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M Losa

Publications and source records attributed to M Losa.

105 records · Page 6Linked to original sources
PubMed1985

Growth hormone releasing factor-test in acromegaly: comparison with other dynamic tests.

Human pancreatic growth hormone releasing factor (hpGRF1-44) was given intravenously as a 100 micrograms bolus to 20 patients with active acromegaly. The GH-responses were variable, ranging from an increase of 8 to 2813% from the basal level (mean +/- SE, 428 +/- 136%). Sixteen GRF-responders (delta% greater than or equal to 100%) were arbitrarily distinguished from four GRF non-responders, whose GH-levels increased less than 100% from basal level after GRF-administration. The outcome of the GRF-test did not correlate with the results of other dynamic tests of GH-secretion in acromegaly (oral glucose tolerance test, insulin hypoglycaemia, TRH-, LHRH-, CRF-stimulation). In 10 patients who had not been treated before, the GH-increments after GRF were higher than those in seven patients who had previously been subjected to transsphenoidal surgery, though they still had clinically and biochemically active acromegaly. Ten acromegalics, who were tested with GRF, were later treated surgically by the transsphenoidal route and were reevaluated with GRF-stimulation 2 months after surgery. Eight patients appeared clinically cured of whom four had complete normalization and four had significantly lower basal and conventionally stimulated GH-levels postoperatively. These patients also had normal postoperative GH-responses to GRF, which had been significantly higher before surgery compared with normal controls. It is concluded that the GRF-test in acromegaly does not help in establishing the diagnosis. The normalization of the GH-response to GRF after transsphenoidal surgery seems to represent additional evidence for normalization of GH-secretion, though the latter is not proven by the normal outcome of this test.

Acromegaly↗
PubMed1985

Free thyroid hormone levels and TSH response to TRH in patients with autonomous thyroid adenomata and normal T3 and T4.

Free thyroid hormone levels together with basal and TRH stimulated TSH levels, have been determined in 50 patients with autonomous thyroid adenomata, who had normal serum total T3 and T4 values. Similar measurements were made in 33 healthy subjects. FT3 and FT4 plasma levels were significantly higher (P less than 0.01 and P less than 0.05 respectively), and basal and TRH stimulated TSH were significantly lower (P less than 0.05 and P less than 0.001 respectively) in the patients than in the controls. The TSH response to TRH was decreased in spite of normal free thyroid hormones in 25 patients and in a further ten both the delta TSH after TRH and the free fractions were normal. Eighteen patients were studied over periods from 4 37 months by repeating thyroid hormone levels and TRH tests. In six of them a change of these parameters toward toxicity was observed. The data obtained in the longitudinal study indicate that the values of free thyroid hormones and the result of the TRH test obtained by a single determination may represent different steps in the evolution of autonomous thyroid adenomata rather than a distinct pathophysiological condition.

Adenoma↗
PubMed1985

Interaction between growth hormone releasing factor (GRF) and somatostatin analogue (SMS 201-995) in normal subjects.

Continuous infusion or pulsatile administration of growth hormone releasing factor leads to decreasing GH levels and GH responses in normal subjects. We have given 50 micrograms GRF 1-44 i.v. four times in 2-hourly intervals to five normal subjects. After 1 week the same protocol was repeated after s.c. administration of 50 micrograms of the synthetic octapeptide somatostatin (SMS 201-995). The GH response to the same GRF doses was higher after the initial GRF pulse and blunted to the following GRF pulses (pulse I: 37:0 +/- 11.2 ng/ml; Pulse II: 5.3 +/- 1.2 ng/ml; pulse III: 5.9 +/- 2.5 ng/ml; pulse IV: 5.9 +/- 3.2 ng/ml; mean +/- SE). When SMS 201-995 was given 60 min before pulsatile GRF administration, the GH secretion pattern was reversed (pulse I: 2.4 +/- 0.7 ng/ml; pulse II: 2.0 +/- 0.9 ng/ml; pulse III: 4.4 +/- 2.1 ng/ml; pulse IV: 11.4 +/- 3.6 ng/ml). Radioimmunoassayable GRF levels were not different before and after administration of SMS 201-995. The half time of disappearance was 8.6 +/- 0.4 min before and 8.0 +/- 0.5 min after SMS 201-995. Basal thyrotrophin and insulin levels, which remained constant over the 8 h period with GRF only, decreased significantly after SMS 201-995 administration. These findings are compatible with a limited releasable GH pool which is exhausted by chronic GRF stimulation but can be conserved by prior administration of the somatostatin analogue. Thus, when somatostatin bioactivity tapers off, there is recovery of GRF-stimulated GH secretion.

Adult↗
PubMed1985

Growth hormone releasing factor induces prolactin secretion in acromegalic patients but not in normal subjects.

The effect of an iv injection of growth hormone releasing factor (GRF) on Prl secretion in healthy volunteers and patients with active acromegaly was investigated. Thirteen normal subjects received 100 micrograms GRF 1-44, and 19 acromegalics received 100 micrograms GRF 1-44. Nine normals and 9 patients were given the diluent only and served as placebo control. In healthy volunteers GRF did not affect Prl secretion significantly when compared to placebo, whereas in acromegalics Prl levels after GRF were higher than after placebo. We have divided acromegalics in Prl-responders to GRF (n = 11) and Prl-non-responders (n = 8) using the criterion of strict parallelism between GH and Prl secretion after GRF. In cases with no GH response to GRF a clear increase of Prl levels with the maximum 15-30 min after GRF was also regarded as a Prl response. Acromegalic Prl-responders and Prl-non-responders did not significantly differ in age, sex, previous therapy, and basal GH and Prl levels. However, Prl-non-responders had a significantly reduced response of both GH and Prl to TRH (GH: 147.3 +/- 16.0 vs 590.1 +/- 127.8%; mean +/- SE; Prl: 159.4 +/- 32.6 vs 504.9 +/- 109.3%). It is concluded that 50 or 100 micrograms GRF does not affect Prl secretion in normal subjects. In contrast, in acromegaly GRF leads to Prl secretion in more than half of all patients.

Acromegaly↗
PubMed1984

Stimulation of growth hormone secretion with human growth hormone releasing factors (GRF1-44, GRF1-40, GRF1-29) in normal subjects.

Peptides of different chain lengths (GRF1-44, GRF1-40, GRF1-29) were given as a 50 micrograms i.v. bolus to five normal volunteers. Blood was collected before and until 120 min after GRF injection. No serious side effects were recorded. All GRF peptides led to a clearcut and significant increase of GH levels compared to placebo controls with the maximum occurring 15-30 min after GRF injection. There was no significant difference in the maximal GH increase after the different GRF peptides. When GRF1-44 was administered to five normal subjects over 2 days in 6- and 18-h intervals, respectively, significant increase of GH levels were recorded after each injection compared to placebo controls. Again, there was no significant difference between the maximal GH rises during the different tests. These findings show that the short GRF1-29 peptide may be used for diagnosis and therapy. In addition, in contrast to continuous infusion and administration of GRF in short intervals, GRF application in 6-h intervals leads to adequate GH responses.

Adult↗
PubMed1984

Growth hormone releasing factor (hpGRF)-stimulation test in normal controls and acromegalic patients.

Recently a growth hormone releasing factor (GRF) has been isolated from a pancreatic tumor of an acromegalic patient. This peptide with 44 aminoacids (hpGRF1-44) has been synthesized and has been shown to have growth hormone releasing property in vivo and in vitro. We have examined the growth hormone response to synthetic hpGRF1-44 in 10 normal male and 5 normal female subjects, in 4 patients with active acromegaly and in one patient with hypothalamic pituitary insufficiency. After the injection of 100 micrograms hpGRF1-44, growth hormone increased in all normal controls within 5-15 min from a mean basal level of 0.64 +/- 0.06 ng/ml +/- SE to a peak of 16.7 +/- 3.3 ng/ml 30 min after hpGRF1-44. No significant side effects were recorded. All other anterior pituitary hormones showed no increase after hpGRF1-44. In addition, no significant change of blood glucose, pulse rate or blood pressure was recorded after hpGRF1-44. In 4 normal subjects the growth hormone response to 100 micrograms hpGRF1-44 was compared with the response to insulin-induced hypoglycemia. There was no significant difference between the maximum increase of growth hormone after hpGRF1-44 and hypoglycemia. In 3 out of 4 patients with active acromegaly 100 micrograms hpGRF1-44 led to a clear-cut increase with a peak value at 15 min, whereas one patient with postoperative active acromegaly showed no GH increase after 100 micrograms hpGRF1-44. One acromegalic was tested before and 6 weeks after incomplete transsphenoidal surgery with the same response from a lower basal level after surgery as before.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1984

Growth hormone releasing factor infusion does not sustain elevated GH-levels in normal subjects.

To evaluate the dynamics of GH-secretion after infusion of growth hormone releasing factor, human pancreatic growth hormone releasing factor (hpGRF1-44) was infused over 2 and 5 h at a dosage of 100 micrograms hpGRF1-44/h into 11 healthy subjects. The infusion was started and terminated with a 50 micrograms hpGRF1-44 bolus injection. In 5 subjects 200 micrograms TRH was given 4 h after starting the infusion. In addition, 4 healthy subjects received 50 micrograms hpGRF1-44 bolus injection every 2 h. GRF, somatostatin, GH, Prl, and TSH were measured by radioimmunoassay. The initial 50 micrograms GRF bolus increased GH-levels in all 11 subjects with a maximum at 30 min (24.1 +/- 5.1 ng/ml +/- SE). However, though hpGRF1-44 was continuously infused and GFR-levels remained elevated, GH decreased to a minimum 270 min after start of infusion (2.6 +/- 0.6 ng/ml). The GH-response to the second bolus at the end of the infusion was lower compared to the first response (14.6 +/- 3.4 ng/ml after 2 h and 7.6 +/- 2.5 ng/ml after 5 h). TRH did not lead to a GH-increase during hpGRF1-44 infusion though Prl and TSH rose normally. The intermittent bolus injection of 50 micrograms hpGRF1-44 led to continuously decreasing GH-responses to the same GRF-dosage (I. bolus: 16.5 +/- 1.6 ng/ml; II. bolus: 4.2 +/- 0.8 ng/ml; III. bolus: 3.4 +/- 0.5 ng/ml). No change in somatostatin levels was observed. These findings show that GRF infusion or bolus injection in short intervals does not sustain elevated GH-levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Human pancreatic growth hormone-releasing factor (hpGRF): dose-response of GRF- and GH-levels.

Synthetic human pancreatic growth hormone-releasing factor (hpGRF1-44) was given as an i.v. bolus to 8 healthy volunteers in 5 different dosages. Blood was collected before and up to 120 min after GRF-injection. Four subjects received only placebo, five received 3.3 micrograms, three 12.5 micrograms, four 50 micrograms, 5 received 100 micrograms, and three 200 micrograms hpGRF1-44. No serious side effects were recorded after hpGRF1-44. All dosages with the exception of the 3.3 micrograms-dosage lead to a clearcut and significant increase of GH-levels with a maximum occurring 15 to 30 minutes after hpGRF1-44. A dose-response-relationship between the injected GRF-dosage and growth hormone levels was only found from 3.3 to 50 micrograms hpGRF1-44. The administration of 100 or 200 micrograms hpGRF1-44 did not lead to a further increase of GH-levels compared to the 50-micrograms-dose. This was in contrast to the clearcut dose dependency of hpGRF1-44-levels measured by a specific radioimmunoassay over the whole dose range with a maximum occurring 5 minutes after the injection. The mean halftime of disappearance for the 200-micrograms-dose of hp-GRF1-44 was 7.6 +/- 1.7 minutes (+/- SE). We conclude that there is a marked heterogeneity of the GH-response to hpGRF1-44 in healthy volunteers though a dose-response-relationship over the range from 3.3 to 50 micrograms hpGRF i.v. could be established. The dose-response-dependency of hpGRF1-44-levels up to the 200-micrograms-dose indicates that the maximal GH-response is reached when 50 micrograms hpGRF1-44 are administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

The epidermal melanocyte population in the skin of ultraviolet-irradiated crested newt.

The response of the epidermal melanocyte population to repeated ultraviolet (UV) exposure (wavelength spectrum 275-350 nm) has been investigated in the crested newt, Triturus cristatus carnifex. The effects of different doses of UV light were studied. The animals were killed 7 months after the first UV exposure. Only a slight decrease in the number of pigment cells was found after 85 sequential irradiations with a total dose of 1.3 x 10(5) J/m2, whereas striking decreases were observed when the same total dose was fractionated into 14 exposures or when a double dose was given in 57 exposures. The relationship between the square roots of the epidermal melanocyte densities and single doses appeared to be roughly linear, at least over the range of doses administered. The main factor in melanocyte damage seemed to be the single dose of irradiation rather than the cumulative dose administered. Decreased melanin content of the keratinocytes was observed in most irradiated animals.

Animals↗
PubMed1981

Skin damage in adult amphibians after chronic exposure to ultraviolet radiation.

The effects of repeated UV exposure on the skin of the European crested newt, Triturus cristatus carnifex, have been investigated. The animals were irradiated 3 times per week with a Westinghouse FS40T12 fluorescent sun lamp (wavelength spectrum 275-350 nm). Two groups of animals received the same total fluence of 1.3 x 10(5) J/m(2) in single fluences of either 1570 J/m(2) (group A) or 9430 J/m(2) (group C), and one group received a total fluence of 2.6 x 10(5) J/m(2) in single fluences of 4710 J/m(2) (group B). All the animals were killed in 7 months after the first UV exposure, but at different intervals after the last exposure. Striking epidermal hyperplasia was found in the newts irradiated at the lower fluence rate group (group A). In the animals given the higher total fluence (group B), the most prominent skin changes were dermal fibrosis and irregular thinning and thickening of the epidermis. No significant skin changes were found in group C, in which if there had been UV lesions, they had been repaired during the 5 month interval between the last irradiation and the killing of the animals. No skin tumors developed in any experimental group.

Animals↗
PubMedDate not supplied

Modern imaging techniques in GH secretory disorders.

Magnetic resonance images of the pituitary-hypothalamic area in patients with GH secretory disorders, divided into two groups (hypersecretory and hyposecretory), were studied. In the first group there were 42 patients with pituitary adenoma; size, signal characteristics, direction of growth, and type of enhancement were analyzed and compared with similar studies in 40 age and sex matched control patients with non-GH secreting pituitary adenomas. No significant differences were found except for a higher frequency of chiasm involvement and a more pronounced contrast enhancement in the control group. The hyposecretory group was composed of 101 patients with congenital idiopathic growth hormone deficiency (CIGHD). MR revealed morphological abnormalities consisting of hypoplastic anterior pituitary and ectopic posterior pituitary (PPE) in 59 patients, without evidence of a complete pituitary stalk; in 42 patients the posterior pituitary was in normal position and the pituitary stalk visible. The group with PPE showed a greater frequency of multiple pituitary hormone deficiency (51% vs 12%), breech delivery (30% vs 7%) and associated congenital brain anomalies (12% vs 7%). These data suggest that CIGHD could be the result of a congenital midline brain anomaly in a significant proportion of patients.

Adenoma↗