Pituitary-hormone secretion by thyrotropinomas

Hormone secretion by somatotropinomas, corticotropinomas and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness. Increased concentrations of growth hormone (GH) or prolactin (PRL) are observed in about 30% of thyrotropinomas leading to acromegaly or disturbed sexual functions beyond thyrotropin (TSH)-induced hyperthyroidism. Regulation of non-TSH pituitary hormones in this context is not well understood. We there therefore evaluated TSH, GH and PRL secretion in 6 patients with up-to-date analytical and mathematical tools by 24-h blood sampling at 10-min intervals in a clinical research laboratory. The profiles were analyzed with a new deconvolution method, approximate entropy, cross-approximate entropy, cross-correlation and cosinor regression. TSH burst frequency and basal and pulsatile secretion were increased in patients compared with controls. TSH secretion patterns in patients were more irregular, but the diurnal rhythm was preserved at a higher mean with a 2.5 h phase delay. Although only one patient had clinical acromegaly, GH secretion and IGF-I levels were increased in two other patients and all three had a significant cross-correlation between the GH and TSH. PRL secretion was increased in one patient, but all patients had a significant cross-correlation with TSH and showed decreased PRL regularity. Cross-ApEn synchrony between TSH and GH did not differ between patients and controls, but TSH and PRL synchrony was reduced in patients. We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas. In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although not always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells

Cardiovascular complications in AIDS

Cardiovascular complications in acquired immunodeficiency syndrome. AIDS miocardiopathy has been described since 1983. Physiopathologic events leading to AIDS myocardiopathy are largely unknown: viral miocardiopathy, cytokines induced lesions, nutritional status, microvascular and ischemic miocadiopathy have been suspected. We describe a consecutive series of 50 patients (43 males, 7 women) with HIV infection and severe immunodepression (CD4<200/ml) that had clinical, ECG and echocardiographic evaluation. There were 24 drug addicted patients, 17 homosexual patients, and 10 heterosexuals. Some of these patients had the following opportunistic infections: tuberculosis (n=20), Pneumocystis carinii (n=9), Criptocococis (n=9), oropharyngeal candidosis (n=5), toxoplasmosis (n=5), histoplasmosis (n=1) and Kaposi’s sarcoma (n=2). After clinical evaluation 15/50 patients had some kind of cardiovascular complication: 6 patients had congestive heart failure, 5 patients presented with pericardial effusion, one patient has a reversible cardiac arrest, and one patient had pulmonary valvular endocarditis. After Doppler echocardiographic evaluation (according to the American echocardiography association), we found 20 patients with left ventricular diastolic dysfunction, 9 patients with right ventricular diastolic dysfunction and 6 patients with left ventricular systolic dysfunction. In conclusion, our series found left diastolic dysfunction in nearly 40 % of cases and cardiavasular events (pericarditis, heart congestive failure, arrhythmias) in 26% of cases. Cardiovascular complications have prognostic implications in AIDS and shoul be early detected. Further pathological and immunohistochemical studies are needed to clarify the phyiopathological etiologies in AIDS miocardiopathy