Effect of Chronic Metoclopramide Therapy on Serum Pituitary Hormone Concentrations

Tamagna, Ellen I.; Lane, W.Kenneth; Hershman, Jerome M.; Carlson, Harold E.; Sturdevant, Richard A.L.; Poland, Russell E.; Rubín, Robert T.

doi:10.1159/000179051

Cited by 28 publications

(15 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Administration of metoclopramide, a do pamine antagonist, produced no change in the basal or TRH-stimulated TSH release, findings which are in agreement with pre vious reports on the effects of acute and chronic metoclopramide administration on thyrotropin secretion [18,19]. Other authors have, however, described a stimulatory effect of metoclopramide on basal and TRH-stimu lated TSH release [20,21], Variations in assay sensitivity may have accounted for the dis crepancies in earlier reports.…”

Section: Discussionsupporting

confidence: 84%

“…In humans, GABA, its analogues, and GABA-transaminase inhibitors have been shown to influence the secretion of GH [3], ACTH [4. 5], LH and FSH [6,7], prolactin [8] and TSH [9], There is some evidence to suggest that the effect of GABA on TSH secretion is dopamine dependent [19], In the present study, we attempted to investigate the effect of the GABA analogue, baclofen, on basal and TRH-stimulated TSH release, in normal adult males without and with prior administration of metoclopramide. a dopa mine antagonist.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gaba-Ergic and Dopaminergic Regulation of Thyroid Stimulating Hormone

Elias¹,

Szekeres²,

Stone³

et al. 1984

Horm Res

View full text Add to dashboard Cite

The effects of the GABA analogue, baclofen, and the dopamine antagonist, metoclopramide, on basal and TRH-stimulated TSH release were studied in 6 normal male volunteers. Basal TSH secretion was not influenced by baclofen (10 mg orally three times daily for 3 days) or metoclopramide (10 mg i.v.), given alone or together. Baclofen produced a blunting of the TRH-stimulated TSH release (p < 0.05), which persisted after metoclopramide administration. It is speculated that GABA and its analogues exert an inhibitory effect on TSH secretion, presumably at the level of the pituitary, and this effect is not mediated by dopamine.

show abstract

Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Gaba-Ergic and Dopaminergic Regulation of Thyroid Stimulating Hormone

Elias¹,

Szekeres²,

Stone³

et al. 1984

Horm Res

View full text Add to dashboard Cite

show abstract

“…Metoclopramide has been both used in diagnostic studies of pituitary function, [16][17][18][19] and administered chronically. 20,21 Our patient received metoclopramide at a time that her Hct was 17% to 22% and had a dramatic response (Figure 2). Because a normal Hct was maintained with 10 mg metoclopramide daily, which caused intermittent (but not sustained) elevations in the serum prolactin level, and also when breast-feeding as infrequently as once each day, it appears that repetitive increases in the serum prolactin level are sufficient to support erythropoiesis.…”

Section: Discussionmentioning

confidence: 97%

“…Five years after beginning metoclopramide, the kinetics of the prolactin response was studied quantitatively and was similar to that reported in pharmacologic studies. [17][18][19][20] The baseline serum prolactin level was 3 ng/mL. Two hours after ingestion of 10 mg metoclopramide, prolactin was measured at 140 ng/mL.…”

mentioning

confidence: 99%

Response of Diamond-Blackfan anemia to metoclopramide: evidence for a role for prolactin in erythropoiesis

Abkowitz

Schaison

Boulad

et al. 2002

Blood

View full text Add to dashboard Cite

A 47-year-old woman with severe macrocytic anemia markedly improved during the second and third trimesters of 3 pregnancies and when breast-feeding her 2 children. Because the serum prolactin level is elevated at these times, we later treated her with metoclopramide (10 mg orally 3 times daily), a medication known to induce prolactin release. Her serum prolactin levels increased from 7 to 133 ng/mL (normal < 20 ng/mL) and hematocrit from 17% to 22% to 35%. With continued therapy (now 10 mg orally daily), her hematocrit has ranged from 30% to 40% for 6 years, although the macrocytosis persists (mean corpuscular volume, 100-112 fL). On the basis of this observation, a pilot study was undertaken of metoclopramide therapy in patients with DiamondBlackfan anemia who were refractory to low doses of corticosteroids. Fifteen patients were enrolled and 9 completed the planned 16 weeks of therapy. Three individuals responded, suggesting that this therapeutic approach may benefit others. As with the index case, the anemia did not improve until 12 to 15 weeks of therapy had been completed. IntroductionDiamond-Blackfan anemia is a congenital macrocytic anemia, characterized by a low reticulocyte count, the absence or severe reduction of hemoglobin (Hgb)-containing cells in the marrow, and normal megakaryocytic and granulocytic differentiation. 1-3 Approximately 30% of patients have physical anomalies, including short stature and craniofacial, neck, and thumb malformations. [2][3][4][5] Ten percent have a family history of anemia, generally with a dominant inheritance pattern. The genetic basis of Diamond-Blackfan anemia is likely heterogeneous. Abnormalities of the gene encoding ribosomal protein S19 (localized to chromosome 19q13.2) have been reported in 25% of families (as well as 25% of sporadic cases), 6-8 whereas linkage to different chromosomes has been implicated in other families. 5,7,9,10 Although the anemia may initially respond to corticosteroid therapy, many patients require life-long red blood cell (RBC) transfusions, leading to infectious complications and iron overload. [2][3][4][5] Other therapies include androgens, cyclosporine, and interleukin 3 (IL-3), which appear to be efficacious in 10% to 15% of patients, 2-5,11-13 and marrow transplantation. 4,5,14 Spontaneous remissions, especially during adolescence, have been reported 3 .Our observations in a unique patient suggest that metoclopramide may also be an effective therapy. The patient's severe macrocytic anemia remitted during each of 3 pregnancies and when breast-feeding her 2 children, times when the serum prolactin level is elevated. 15 Thus, when she finished childbearing and was again symptomatically anemic (hematocrit [Hct], 17%-22%), we treated her with metoclopramide, which is known to induce the release of prolactin from the pituitary. [16][17][18][19][20][21] The Hct slowly increased and she has remained asymptomatic and transfusion independent (Hct, 30%-40%, mean corpuscular volume [MCV], 100-112 fL) for 6 years. The mechanism by which prola...

show abstract

“…However, metoclopramide has an additional inhibitory effect on serotonin receptors of the chemoreceptor trigger zone of the central nervous system. Therefore, metoclopramide is considered to be one of the potent stimuli for prolactin release and the levels can be high as 15-fold in patients on chronic metoclopramide therapy (24). It can be associated with amenorrhoea, galactorrhoea, gynaecomastia and impotence (25).…”

Section: Prokineticsmentioning

confidence: 99%