A multicenter study of Turner syndrome (TS) patients was carried out to estimate the prevalence of celiac disease (CD) and to detect clinical characteristics and laboratory data of affected patients. Three hundred eighty-nine girls with TS were screened by IgA antigliadin antibodies and/or antiendomysial antibodies. Intestinal biopsy was offered to positive cases. CD was diagnosed in 25 patients. In celiac subjects, anemia, anorexia, and delayed growth (with respect to Italian TS curves) were frequently present; whereas distended abdomen, chronic diarrhea, constipation, and vomiting occurred more rarely. In addition, low serum iron levels, hemoglobinemia, and high values of aminotransferases were observed. Ten patients showed classic CD, 8 showed atypical symptoms, and 7 showed a silent CD. In 11 symptomatic patients, the diagnosis of CD was made at the onset of symptoms, whereas 7 of them showed a median delay of 79 months in diagnosis. Other autoimmune disorders were observed in 40% of the patients. Our study confirms the high prevalence (6.4%) of CD in a large series of TS patients. Moreover, the subclinical picture in 60% of the cases, the diagnostic delay, and the incidence of other autoimmune disorders suggest that routine screening of CD in TS is indicated.
SUMMARYThe relationship between plasma levels of norepinephrine (NE) and sympathetic neural activity is discussed with special reference to human primary hypertension. Since sympathetic discharge is differentiated, neural activity to a given target organ will contribute variably to plasma NE levels in different situations. Hemodynamically, early primary hypertension is often characterized by a mild defense reaction-like pattern with signs of increased sympathetic activity to the heart and vasoconstriction in the renal and splanchnic vascular beds. Although important hemodynamically, these organs seem to be ofless importance as contributors to peripheral plasma NE levels. In contrast, muscle sympathetic activity and muscle vascular resistance is unchanged or reduced. Since this organ mass contributes importantly to plasma NE levels, especially in peripheral venous blood, it is not surprising that most patients with primary hypertension have normal NE levels. It is concluded that NE concentrations in forearm or mixed venous blood are unreliable indicators of sympathetic neural contributions to essential hypertension, tending to underestimate this element, and that regional measurements of NE overflow are needed for a reliable analysis. cholamine concentrations in body fluids have reached high sensitivity and accuracy and can for some purposes be a valuable tool, particularly for studies in humans when simple and safe indicators of sympathetic activity are needed. Such measurements have also become widely used for assessing the involvement of neurogenic elements in primary hypertension (recently surveyed by Goldstein 1 -2 ). It should be realized, however, that norepinephrine (NE) is a locally released transmitter, rather than a hormone, and that the autonomic nervous system operates quite differently from hormonal systems. Thus, there are good reasons for considerable caution when interpreting plasma NE levels, particularly in hypertension, as will be outlined below.
Turner syndrome (TS) is the most common sex-chromosome abnormality in females. Short stature and hypogonadism are the classical clinical findings. The spontaneous final height (FH) ranges between 139 and 147 cm, representing a growth deficit of about 20 cm with respect to the unaffected population. GH therapy improves FH and should be started during childhood at a high dose of about 1 IU/kg/week (range 0.6-2 IU/kg/week). Some authors advocate combined therapy with an anabolic steroid at various doses (e.g. oxandrolone 0.05-0.1 mg/kg/day). This treatment results in a significantly increased FH, .a large proportion of treated girls reaching a FH of more than 150 cm. Gonadal function is compromised during adolescence in about 80% of girls with TS, whilst in about 20% pubertal development occurs spontaneously. Oestrogen therapy should be started at the age of 13-14 years in hypogonadic patients; early onset of treatment (before 12 years) seems to compromise FH. Other concerns in these patients are fertility and osteopenia.
Intravenous injection of growth hormone in anaesthetized pigs has been shown to cause coronary vasoconstriction by antagonizing the vasodilatory effects of β2‐adrenergic receptors. Because nitric oxide is believed to modulate or mediate β2‐adrenergic effects, the present study was undertaken in the same experimental model to determine the role of nitric oxide in the above response to growth hormone. In fourteen pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous injection of 0.05 i.u. kg‐1 of growth hormone at constant heart rate and arterial blood pressure were assessed using electromagnetic flowmeters. In a first control group of six pigs, growth hormone caused a decrease in coronary blood flow which averaged 13.1% of the baseline values. In a second group of eight pigs, intravenous administration of Nω‐nitro‐L‐arginine methyl ester (L‐NAME) was used to block the endothelial release of nitric oxide. In these pigs, the subsequent injection of growth hormone did not cause any significant changes in coronary blood flow, even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L‐NAME with continuous intravenous infusion of papaverine. These results indicated that the coronary vasoconstricting effect of growth hormone, known to involve antagonism of β2‐adrenergic vasodilatory effect, was mediated by inhibition of nitric oxide release.
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