scholarly journals Natural History of Growth Hormone Deficiency in a Pediatric Cohort

2015 ◽  
Vol 83 (4) ◽  
pp. 252-261 ◽  
Author(s):  
Eva Deillon ◽  
Michael Hauschild ◽  
Mohamed Faouzi ◽  
Sophie Stoppa-Vaucher ◽  
Eglantine Elowe-Gruau ◽  
...  
2012 ◽  
Vol 32 (1) ◽  
pp. 81-84
Author(s):  
SK Kota ◽  
S Jammula ◽  
PR Tripathy ◽  
Siva Krishna Kota ◽  
LK Meher ◽  
...  

Langerhans cell histiocytosis is a multi system disorder with a certain predilection for involving hypothalamic pituitary axis. We hereby report a 7 year old girl presenting with polyuria, polydipsia and growth retardation. The girl had a past history of pain in right hip joint and nodular region over chest. Water deprivation test confirmed the diagnosis of central diabetes inspidus. Other investigations revealed Growth hormone deficiency and central hypothyroidism. X-ray and MRI hip revealed absent right inferior pubic ramus with bone marrow biopsy confirming the diagnosis of histiocytosis. Patient was treated with nasal Arginine Vasopressin spray, subcutaneous growth hormone and oral thyroxine. Key words: Histiocytosis; Diabetes inspidus; Growth hormone deficiency; Central hypothyroidism DOI: http://dx.doi.org/10.3126/jnps.v32i1.5343 J. Nepal Paediatr. Soc. Vol.32(1) 2012 81-84


2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Rohan K. Henry ◽  
Ram K. Menon

In a seminal report, a 17-year-old boy with panhypopituitarism had fatty liver (FL) amelioration with growth hormone (GH). By extension, since hepatic insulin resistance (IR) is key to FL and type 2 diabetes mellitus (T2DM), GH then may ameliorate the IR of T2DM. We present a 17-year-old nonobese female with untreated childhood onset growth hormone deficiency (CO-GHD) who developed type 2 diabetes mellitus (T2DM) and steatohepatitis with bridging fibrosis. Based on height z-score of – 3.1 and a history of radiation therapy as treatment for a medulloblastoma at 7 years of age, GHD was quite likely. GH therapy was, however, not initiated at 15 years of age (when growth was concerning) based on full skeletal maturity. After she developed T2DM, GHD was confirmed and GH was initiated. With its initiation, though insulin dose decreased from 2.9 (~155 units) to 1.9 units/kg/day (~ 100 units), her T2DM was, however, not fully reversed. This illustrates the natural history of untreated CO-GHD and shows that though hepatic IR can be ameliorated by GH, full reversal of T2DM may be prevented with irreversible hepatic changes (fibrosis). Clinicians caring for pediatric patients and otherwise should remember that, even in patients beyond the cessation of linear growth, GH can have a crucial role in both glucose and lipid metabolism.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jeongju Hwang ◽  
Jeesuk Yu

Abstract Introduction: Sturge-Weber syndrome (SWS) is a congenital neurocutaneous disorder characterized by a port wine stain on the skin in the distribution of the ophthalmic branch of the trigeminal nerve (vascular malformation of skin), glaucoma, and leptomeningeal angiomas. Central nervous system abnormalities may increase the risk of hypothalamic-pituitary dysfunction. One previous study showed that SWS patients had higher prevalence of growth hormone deficiency than the general population although the etiology is unclear. This case report describes a patient who was initially diagnosed with SWS and later confirmed with complete growth hormone deficiency. Case: A 7-year-and-11-month-old boy who had been diagnosed with SWS visited a tertiary center for the evaluation of short stature [111.1cm (<3 percentile)]. He was born at 37 weeks of gestational age with birth weight of 3230g by cesarean section and had a port wine nevus on the right side of the face since birth. He had a history of epilepsy first occurring at 6 months of age when he was diagnosed with SWS. There were two more attacks of seizure till 32 months of age. Brain magnetic resonance imaging revealed leptomeningeal angioma, choroidal hemangioma, and diffuse brain atrophy. He was diagnosed with glaucoma and had been managed with surgery and medication. There was no family history of SWS or any other brain anomaly. His mid-parental height was 167.7cm. All blood tests were normal including complete blood count, chemistry, and thyroid function test. Hand x-ray showed delayed bone age. Cocktail test was performed for the evaluation of short stature. As a result, he was diagnosed with complete growth hormone deficiency (peak GH on L-dopa test: 2.46 ng/mL, peak GH on glucagon test: 3.71 ng/mL). The recombinant growth hormone therapy was started at the age of 8 years and 1 month. He showed good response to GH treatment. His height became 125.8cm at the age of 9 years and 5 months (height velocity 9.2 cm/year), and 134.3cm at the age of 10 years and 6 months. Conclusion: We experienced a case with Sturge-Weber syndrome and complete growth hormone deficiency which was successfully managed by recombinant growth hormone therapy. It may be better to consider the possibility of GH deficiency even if there are certain conditions that affect the growth itself.


PEDIATRICS ◽  
1982 ◽  
Vol 69 (4) ◽  
pp. 486-488
Author(s):  
Alan N. Lindsay ◽  
Margaret H. MacGillivray ◽  
Mary L. Voorhess

Idiopathic growth hormone deficiency is unusual in twin sibships. We report three twins with growth hormone deficiency whose co-twins are growing normally and have no evidence of hypothalamicpituitary dysfunction. It is likely that the affected children sustained perinatal insult. The data illustrate that idiopathic growth hormone deficiency should be considered in the differential diagnosis when there is a major discrepancy in height between twins. CASE REPORTS Case 1 Male twins I were born at 36 weeks' gestation to a 27-year-old gravida 3, para 2. There was no history of abnormal vaginal bleeding, infection or, toxemia. Labor was spontaneous and lasted two hours.


1977 ◽  
Vol 85 (4) ◽  
pp. 684-691 ◽  
Author(s):  
J. H. Vogt

ABSTRACT The case history of a woman born in 1946 is given. In 1968 she developed a syndrome of headache, fever, elevated antistreptolysin titer, enlarged and ballooned sella turcica, hypothyroidism secondary to TSH deficiency, secondary amenorrhoea of pituitary genesis, probable growth hormone deficiency, and secondary adrenocortical insufficiency. From 1972 all the mentioned pituitary defects of function disappeared, and the sella turcica gradually became normal in size as shown by X-ray examination.


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