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A case of hypothalamic hypopituitarism accompanied by recurrent severe hypoglycemia.

Takai M, Kaneto H, Kamei S, Mune T, Kaku K - Springerplus (2015)

Bottom Line: Therefore, we stopped hydrocortisone and instead started an alternative treatment with prednisolone.We diagnosed this subject as hypothalamic hypopituitarism mainly by the following two findings: (1) excess and delayed reaction of ACTH in CRH load test, (2) delayed reaction of LH and FSH in LHRH load test.We should be aware of the possibility of hypothalamic hypopituitarism as a cause of recurrent severe hypoglycemia.

View Article: PubMed Central - PubMed

Affiliation: Division of Diabetes, Metabolism and Endocrinology, Kawasaki Medical School, 577 Matsushima, Kurashiki, 701-0192 Japan.

ABSTRACT

Introduction: Hypothalamic hypopituitarism is relatively rare cause of secondary adrenal deficiency which is often accompanied by severe hypoglycemia. Hydrocortisone replacement therapy is essential for this condition, but gastrointestinal symptom such as nausea and vomiting is not well-recognized adverse effect of hydrocortisone.

Case description: A 64-year-old-woman was referred to our hospital because of frequent severe hypoglycemia. She was diagnosed as type 2 diabetes when she was 58 years old but had not been treated since she was 60. We ruled out the possibility of exogenous administration of insulin or other anti-diabetic drugs, insulinoma and insulin autoimmune syndrome. After glucose injection, she once became conscious, but severe hypoglycemia was often observed even after that. In addition, counter-regulatory hormone levels were not increased even at the time of hypoglycemia. We conducted several hormone load tests. In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ACTH was observed. In thyrotropin-releasing hormone (TRH) load test, TSH and prolactin were normally secreted in response to TRH. In luteinizing hormone-releasing hormone (LHRH) load test, delayed reaction of LH and FSH was observed. Based on such hormone loading tests, we diagnosed this patient as idiopathic hypothalamic hypopituitarism and consequent adrenal deficiency. We immediately intravenously injected hydrocortisone and started oral hydrocortisone therapy. However, just after taking hydrocortisone, vomiting was often observed which disturbed sufficient steroid hormone replacement, leading to recurrent hypoglycemia. Therefore, we stopped hydrocortisone and instead started an alternative treatment with prednisolone. After that, vomiting and hypoglycemia were not observed at all.

Discussion and evaluation: We diagnosed this subject as hypothalamic hypopituitarism mainly by the following two findings: (1) excess and delayed reaction of ACTH in CRH load test, (2) delayed reaction of LH and FSH in LHRH load test.

Conclusions: We should be aware of the possibility of hypothalamic hypopituitarism as a cause of recurrent severe hypoglycemia. Also, we should be aware that hydrocortisone could induce gastrointestinal symptom and that in such a case we should stop hydrocortisone and start prednisolone to sufficiently replace steroid hormone and avoid recurrent hypoglycemia.

No MeSH data available.


Related in: MedlinePlus

Corticotropin-releasing hormone (CRH) load test: after intravenous injection of CRH (0.1 mg), ACTH and cortisol levels were examined. Thyrotropin-releasing hormone (TRH) load test: after intravenous injection of TRH (0.5 mg), TSH and PRL levels were examined. Luteinizing hormone-releasing hormone (LHRH) load test: after intravenous injection of LHRH (0.1 mg), LH and FSH levels were examined. Arginine load test: after intravenous injection of arginine (10%, 300ml), GH level was examined. Growth hormone releasing hormone (GHRH) load test: after intravenous injection of GHRH (0.1 mg), GH level was examined.
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Fig1: Corticotropin-releasing hormone (CRH) load test: after intravenous injection of CRH (0.1 mg), ACTH and cortisol levels were examined. Thyrotropin-releasing hormone (TRH) load test: after intravenous injection of TRH (0.5 mg), TSH and PRL levels were examined. Luteinizing hormone-releasing hormone (LHRH) load test: after intravenous injection of LHRH (0.1 mg), LH and FSH levels were examined. Arginine load test: after intravenous injection of arginine (10%, 300ml), GH level was examined. Growth hormone releasing hormone (GHRH) load test: after intravenous injection of GHRH (0.1 mg), GH level was examined.

Mentions: To explore the pathogenesis of severe hypoglycemia, we performed several examination. First, magnetic resonance imaging (MRI) of the brain showed no obvious abnormalities; pituitary abnormality such as adenoma and pituitary stalk interruption was not observed. Second, we conducted several hormone load tests (FigureĀ 1). In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ACTH (adrenocorticotropic hormone) was observed, indicating the dysfunction of the hypothalamus. In thyrotropin-releasing hormone (TRH) load test, TSH and prolactin were normally secreted in response to TRH. In luteinizing hormone-releasing hormone (LHRH) load test, delayed reaction of LH and FSH (follicle stimulating hormone) was observed, which was also compatible with the possible dysfunction of the hypothalamus. Furthermore, in arginine load test, GH reaction was very poor, which strengthened the idea that the hypothalamus in this subject does not function well. Based on these findings, we diagnosed this subject as hypothalamic hypopituitarism although its cause remained unknown. In growth hormone-releasing hormone (GHRH) load test, GH reaction was poor. Although the results in this GHRH load test suggest the possibility of adult GH deficiency, serum IGF-1 (insulin-like growth factor-1) level was within normal range. Therefore, we followed up without any medication for this poor GH response.Figure 1


A case of hypothalamic hypopituitarism accompanied by recurrent severe hypoglycemia.

Takai M, Kaneto H, Kamei S, Mune T, Kaku K - Springerplus (2015)

Corticotropin-releasing hormone (CRH) load test: after intravenous injection of CRH (0.1 mg), ACTH and cortisol levels were examined. Thyrotropin-releasing hormone (TRH) load test: after intravenous injection of TRH (0.5 mg), TSH and PRL levels were examined. Luteinizing hormone-releasing hormone (LHRH) load test: after intravenous injection of LHRH (0.1 mg), LH and FSH levels were examined. Arginine load test: after intravenous injection of arginine (10%, 300ml), GH level was examined. Growth hormone releasing hormone (GHRH) load test: after intravenous injection of GHRH (0.1 mg), GH level was examined.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4402679&req=5

Fig1: Corticotropin-releasing hormone (CRH) load test: after intravenous injection of CRH (0.1 mg), ACTH and cortisol levels were examined. Thyrotropin-releasing hormone (TRH) load test: after intravenous injection of TRH (0.5 mg), TSH and PRL levels were examined. Luteinizing hormone-releasing hormone (LHRH) load test: after intravenous injection of LHRH (0.1 mg), LH and FSH levels were examined. Arginine load test: after intravenous injection of arginine (10%, 300ml), GH level was examined. Growth hormone releasing hormone (GHRH) load test: after intravenous injection of GHRH (0.1 mg), GH level was examined.
Mentions: To explore the pathogenesis of severe hypoglycemia, we performed several examination. First, magnetic resonance imaging (MRI) of the brain showed no obvious abnormalities; pituitary abnormality such as adenoma and pituitary stalk interruption was not observed. Second, we conducted several hormone load tests (FigureĀ 1). In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ACTH (adrenocorticotropic hormone) was observed, indicating the dysfunction of the hypothalamus. In thyrotropin-releasing hormone (TRH) load test, TSH and prolactin were normally secreted in response to TRH. In luteinizing hormone-releasing hormone (LHRH) load test, delayed reaction of LH and FSH (follicle stimulating hormone) was observed, which was also compatible with the possible dysfunction of the hypothalamus. Furthermore, in arginine load test, GH reaction was very poor, which strengthened the idea that the hypothalamus in this subject does not function well. Based on these findings, we diagnosed this subject as hypothalamic hypopituitarism although its cause remained unknown. In growth hormone-releasing hormone (GHRH) load test, GH reaction was poor. Although the results in this GHRH load test suggest the possibility of adult GH deficiency, serum IGF-1 (insulin-like growth factor-1) level was within normal range. Therefore, we followed up without any medication for this poor GH response.Figure 1

Bottom Line: Therefore, we stopped hydrocortisone and instead started an alternative treatment with prednisolone.We diagnosed this subject as hypothalamic hypopituitarism mainly by the following two findings: (1) excess and delayed reaction of ACTH in CRH load test, (2) delayed reaction of LH and FSH in LHRH load test.We should be aware of the possibility of hypothalamic hypopituitarism as a cause of recurrent severe hypoglycemia.

View Article: PubMed Central - PubMed

Affiliation: Division of Diabetes, Metabolism and Endocrinology, Kawasaki Medical School, 577 Matsushima, Kurashiki, 701-0192 Japan.

ABSTRACT

Introduction: Hypothalamic hypopituitarism is relatively rare cause of secondary adrenal deficiency which is often accompanied by severe hypoglycemia. Hydrocortisone replacement therapy is essential for this condition, but gastrointestinal symptom such as nausea and vomiting is not well-recognized adverse effect of hydrocortisone.

Case description: A 64-year-old-woman was referred to our hospital because of frequent severe hypoglycemia. She was diagnosed as type 2 diabetes when she was 58 years old but had not been treated since she was 60. We ruled out the possibility of exogenous administration of insulin or other anti-diabetic drugs, insulinoma and insulin autoimmune syndrome. After glucose injection, she once became conscious, but severe hypoglycemia was often observed even after that. In addition, counter-regulatory hormone levels were not increased even at the time of hypoglycemia. We conducted several hormone load tests. In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ACTH was observed. In thyrotropin-releasing hormone (TRH) load test, TSH and prolactin were normally secreted in response to TRH. In luteinizing hormone-releasing hormone (LHRH) load test, delayed reaction of LH and FSH was observed. Based on such hormone loading tests, we diagnosed this patient as idiopathic hypothalamic hypopituitarism and consequent adrenal deficiency. We immediately intravenously injected hydrocortisone and started oral hydrocortisone therapy. However, just after taking hydrocortisone, vomiting was often observed which disturbed sufficient steroid hormone replacement, leading to recurrent hypoglycemia. Therefore, we stopped hydrocortisone and instead started an alternative treatment with prednisolone. After that, vomiting and hypoglycemia were not observed at all.

Discussion and evaluation: We diagnosed this subject as hypothalamic hypopituitarism mainly by the following two findings: (1) excess and delayed reaction of ACTH in CRH load test, (2) delayed reaction of LH and FSH in LHRH load test.

Conclusions: We should be aware of the possibility of hypothalamic hypopituitarism as a cause of recurrent severe hypoglycemia. Also, we should be aware that hydrocortisone could induce gastrointestinal symptom and that in such a case we should stop hydrocortisone and start prednisolone to sufficiently replace steroid hormone and avoid recurrent hypoglycemia.

No MeSH data available.


Related in: MedlinePlus