Breast cancer and thyroid diseases: analysis of 867 consecutive cases.

INTRODUCTION: The aim of this study was to evaluate the association of breast cancer with thyroid diseases. Many authors have already studied the possible relationship between these two diseases, but the results are nowadays conflicting. MATERIALS AND METHODS: Our study examining 867 patients with breast cancer (862 women and 5 men, average age = 61 years old) of whom 141 also had thyroid disease evaluated the recurrence of thyroid diseases and their association with different types of breast cancer. Statistical analyses were performed using SPSS software for Windows; we used nonparametric tests (Chi-square and Mann-Whitney), and the level of significance was set at p < 0.05. RESULTS: We found a significant association between breast cancer diagnosed after menopause and thyroid disease (p < 0.003). Moreover, we analyzed the role of thyroid autoimmunity identifying an association between chronic autoimmune thyroiditis and breast cancer diagnosed before menopause (p < 0.05). Regarding receptor profile of breast carcinoma, we have found an increased expression of estrogen receptors in patients with autoimmune thyroiditis compared to patients with any other thyroid diseases (p < 0.03). Contrariwise, we do not have found any difference between the group with every thyroid disease and the group without thyroid disease (p < 1.00). We did not find other statistically significant associations with breast cancer's parameters like family history, tumor size, lymph node metastasis, distant metastasis, cancer clinical and pathological stage, differentiation grade and expression of Ki67, p53 and Her2 in the two main groups with or without thyroid disease. Likewise, we did not found other statistically significant association between hypothyroidism or hyperthyroidism and breast cancer.

Longitudinal changes of insulin sensitivity in essential hypertension: influence of blood pressure control and familial predisposition to hypertension.

The aim of this study was to evaluate the influence of blood pressure (BP) control and familial predisposition to hypertension on longitudinal changes in insulin sensitivity in essential hypertension. We evaluated 6 groups of subjects twice (basal: before any treatment; 2nd: after at least 18 months): 42 hypertensives (H) with a family history of hypertension (F+) and 30 H without a family history of hypertension (F-) successfully treated with angiotensin-converting enzyme inhibitors and/or calcium channel blockers (2nd: 24-h BP < or = 130/80 mm Hg); 22 untreated (UT) HF+ and 18 UTHF- (2nd: 24-h BP >140 and/or 90 mm Hg); 18 normotensives F+ and 15 normotensives F-. The parameters evaluated were as follows: glucose, insulin, and C-peptide (Cp) response to an oral glucose load. Glucose was normal in all of the subjects, similar among the 6 groups, and unchanged at the 2nd evaluation. At the basal evaluation insulin and Cp were higher and the metabolic clearance rate (MCR) of glucose was lower in the three F+ groups compared with the corresponding F- groups. In the 2nd evaluation insulin and Cp were reduced and the MCR of glucose increased in THF-, whereas all metabolic parameters were unchanged in THF+; in both UT hypertensive groups insulin and Cp increased and the MCR of glucose decreased, more so in F+ than in F-; in normotensive groups metabolic parameters did not change. A familial predisposition to hypertension influences insulin sensitivity changes during successful antihypertensive therapy, with an improvement in insulin sensitivity in F- and no changes in F+. A persistently high BP has a negative influence on insulin sensitivity in F+ and F-; this influence is greater when high BP is associated with a familial predisposition to hypertension.

Insulin and diastolic dysfunction in lean and obese hypertensives: genetic influence.

We investigated the influence of genetic predisposition to hypertension by studying the relation between insulin sensitivity and left ventricular (LV) mass and function in untreated lean and obese hypertensives. We selected 50 lean hypertensives with normotensive parents (negative family history of hypertension [F-]), 64 lean hypertensives with 1 or both parents hypertensive (positive family history of hypertension [F+]), 40 obese F- hypertensives, and 43 obese F+ hypertensives. The 4 groups were comparable regarding age, gender, 24-hour blood pressure profile, and known duration of hypertension. We measured glucose, insulin, and C-peptide during fasting and during an oral glucose tolerance test; LV morphology and function were assessed by digitized M-mode echocardiography. Glucose (fasting and test) levels were normal in all and similar among the 4 groups. Insulin and C-peptide (fasting and stimulated) levels were higher in obese hypertensives than in lean hypertensives; at similar body mass index, insulin and C-peptide levels were higher in F+ than in F- groups. Compared with lean hypertensives, obese hypertensives had greater LV mass index; LV systolic function was normal in all and similar among the groups. The indices of LV diastolic function were significantly lower in F+ than in F- groups. LV mass index did not correlate with metabolic parameters; the indices of LV diastolic function were inversely correlated with insulin area during test in only the 2 F+ groups. In conclusion, genetic predisposition to hypertension is associated with a reduced insulin sensitivity and affects the response of the myocardium to increased insulin levels, inducing a greater impairment of diastolic function. Insulin sensitivity and genetic predisposition to hypertension seem to have no influence on LV mass.

Insulin sensitivity in obese normotensive adults: influence of family history of hypertension.

OBJECTIVE: To evaluate the influence of family history of hypertension on insulin sensitivity in obese normotensive adults, comparing them with lean subjects. SUBJECTS: 136 normotensives (N)(mean 24 h blood pressure < 130/80 mmHg; age range 35-45 y): 32 lean (body mass index, BMI < or = 25 kg/m2) N with normotensive parents (F-), 37 lean N with one or two parents hypertensive (F+), 32 obese (BMI > or = 30 kg/m2) NF- and, 35 obese NF+. METHODS: 24 h ambulatory blood pressure monitoring; glucose, insulin and C-peptide before and 30, 60, 90 and 120 min after an oral glucose load; index of insulin peripheral activity (Ia: 10(4)/insulin x glucose values at glucose peak); fasting insulin/C-peptide ratio (I/Cp). RESULTS: The four groups were comparable for age, gender and blood pressure values throughout the 24 h. Glucose, fasting and during test, and I/Cp were similar among the four groups; insulin and C-peptide, fasting and stimulated, were significantly higher and Ia lower in obese N than in lean N; at similar BMI, insulin and C-peptide were significantly higher and Ia lower, in F+ than in F-. The correlation between insulin and BMI was significantly closer in F- than in F+. CONCLUSIONS: Family history of hypertension appears to be significantly associated with insulin sensitivity in both lean and obese normotensive adults; moreover, overweight and a genetic predisposition to hypertension may have additive adverse effects on insulin sensitivity in normotensive adult subjects.

Influence of family history of hypertension on insulin sensitivity in lean and obese hypertensive subjects.

We evaluated the influence of family history of hypertension on insulin sensitivity in lean and obese hypertensive subjects (H): 40 lean [body mass index (BMI) < or = 25 kg m-2] H with normotensive parents (F-), 50 lean H with one or two parents hypertensive (F+), 30 obese HF- (BMI > or = 30 kg m-2) and 35 obese HF+. The four groups were comparable in terms of age, sex and ambulatory blood pressure values. We evaluated glucose, insulin and C-peptide before and 30, 60, 90 and 120 min after an oral glucose load, insulin sensitivity index (ISI, fasting glucose/insulin ratio), fasting insulin/C-peptide ratio (I/Cp). Glucose, fasting and during test, and I/Cp were similar among the four groups; insulin and C-peptide, fasting and stimulated, were significantly higher and ISI lower in obese H than in lean H; at similar BMI, insulin and C-peptide were significantly higher in F+ than in F-. Insulin directly correlated with night-time blood pressure only in lean HF-. The correlation between insulin and BMI was significantly closer in F-than in F+. In conclusion, family history of hypertension appears to play a relevant role in insulin sensitivity in hypertensive subjects also in the presence of obesity.

The clinical use of 99m-Tc-labeled WBC scintigraphy in critically ill surgical and trauma patients with occult sepsis.

OBJECTIVE: To evaluate the clinical use of radionuclide-labeled white blood cell scintigraphy in the detection of focal sepsis. DESIGN: Prospective clinical study. SETTING: A medical/surgical 12-bed intensive care unit (ICU) in a university hospital. PATIENTS: 26 trauma and surgical patients affected by sepsis of unknown origin were studied. MEASUREMENTS AND RESULTS: After the usual diagnostic approach, patients were submitted to a total body scan by using the patient's leukocytes labeled with technetium-99m (99m-Tc) HMPAO; three scintigraphy were performed within 20 h of tracer injection; the result of scan was completed with all clinical and instrumental data, including ultrasound (US) arnd computed tomography (CT), and the diagnostic efficacy was demonstrated for each patient on discharge from the ICU. The scan was able to detect 20 sites of infection; it was possible to rule out 11 suspected sites; only in two cases was the result considered to be false positive or false negative; in two cases the result was considered to be uncertain. These results show the high sensitivity (95%), specificity (91%) and accuracy (94%) of the method. CONCLUSIONS: In ICU patients with sepsis, nuclear medicine can provide additional data, as the injection of radionuclide-labeled white blood cells (WBCs) allows the imaging of sites of infection. Analysis of our results suggests that scintigraphy with 99m-Tc-labeled WBCs can be considered a useful tool in the detection of the source of infection.

Hyperinsulinemia, family history of hypertension, and essential hypertension.

The aim of this study was the evaluation of the relationships among hyperinsulinemia, a family history of hypertension, and essential hypertension. Insulin and C-peptide responses to an oral glucose load were studied in 175 lean normotensives (N) and untreated hypertensives (H) with (F+) and without (F-) a family history of hypertension: 30 NF-, 30 NF+, 45 HF-, and 70 HF+. The groups were comparable for age, sex, body mass index, and blood pressure. The following parameters were evaluated: plasma glucose (G), serum insulin (I), and C-peptide (Cp) before and 30, 60, 90, and 120 min after the glucose load, fasting glucose/insulin ratio (ISI), fasting insulin/C-peptide ratio (I/Cp), and 24-h ambulatory blood pressure monitoring. Plasma glucose was measured, fasting and during the test, and it and I/Cp were similar in the four groups. Serum insulin and Cp, both fasting and stimulated, were significantly higher and ISI lower in normotensives and hypertensives with hypertensive parents. Grouping the subjects first on the basis of blood pressure and then on the basis of family history, no differences were found between normotensives and hypertensives, whereas I and Cp, fasting and stimulated, were significantly higher and ISI lower in subjects with positive as compared to negative family history. The closest correlations between insulin and ambulatory blood pressure were found in normotensive with hypertensive parents; in hypertensives with hypertensive parents we only found a direct correlation between fasting Cp and nocturnal blood pressure fall; in hypertensives with normotensive parents insulin inversely correlated with nocturnal blood pressure fall. Insulin resistance seems to have a familial basis, independently of the presence of hypertension. Instead of showing a causal relationship between insulin resistance and hypertension, our results indicate that the two are partly independent components of a common familial pattern.

[Changes in hormonal and biochemical parameters in gastric adenocarcinoma]. / Modificazioni di parametri ormonali e biochimici nell'adenocarcinoma gastrico.

In 51 patients with gastric adenocarcinoma the fasting blood concentrations of hCG, beta hCG, alpha subunits, ADH, calcitonin, enteroglucagon, gastrin, GH, melatonin, somatostatin, estradiol, CEA and pepsinogen I in the peripheral vein were estimated by radioimmunoassay at the time of diagnosis and, in those who underwent surgery, 7 days after the operation, to determine the incidence of the modifications of the above mentioned substances' blood levels and the existence of possible markers. In presence of increases of the examined parameters greater than 50%, considering M +/- 2 SD of 10 control subjects as normal range, the tumours were examined immunohistochemically. In patients with gastric adenocarcinoma, in comparison with normal subjects, we found significant higher blood levels of hCG alpha subunits, gastrin and CEA and lower of melatonin, pepsinogen I and GH. The immunohistological results demonstrated CEA in both examined cases, alpha subunits in 2 of 6 (respectively in dysplasic areas and in surrounding non neoplastic mucosa) and enteroglucagon in 1 of 3 (dysplasic areas). Our results indicate that none of the parameters we examined, because of their non-specificity or of the low incidence of their modifications, can be considered a marker of gastric adenocarcinoma.

[Comparison of the results obtained using 99mTc HM-PAO tomoscintigraphy and computer tomography in ischemic lesions of the brain]. / Confronto tra i risultati ottenuti con la tomoscintigrafia con 99mTc HM-PAO e con la TC nelle lesioni ischemiche cerebrali.

Fifty patients suffering from cerebral ischemic attacks, transient or not, were studied with both 99mTc HM-PAO single photon emission computed tomography (SPECT) and computed tomography (CT). In 31 patients both SPECT and CT showed pathologic areas, the max diameters of which were measured on CT images and SPECT orbitomeatal reconstructed sections, and then compared. We observed that: only SPECT images are positive for pathologic conditions in transient ischemic attacks and in the very early phases of infarctions; in recent infarctions (less than 15 days earlier) both SPECT and CT scans are positive but SPECT lesion areas are greater than CT ones; pathologic areas, with clear-cut outlines, having the same dimensions on both CT and SPECT images, are supposed to result from old static infarctions. A persistent perilesional hypoactive area on SPECT images means, in our opinion, a hypoperfusional area liable to new vascular troubles; in which case, medical/surgical therapy seems necessary.

Modulation of mitochondrial F0F1 catalysis by boundary and bulk phase phospholipids.

The importance of boundary and bulk phase phospholipids was studied on a mitochondrial ATPase complex isolated by AH-Sepharose chromatography as described by Dreyfus et al (1984, Anal. Biochem. 142,215-220), this preparation was devoid of the adenine nucleotide carrier. The presence of isoelectric or acidic phospholipids during the purification in the column allows the exchange of tightly bound phospholipids up to 95%. ATP hydrolysis and oligomycin sensitivity were slightly affected by the nature of boundary and bulk phase phospholipids, while Pi-ATP exchange was highly inhibited.

Differences in cortisol, aldosterone and testosterone responses to ACTH 1-17 administered at two different times of day.

The effects of 100 micrograms, i.m. of the analog ACTH 1-17 administered at 0800 and 1800 on the secretion of cortisol, aldosterone and testosterone have been studied in normal subjects: 8 male and 8 female. The group as a whole and the males had significantly greater absolute and percent increments in plasma cortisol after administration at 1800. In the females, there was only a greater percent increment in cortisol after the evening administration. The heptadecapeptide always significantly stimulated serum aldosterone, with no difference between the two times of administration. In the females, ACTH 1-17 significantly stimulated testosterone, with a more protracted secretion after the evening administration. In the males, there was always a significant testosterone decrease after the administration of the drug, with no difference between morning and evening. In conclusion, 100 micrograms i.m. of the analog ACTH 1-17 stimulates cortisol secretion more when given during the circadian nadir of plasma cortisol, but only in men. ACTH 1-17 increases testosterone in women and decreases it in men, whereas it seems to increase aldosterone secretion in both sexes.

Nomifensine, TRH and insulin-induced hypoglycemia tests in the diagnosis of prolactinomas.

Nomifensine, TRH and insulin-induced hypoglycemia tests were carried out in 37 cases of hyperprolactinemia: 25 were due to PRL-secreting pituitary tumors, 6 cases to GH and PRL-secreting pituitary tumors and 6 to pituitary and suprasellar non secreting tumors. Nomifensine failed to suppress the serum PRL in all subjects and PRL responses to TRH and insulin-induced hypoglycemia were impaired in all patients, irrespective of the origin of hyperprolactinemia. The uniform pattern of PRL response to the above tests in patients with hyperprolactinemia of variable etiology suggests that none of them is specific for prolactinomas.

[Blood folates in chronic uremic patients in dialysis treatment]. / La folatemia negli uremici cronici in trattamento dialitico.

The authors, after having reviewed folic acid and folates chemical and biochemical characteristics and their absorption and excretion modalities, determine serum folate levels by radioassay method on 30 patients with renal failure in chronic dialysis and on 24 normal controls. Low serum folate levels concerned 14 uremic patients (46.6% of th cases): 10 in hemodialysis and 4 in peritoneal dialysis. The mean serum folate values was 3.31 ng/ml (+/- 1.93) for the uremic patients' group and 4.29 ng/ml (+/- 1.21) for the control group. The difference between the mean level of these groups was statistically significant (p less than 0.05). No significant difference was observed among the mean serum folate levels of the uremic patients in peritoneal dialysis and of those in hemodialysis. Significantly low serum folate levels were finally found for the uremic HBsAg-positive patients, but in the same subjects the dialytic treatment period had been very prolonged. The authors conclude emphasizing the usefulness of folic acid treatment in uremic patients on dialysis, also without having an evident hematologic picture of megaloblastic anemia.