Paradoxical GH response to TRH during status epilepticus in man

Lindbom, Ulla; Al, Hulting; Tomson, Torbjörn

doi:10.1530/eje.0.1400307

Cited by 6 publications

(4 citation statements)

References 36 publications

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“…TRH is known to have age-and endocrine environment-dependent effects on GH release in rats (50)(51)(52), but whether this translates to the human phenotype is unknown. A paradoxical GH response to TRH may also be observed in nonacromegalic conditions (eg, depression, anorexia nervosa, untreated primary congenital hypothyroidism) where it has been hypothesized to reflect dysregulation of the normal dopaminergic or somatostatin-mediated inhibitory effects on GH release, supporting the argument that although a somatotrope-autonomous role for IGSF1 is possible, additional hypothalamic dysfunction may also contribute to GH excess (53,54).…”

Section: Discussionmentioning

confidence: 89%

IGSF1 Deficiency results in human and murine somatotrope neurosecretory hyperfunction

Sd¹,

Roelfsema²,

Trotsenburg³

et al. 2020

ESPE

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The X-linked immunoglobulin superfamily, member 1 (IGSF1), gene is highly expressed in the hypothalamus and in pituitary cells of the POU1F1 lineage. Human loss-of-function mutations in IGSF1 cause central hypothyroidism, hypoprolactinemia, and macroorchidism. Additionally, most affected adults exhibit higher than average IGF-1 levels and anecdotal reports describe acromegaloid features in older subjects. However, somatotrope function has not yet been formally evaluated in this condition. Objective:We aimed to evaluate the role of IGSF1 in human and murine somatotrope function.Patients, Design, and Setting: We evaluated 21 adult males harboring hemizygous IGSF1 lossof-function mutations for features of GH excess, in an academic clinical setting. Main Outcome Measures:We compared biochemical and tissue markers of GH excess in patients and controls, including 24-hour GH profile studies in 7 patients. Parallel studies were undertaken in male Igsf1-deficient mice and wild-type littermates.Results: IGSF1-deficient adult male patients demonstrated acromegaloid facial features with increased head circumference as well as increased finger soft-tissue thickness. Median

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Section: Discussionmentioning

confidence: 89%

IGSF1 Deficiency results in human and murine somatotrope neurosecretory hyperfunction

Sd¹,

Roelfsema²,

Trotsenburg³

et al. 2020

ESPE

View full text Add to dashboard Cite

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“…They typically occur when the tumor invades the suprasellar area due to mass effect on the brain in large pituitary adenomas ( 9 ). The mechanism by which status epilepticus may occur in patients with pituitary macroadenoma is by local effect and hormone dysfunction ( 10 ). The seizure disorder in the first case is likely to have been secondary to the small acute hemorrhage reported in the right frontal lobe which in turn may have been secondary to the acute infarction reported in the macroadenoma.…”

Section: Discussionmentioning

confidence: 99%

Status epilepticus and diabetes ketoacidosis: uncommon clinical presentations of acromegaly

Chamba

Amour²,

Sadiq

et al. 2021

Endocrinology, Diabetes &Amp; Metabolism Case Reports

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Summary Acromegaly is a rare disease caused by hypersecretion of the growth hormone (GH). Most cases are caused by either pituitary microadenoma or macroadenoma. The GH producing tumors present with clinical manifestations of acromegaly due to excessive GH secretion or symptoms resulting from mass effects of the enlarging tumor. The physical changes are usually slow and, therefore, recognition of the disease is delayed. These adenomas are never malignant but can have significant morbidity and mortality. A subgroup of patients with acromegaly present with severe hyperglycemia resulting in diabetic ketoacidosis (DKA) which requires insulin. Rarely are pituitary tumors responsible for generalized convulsions except when they are too large. We hereby present two cases, the first is that of a 26-year-old female who presented with new onset status epilepticus, DKA with a 1-year history of diabetes mellitus (DM). On examination, she had clinical features of acromegaly. The second case is that of a 34-year-old female who presented with new onset status epilepticus, hyperglycemia with a history of recently diagnosed DM, and features of gigantism. In both cases, their diagnosis was confirmed by elevated serum GH and later by elevated insulin-like growth factor type 1 levels, and CT of the head demonstrating large pituitary macroadenoma. The importance of clinical history and examination, as well as investigations is vital in the recognition of acromegaly. The prognosis of acromegalic patients depends on early clinical recognition and tumor size reduction by either medical or surgical therapy. Learning points Conditions such as status epilepticus and DKA may be clinical presentations in patients presenting with acromegaly. Seizures are rare in people with pituitary adenoma and typically occur when the tumor invades the suprasellar area due to mass effect on the brain. This article shows how best we were able to manage the acromegaly complications in a low resource setting. Hyperprolactinemia in acromegaly may be due to disruption of the normal dopaminergic inhibition of prolactin secretion due to mass effect of the macroadenoma, and around 25% of GH-secreting adenomas co-secrete prolactin.

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“…However, abnormal GH responses to TRH have also been reported in patients with hypothyroidism (35), anorexia nervosa (36), diabetes mellitus (37), liver cirrhosis (38) and status epilepticus (39). Investigations of these conditions suggest that the paradoxical GH reaction to TRH may be a functional consequence of several pathological states characterized by altered somatostatin control of GH secretion.…”

Section: Discussionmentioning

confidence: 99%

Effects of acute infusion of erythropoietin on paradoxical responses of growth hormone to thyrotropin-releasing hormone in acromegalic patients

Iglesias²,

Sastre³

et al. 2000

European Journal of Endocrinology

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Objective: Our aim has been to evaluate the effects of i.v. infusion of recombinant human erythropoietin (rhEPO) on the responses of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) stimulation in acromegalic patients. Methods: We studied 16 patients (8 females, aged 29±68 years) with active acromegaly and 12 control subjects (7 females, 24±65 years). All participants were tested with TRH (400 mg i.v. as bolus) and with TRH plus rhEPO (40 U/kg at a constant infusion rate for 30 min, starting 15 min before TRH injection) on different days. Blood samples were obtained between À30 and 120 min for GH and PRL determinations, and between À30 and 90 min for TSH determinations. Hormone responses were studied by a time-averaged (area under the secretory curve (AUC)) and time-independent (peak values) analysis. Results: Twelve patients exhibited a paradoxical GH reaction after TRH administration with great interindividual variability in GH levels. When patients were stimulated with rhEPO plus TRH there were no changes in the variability of GH responses or in the peak and AUC for GH secretion. Infusion with rhEPO did not induce any signi®cant change in GH secretion in normal subjects. Baseline and TRH-stimulated PRL concentrations in patients did not differ from those values found in controls. When TRH was injected during the rhEPO infusion, a signi®cant (P < 0.05) increase in PRL concentrations at 15±120 min was found in acromegalic patients. Accordingly, the PRL peak and the AUC for PRL secretion were signi®cantly increased in patients. Infusion with rhEPO had no effect on TRH-induced PRL release in control subjects. Baseline TSH concentrations, as well as the TSH peak and the AUC after TRH, were signi®cantly lower in patients than in controls. Infusion with rhEPO modi®ed neither the peak TSH reached nor the AUC for TSH secretion after TRH injection in acromegalic patients and in healthy volunteers. Conclusion: Results in patients with acromegaly suggest that (i) the paradoxical GH response to TRH is not modi®ed by rhEPO infusion, (ii) rhEPO has no effect on TRH-induced TSH release, and (iii) acute rhEPO administration increases the TRH-induced PRL release in acromegalic patients.

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Paradoxical GH response to TRH during status epilepticus in man

Cited by 6 publications

References 36 publications

IGSF1 Deficiency results in human and murine somatotrope neurosecretory hyperfunction

IGSF1 Deficiency results in human and murine somatotrope neurosecretory hyperfunction

Status epilepticus and diabetes ketoacidosis: uncommon clinical presentations of acromegaly

Effects of acute infusion of erythropoietin on paradoxical responses of growth hormone to thyrotropin-releasing hormone in acromegalic patients

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