions we studied stimulated TSH secretion in 24 untreated hospitalized patients (8 males and 16 females), aged from 21 to 76, in whom the psychiatric examination disclosed mild but inequivocal signs of persistent depression (score range on Rufin and Ferreri Iventory from 20 to 35). The TRH-test (200 mcg i.v.) was started between 9.00 and 9.30 a.m.. The same test was performed also in 14 sex- and age-matched volunteers defined without psychiatric disorders. As comparison parameter, delta-TSH (maximum increase during TRH stimulation) was accounted. All the patients had normal serum thyroid hormone levels. TSH responsiveness of patients with minor depressive disorders was not found statistically different when compared with normal control volunteers, but a reverse significant correlation was found between delta-TSH and percentage score of anxiety in group of patients (with blunted TSH response in 6 (25%) patients), that was not found in normal subjects. A significant correlation between delta-TSH and depression degree was not found. The present data, although preliminary, could indicate the existence of depressed subjects in whom blunted TSH response to TRH seems related to anxiety degree. Additional studies, particularly on the medullo-adrenal function, might clarify the nature of these alterations, that at state is unclear, although the mechanisms suggested also for alterations of pituitary hormone responses in major depression could be taken in account.

The aim of the present investigation was to study the clearance of 99mTc-p-butyl IDA in some acute and chronic liver diseases, it being considered that the typical parameters obtained with this method are as indicative as any of the others put forward for the study of liver function using radioisotopes. 46 subjects were examined: 6 with acute hepatitis, 10 with chronic hepatitis, 18 with liver cirrhosis and 12 with dyspepsia but otherwise normal haematochemical tests. Two basic 99mTc-p-butyl IDA clearance parameters, Tu (semi-take up time) and Te (semi-excretion time), were determined plotting the data obtained using a Gamma-Camera on semi-logarithmic paper. Mean Tu values were as follows: 5'06'' +/- 1'24'' in dyspeptics, 12'30'' +/- 6'31'' in subjects with acute hepatitis, 6'30'' +/- 1'45'' in subjects with chronic hepatitis and 13'30'' +/- 4'30'' in subjects with cirrhosis. The values were: 34'30'' +/- 4'30'' in dyspeptics, 49'54'' +/- 2'36'' in subjects with acute hepatitis, 42'24'' +/- 12'24'' in subjects with chronic hepatitis and 65'30'' +/- 39'36'' in subjects with cirrhosis. The Tu parameter was found to be delayed more significantly in cirrhotic patients and less in subjects with acute or chronic hepatitis, compared to dyspeptics with normal haematochemical parameters. Te was significantly delayed in subjects with cirrhosis and acute hepatitis, while there was no difference for subjects with chronic hepatitis. Of the routine haematochemical tests, the albumin/gamma-globulin ratio and unconjugated bilirubin were found to correlate significantly with the Tu parameter, whereas conjugated bilirubin was found to bear a significant correlation to the Te parameter.

The aim of this study was to evaluate the in vitro effects of verapamil on platelet aggregation and serum thromboxane formation. We also studied the in vivo effects of verapamil retard on platelet aggregation and serum thromboxane formation. The incubation of verapamil with PRP produced a dose-dependent decrease of in vitro platelet aggregation for all the agents used. Potentiation by verapamil of antiaggregating activity of prostacyclin was also demonstrated; in fact when verapamil and prostacyclin were added simultaneously a synergistic inhibition of platelet aggregation by ADP was observed. In whole blood verapamil partially inhibited thromboxane production only at a higher concentration. In vivo verapamil significantly decreased platelet aggregation induced by ADP and epinephrine while no changes were observed after arachidonic acid. No significant changes occurred in serum TXB2 levels. The observations suggest a potential role for verapamil in antithrombotic therapy as an antiplatelet agent.

Present study was carried out in order to control if glucose tolerance and insulin secretion changed during nicardipine treatment in healthy or in non-insulin dependent diabetics. In the 8th day of therapy with nicardipine (40 mg/day), glucose tolerance and insulin secretion were unmodified in a group of 20 non-diabetic patients. At the same time glucose tolerance was found improved in the group of 14 non-insulin dependent diabetic without a contemporary variation of insulin secretion. Such a result, note-worthy for a drug frequently administered to diabetics, could be due to inhibited glucagon secretion, or to increased glucose uptake by hepatocytes.

Hormonal and clinical data on 38 tests performed in 7 hypothyroid patients given substitutive treatment with L-thyroxin were analysed. The aim of the survey was to assess the dependability of the various parameters used to estimate dose adequacy in substitutive treatment. Examination of individual cases revealed that overdoses of thyroxin increased T4 to above normal limits without increases in T3, FT3, FT4 or hypophyseal suppression. Chronological discrepancies between clinical data and normal parameters were also noted. However on the data as a whole significant correlations were noted between T4 and TSH (p less than 0.001), between T4 and delta-TSH (p less than 0.001), between T3 and TSH p less than 0.01), between FT3 and delta-TSH (p less than 0.01), between FT4 and delta-TSH (p less than 0.01). FT4 and delta-TSH were also significantly correlated (p less than 0.02) with the Billewicz clinical index of hypothyroidism. It is concluded that the clinical and hormonal data in treated hypothyroid cases have the same significance as in normal or untreated hypothyroid cases. However, it must be borne in mind that unusual relations between the various thyroid hormone fractions including TSH and the standardised clinical examination may arise while doses are being established. In this case the data cannot be automatically interpreted but merely carefully assessed in the light of experience.

In healthy subjects intravenous glucagon administration induces a prompt (at 1 h) fall in serum T3 concentration and a later (at 4 h) rise in biologically inactive rT3. Since high levels of plasma glucagon have frequently been found in some patients with severe chronic illnesses, together with an anomalous thyroid condition (low serum T3, high serum rT3), it has been supposed that hyperglucagonemia could play a pathogenetic role in causing selective T3 deficiency. In the present study fasting plasma glucagon concentration was measured in 48 patients with low T3 and severe nonthyroidal illnesses: hepatic cirrhosis in 16 cases, chronic non-A non-B hepatitis in 4 cases, uncontrolled type II diabetes mellitus in 5 cases, renal failure in 12 cases, congestive heart failure in 5 cases, tumor in 16 cases. In comparison with a group of 21 healthy controls fasting plasma glucagon concentration was significantly higher in the patients (198.75 +/- 13.20 pg/ml vs. 127 +/- 6.80 pg/ml; p less than 0.001). However, only 29 patients (60.4%) had elevated plasma glucagon levels, whereas 19 (39.5%) had abnormal plasma glucagon levels. Furthermore, no significant difference was found between the thyroid hormone pattern of the patients with hyperglucagonemia and of the patients with normal glucagonemia. On the other hand, a significant correlation between plasma glucagon concentrations and serum T3 and rT3 concentrations was not found. All these findings indicate that in patients with severe chronic illnesses the fall in circulating T3 cannot be due to hyperglucagonemia only which, therefore, might simply be a contributory factor together with other as yet unidentified disorders.

99mTc-p-butyl IDA clearance was measured in three subjects with Gilbert's syndrome at the same time as traditional cholescintigraphy. Cholescintigraphy persistently revealed a delayed liver display together with a normal fast display of the biliary ways. The Tu (semi-uptake time) of 99mTc-p-butyl IDA was higher in all three cases than in normal subjects, whereas Te (semisecretion time) was normal in all cases. The typical liver function profile provided by the association of cholescintigraphy and 99mTc-p-butyl IDA hepatocyte clearance renders the examination, which is both simple and free of side-effects, extremely useful in the clinical identification of subjects with suspected Gilbert's syndrome.

In insulin-dependent diabetes mellitus (IDDM) several organ-specific autoantibodies are found in addition to pancreatic islet cell autoantibodies. In the present study we researched the presence of thyroid microsomal antibodies (anti-TMS) in 33 young patients with IDDM and evaluated contemporaneously their thyroid function. 5 patients (15.4%) are found with significant levels of circulating anti-TMS, among them 4 (12.1%) were also subclinical hypothyroid. However 6 other patients are found with mildly altered thyroid hormone pattern in absence of circulating anti-TMS. Basal and TRH-stimulated TSH were significantly higher, whereas serum FT4 was significantly lower, in patients with IDDM and circulating anti-TMS than in patients with IDDM but without anti-TMS. These observations indicate a significant incidence of mild or subclinical hypothyroidism in patients with IDDM and anti-TMS. Thus the screening for anti-TMS is recommended in all patients with IDDM, then thyroid hormone pattern of anti-TMS positive patients must be periodically followed.

The authors evaluated the existence of serum thyroid microsomal antibodies (anti-TMS) and their correlation, if any, with thyroid function in a group of 120 consecutive patients, who seemed clinically worthy to be studied from that point of view, even if they were lacking of a previous laboratory framing. Present study shows a consistent prevalence (81.8%) of anti-TMS concentrations were not related with any hormone parameter of thyroid function. Instead, the prevalence of anti-TMS positive subjects get to 69% in the 39 over-65 aged patients (32 women) of survey, with a concordance between high anti-TMS concentration and hypothyroidism of 87.5% in the subgroup. In these elderly patients circulating anti-TMS and serum TSH were found directly correlated (p less than 0.001), whereas serum FT4 was found in inverse correlation with the same antibodies (p less than 0.01). The consistent share of hypothyroid-aging patients, although mild or subclinical but clearly related with immunological phenomena, cannot be overlooked.

The aim of the present study was to determine whether the temporary variations in blood thyroid hormone levels secondary to a therapeutic dose administration of L-thyroxine observed in adequately treated hypothyroid patients also occur in spontaneously euthyroid subjects under analogous conditions. Serum levels of T3, T4, FT3, FT4 and TSH were measured over 6 hours following a single oral administration of L-thyroxine (dosage 85 mcg/mq body surface area) in a group of 18 euthyroid volunteers and 8 hypothyroid patients adequately compensated with replacement therapy. In the euthyroid subjects there was a significant increase in T4 and a significant fall in TSH values at 60', while a significant decrease in FT3 and FT4 as compared to initial values was observed at 120'. In the treated hypothyroid patients serum T3 and T4 increased at 120', while FT4 concentrations, already significantly higher at 120', still remained higher than initial levels at 360'. The different behaviour of the hypothyroid patients, in spite of being compensated with therapeutic doses of L-thyroxine, reflects the persistence of a thyroid-metabolic condition substantially different to the physiological feature, which appears to be realized by means of a reduced iodothyronine clearance and a lower sensitivity in TSH feedback.