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Provocative Test (provocative + test)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Effects of hyperventilation on fast goal-directed limb movements in spinocerebellar ataxia type 6

EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001
M.-U. Manto
It has been shown previously that hyperventilation modifies the features of the nystagmus in cerebellar patients (Walker and Zee, 1999). It has been hypothesized that hyperventilation influences the oculomotor control through a metabolic effect on cerebellar calcium channels, which play a critical role in the firing behaviour of neuronal populations in the cerebellum. This hypothesis has been tested here by analysing fast goal-directed limb movements before and after hyperventilation in spinocerebellar ataxia type 6 (SCA-6), a disease associated with a polyglutamine expansion in the , 1-A voltage-dependent calcium channel. Cerebellar hypermetria associated with fast distal single-joint movements was found to be increased following hyperventilation in patients presenting SCA-6 but remained unchanged in patients with idiopathic late-onset cerebellar degeneration (ILOCA). This is a new provocative test to enhance distal dysmetria in SCA-6. The present results strengthen the hypothesis of Walker and Zee. It is suggested that hyperventilation enhances the defective calcium transfers in SCA-6, resulting in an impairment of the calcium influx in particular into Purkinje cells involved in the control of fast goal-directed voluntary movements. [source]

Effect of obesity and morbid obesity on the growth hormone (GH) secretion elicited by the combined GHRH + GHRP-6 test

CLINICAL ENDOCRINOLOGY, Issue 6 2006
Fahrettin Kelestimur
Summary Objective, Obesity is characterized by low basal levels of growth hormone (GH) and impeded GH release. However, the main problem arises in the diagnosis of GH deficiency in adults, as all accepted cut-offs in the diagnostic tests of GH reserve are no longer valid in obese subjects. In this work, the role of obesity in the GH response elicited by the GHRH + GHRP-6 test was assessed in a large population of obese and nonobese subjects. Patients, GHRH + GHRP-6-induced GH peaks were evaluated in 542 subjects. One hundred and five were healthy obese, 50 were morbid obese, and 261 were nonobese (both normal weight and overweight). One hundred and seventy-six GH-deficient patients (obese and nonobese) were also studied. Results, A regression analysis of the 366 subjects with normal pituitary function indicated that adiposity had a negative effect on the elicited GH peak (r = ,0·503, P < 0·0001). A receiver operating characteristic (ROC) curve analysis showed that in subjects with a BMI 35, the currently accepted cut-offs of the GHRH + GHRP-6 test (GH peaks 20 µg/l: normal secretion; GH peaks 10 µg/l: GH deficiency), were fully operative. However, in subjects with a BMI > 35, normality was indicated by GH peaks 15 µg/l and GH deficiency by peaks 5 µg/l (1 µg/l = 2·6 mU/l). Conclusions, This study confirms: (a) that the combined provocative test is adequate to separate normal and GH-deficient subjects; (b) the negative effect of obesity on GH secretion; (c) that obesity accounts for 25% of the reduction of GH release; and (d) that present cut-off values are applicable to normal weight, overweight and grade I obesity subjects, whereas in obese subjects with a BMI exceeding 35, all the normative limits of the GHRH-GHRP +6 test must be reduced by 5 µg/l. [source]

Endocrine responses to ghrelin in adult patients with isolated childhood-onset growth hormone deficiency

CLINICAL ENDOCRINOLOGY, Issue 6 2002
Gianluca Aimaretti
Summary objective Ghrelin, a 28 amino acid acylated peptide, is a natural ligand of the GH secretagogues (GHS) receptor (GHS-R), which is specific for synthetic GHS. Similar to synthetic GHS, ghrelin strongly stimulates GH secretion but also displays significant stimulatory effects on lactotroph and corticotroph secretion. It has been hypothesized that isolated GH deficiency (GHD) could reflect hypothalamic impairment that would theoretically involve defect in ghrelin activity. patients In the present study, we verified the effects of ghrelin (1 µg/kg i.v.) on GH, PRL, ACTH and cortisol levels in adult patients with isolated severe GHD [five males and one female, age (mean ± SEM) 24·7 ± 2·6 years, BMI 25·7 ± 2·7 kg/m2]. In all patients, the GH response to insulin-induced hypoglycaemia (ITT, 0·1 IU regular insulin i.v.) and GH releasing hormone (GHRH) (1 µg/kg i.v.) + arginine (ARG, 0·5 g/kg i.v.) was also studied. The hormonal responses in GHD were compared with those in age-matched normal subjects (NS, seven males, age 28·6 ± 2·9 years, BMI 22·1 ± 0·8 kg/m2). results IGF-I levels in GHD were markedly lower than in NS (69·8 ± 11·3 vs. 167·9 ± 19·2 µg/l, P < 0·003). Ghrelin administration induced significant increase in GH, PRL, ACTH and cortisol levels in all GHD. In GHD, the GH response to ghrelin was higher (P < 0·05) than that to GHRH + ARG, which, in turn, was higher (P < 0·05) than that to ITT (9·2 ± 4·1 vs. 5·3 ± 1·7 vs. 1·4 ± 0·4 µg/l). These GH (1 µg/l = 2 mU/l) responses in GHD were markedly lower (P < 0·0001) than those in NS (ghrelin vs. GHRH + ARG vs. ITT 92·1 ± 16·7 vs. 65·3 ± 8·9 vs. 17·7 ± 3·5 µg/l). In GHD, the highest individual peak GH response to ghrelin was markedly lower than the lowest peak GH response in NS (28·5 vs. 42·9 µg/l). GHD and NS showed overlapping PRL (1 µg/l = 32 mU/l) (10·0 ± 1·4 vs. 14·9 ± 2·2 µg/l), ACTH (22·3 ± 5·3 vs. 18·7 ± 4·6 pmol/l) and cortisol responses (598·1 ± 52·4 vs. 486·9 ± 38·9 nmol/l). conclusions This study shows that ghrelin is one of the most powerful provocative stimuli of GH secretion, even in those patients with isolated severe GHD. In this condition, however, the somatotroph response is markedly reduced while the lactotroph and corticotroph responsiveness to ghrelin is fully preserved, indicating that this endocrine activity is fully independent of mechanisms underlying the GH-releasing effect. These results do not support the hypothesis that ghrelin deficiency is a major cause of isolated GH deficiency but suggest that ghrelin might represent a reliable provocative test to evaluate the maximal GH secretory capacity provided that appropriate cut-off limits are assumed. [source]

Acetylcholine- and ergonovine-induced coronary microvascular spasm reflected by increased coronary vascular resistance and myocardial lactate production

CLINICAL CARDIOLOGY, Issue 3 2000
Masashi Horimoto M.D.
Abstract Diagnosis of coronary microvascular spasm remains largely speculative because it has been mostly based on chest pain and electrocardiographic ST-segment shift with slow filling of contrast medium into the coronary artery. A patient with resting chest pain and normal coronary angiograms underwent provocative tests with intracoronary acetylcholine (ACh) and ergonovine. During the tests, coronary diameter and flow velocity in the left anterior descending (LAD) coronary artery were measured with quantitative coronary angiography and intracoronary Doppler guide wire, respectively. Vascular resistance of the LAD and lactate production were determined separately. With injections of 100 ,g of ACh and 20 ,g of ergonovine, chest pain occurred with ST-segment elevation in the precordial leads in the absence of epicardial coronary spasm. Coronary vascular resistance increased by 2.2- and 1.6-fold of the baseline value with ACh and ergonovine, respectively. Myocardial lactate production was noted during the ST-segment elevation. Coronary microvascular spasm was verified by the increment in coronary vascular resistance and myocardial lactate production with concomitant ST-segment elevation in the presence of normal coronary angiograms. [source]