scholarly journals Heat Intolerance and Hyperhidrosis as the only Presenting Manifestations of Acromegaly: A Case Report

Author(s):  
TN Kamalesh ◽  
HA Vijaya Sarathy ◽  
NT Sreedevi

Acromegaly is a state of Growth Hormone (GH) excess characterised by coarse facial features, acral enlargement, hyperhidrosis, headache, visual disturbances and visceromegaly. The most common cause of acromegaly is pituitary adenoma. The average delay between onset of symptoms and diagnosis is about six years in acromegaly owing to its subtle clinical features at the disease onset.Early diagnosis is important to reduce the morbidities and mortality associated with acromegaly. Familiarisation of physicians with the signs and symptoms of the disease is an effective strategy for the early diagnosis of acromegaly. Here, the authors report a case of 38year-old female patient. After proper clinical examination, history and series of relevant investigations, the serum GH level was estimated and was found to be elevated (40 ng/mL). GH secreting pituitary macroadenoma presenting with heat intolerance and hyperhidrosis without the classical manifestations of acromegaly.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hatem Eid

Abstract Introduction: Secreting pituitary adenoma is exceedingly rare. Less than 15 cases having been reported. Its clinical presentation and diagnosis is challenging. We report a case of pituitary macroadenoma, with features of acromegaly and hyperthyroidism. Case report: A 75 years’ old man presented with new onset atrial fibrillation. He had high FT4 with normal TSH. His ultrasound scan of the neck showed a solitary nodule. He had ablation twice and was started on bisoprolol and anticoagulant. He had MRI scan for headaches and this showed a pituitary macroadenoma. He had high IGF-1. His oral glucose tolerance showed failure of GH suppression. His FT4 was persistently high with normal TSH and he had high a subunits. This suggested the diagnosis of TSH and GH secreting pituitary adenoma. Discussion: TSH-secreting pituitary adenomas are rare and not uncommonly, they co-secrete other pituitary hormones including growth hormones. Somatotrophs and lactotrops share common transcription factors with thyrotrophs. TSH-secreting adenomas are benign but 60% of them are locally invasive. TSH-secreting pituitary adenomas typically present with either symptoms of tumor growth like headache or visual field disturbance or symptoms of hyperthyroidism. Thyroid nodules are common in patients with TSHomas. In patients with TSH-secreting pituitary adenomas, majority will need only surgery and radiation. The medical treatment used to normalize TSH and FT4 levels is somatostatin analogs. This is effective in about 90% of patients with TSH secreting pituitary adenomas TSHoma should be differentiated from resistance to thyroid (RTH). The main difference between TSHoma and RTH is the presence of signs and symptoms of hyperthyroidism in patients with TSHoma, absence of a family history, normal thyroid hormone levels in family members, and the presence of an elevated glycoprotein α-subunit in patients with pituitary tumor. Reference: H Adams and D Adams. A case of a co-secreting TSH and growth hormone pituitary adenoma presenting with a thyroid nodule. EDM case reports 2018 [email protected]


Author(s):  
Nicole Dound ◽  
Sandhya Pajai ◽  
Neema Acharya ◽  
Sourya Acharya ◽  
Chitra Dound

Apoplexy of the Pituitary gland is rarely seen critical disorder marked by acute throbbing of head / altered mental status / visual disturbances /decreased consciousness, due to sudden haemorrhagic changes of the pituitary or infarction of the same. There are numerous factors which precipitate apoplexy of the pituitary, sepsis being one of the least common cause, as is elaborated in this case study.  Inspite of having a distinctive presentation, pituitary apoplexy eludes diagnosis and proper management as it is complicated by related co-morbidities.  Its occurrence in a postpartum lady is an even rarer incident.  This article shows a rare occurrence of apoplexy of macroadenoma in a postpartum woman which was managed conservatively.


JMS SKIMS ◽  
2011 ◽  
Vol 14 (2) ◽  
pp. 75
Author(s):  
Shahnaz Ahmad Mir ◽  
Khalid J Farooqi ◽  
Manzoor Ahmad Bhat ◽  
Souman Koutwal ◽  
Shariq Rashid Masoodi

A 60-year-old woman was referred to our centre for evaluation of Acromegaly. Serum GH level was 60 ng/ml and remained unchanged after OGTT (75 g). Thyroid functions revealed normal TSH and T4 cortisol dynamics showed stimu-lated cortisol of 11 g/dl. MRI revealed pituitary macroadenoma associated with a frontal men ingioma ,JMS 2011;14(2):75  


Author(s):  
K. Kovacs ◽  
L. Stefaneanu ◽  
A. Mayerhofer ◽  
T. E. Wagner ◽  
A. Bartke

Acromegaly and gigantism are due to prolonged oversecretion of growth hormone (GH) most often caused by a somatotroph adenoma of the pituitary. Although the morphologic features of various types of somatotroph adenomas have been extensively investigated by electron microscopy, very little information is available on the ultrastructural changes of non-tumorous somatotrophs in cases of protracted GH excess. Transgenic mice with foreign GH gene incorporated into their genome secrete ectopically increased quantities of GH, have elevated serum GH levels and develop gigantism; thus it seemed conceivable that these animals represent a valuable experimental model to investigate the effects of GH excess on the ultrastructure of pituitary somatotrophs and lactotrophs, the two adenohypophysial cell types which are more likely affected by the foreign GH gene.


1984 ◽  
Vol 18 (11) ◽  
pp. 1206-1206
Author(s):  
A Grossman ◽  
M O Savage ◽  
A Blacklay ◽  
N Lytras ◽  
P N Plowman ◽  
...  

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Nami Mohammadian Khonsari ◽  
Sahar Mohammad Poor Nami ◽  
Benyamin Hakak-Zargar ◽  
Tessa Voth

Abstract Background Linear bone growth is achieved by the division of chondrocytes at the growth plate and is regulated by endocrine and paracrine factors such as growth hormone. Mutations that negatively affect chondrogenesis can be a contributor to short stature. One such mutation can occur in the ACAN gene, causing short stature and advanced bone age. Similarly, mutations in growth hormone receptors (GHR) can lead to Laron syndrome (LS), one of the several disorders that are collectively called growth hormone insensitivity syndrome (GHI). Another example is Floating-Harbor syndrome (FHS), a rare autosomal dominant due to mutations in the SRCAP gene that can also result in short stature. Case presentation We report the case of a 6-year-old female with concomitant mutations in the three genes mentioned above. The mutations reported here were found on genetic studies and are usually benign, causing a variant of undetermined significance. However, our patient’s phenotype could only be explained by the compounded effects of pathogenic mutations of these genes. Some of the same mutations were also found in the patient’s father and her paternal grandfather. Both also presented with short stature, though not to the same degree as our patient. While these mutations are often reported to be insignificant, they gave rise to severe short stature and a specific phenotype in the patient when presented together. We think that even though the GHI spectrum is inherited through an autosomal recessive pattern, the sum of these heterozygous mutations resulted in severe short stature despite the limited GHI seen in our patient, the father, and the grandfather, through a rare ACAN and SRCAP mutation that, to our knowledge, has not been previously reported as a pathogenic mutation in the literature. Conclusion We investigated the possible synergistic effects of these variations on exacerbation or masking of the signs and symptoms of GHI with the hope of providing a better understanding of these genes and their function through our rare case.


1996 ◽  
Vol 271 (2) ◽  
pp. E223-E231 ◽  
Author(s):  
L. Goya ◽  
F. Rivero ◽  
M. A. Martin ◽  
R. Arahuetes ◽  
E. R. Hernandez ◽  
...  

The effect of refeeding and insulin treatment of undernourished and diabetic neonatal rats, respectively, on the regulation of insulin-like growth factor (IGF) and insulin-like growth factor binding protein (IGFBP) was investigated. The changes in body weight, insulinemia, glycemia, serum IGF-I, and growth hormone (GH) as well as the increase of the 30-kDa IGFBP in undernourished and diabetic neonatal rats previously shown elsewhere were reversed by refeeding and insulin treatment, respectively. Also, changes in liver mRNA expression of IGF-I and-II and IGFBP-1 and -2 were restored in refed undernourished and IGF-I and IGFBP-1 levels recovered in insulin-treated diabetic rats. However, serum GH was still below normal after rehabilitation in both situations. Thus the present results support the idea of a GH-independent IGF/ IGFBP regulation mediated by a balance of insulin and nutrients as has already been suggested in previous neonatal studies.


1992 ◽  
Vol 126 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Geoffrey R Ambler ◽  
Bernhard H Breier ◽  
Andrzej Surus ◽  
Hugh T Blair ◽  
Stuart N McCutcheon ◽  
...  

We evaluated the interrelationship between, and regulation of, the hepatic growth hormone receptor and serum GH binding protein (GH BP) in pigs treated with recombinant porcine growth hormone (rpGH). Infant and pubertal male pigs (N = 5 per group) received either rpGH 0.15 mg/kg daily or diluent intramuscularly for 12 days. Somatic growth, serum IGF-I and GH BP and [125I]bovine GH (bGH) binding to MgCl2-treated hepatic membrane homogenates were examined. Marked age-related increases were seen in serum GH BP (p<0.001) and [125I]bGH binding to hepatic membranes (p<0.001). GH BP was increased in rpGH treated animals (p = 0.03), from 13.8±1.2 (mean±1 x sem) (controls) to 17.8±2.0% in infants, and from 35.2±2.6 (controls) to 41.8±3.4% in pubertal animals. [125I]bGH binding to hepatic membranes was also increased by rpGH treatment (p<0.05), from 7.0±1.6 (controls) to 15.4±3.6% in infants and from 53.7±7.1 (controls) to 65.1±11.8% in pubertal animals. No significant interaction between age and treatment was seen. Overall, serum GH BP correlated significantly with [125I]bGH membrane capacity (r=0.82, p<0.001), with a correlation of r= 0.83 in the infant animals but no significant correlation in the pubertal animals considered alone (r=0.13). Serum IGF-I correlated significantly with serum GH BP (r=0.93, p<0.001) and [125]bGH membrane binding capacity (r = 0.91, p< 0.001). These observations suggest that serum GH BP levels reflect major changes of hepatic GH receptor status. In addition, the present study demonstrates that the hepatic GH receptor can be induced by GH in the infant pig, despite a developmentally low GH receptor population at this age, suggesting potential efficacy of GH at earlier ages than generally considered.


PEDIATRICS ◽  
1971 ◽  
Vol 48 (2) ◽  
pp. 190-199
Author(s):  
James R. Humbert ◽  
Ronald W. Gotlin

Recent investigations have raised the possibility that growth hormone (GH) influences intra-uterine weight and length. Moreover, the hypoglycemic tendency of small for gestational age (FSGA) infants and their small size could result from GH deficiency. To verify these hypotheses, a prospective study of daily serum GH and glucose levels was conducted in 46 newborn infants, including 18 FSCA infants, 18-full-term, appropriate for gestational age (FAGA), and 10 premature (PR) infants. Two FSGA babies became hypoglycemic. Both manifested normal GH competence as evidenced by normal daily GH levels, adequate GH response to arginine provocation, and satisfactory growth for over 2 years. Eleven of 12 FSGA babies followed from 14 to 26 months showed no evidence of impaired linear growth. The FSGA babies had GH values similar in magnitude and pattern to those of FAGA and PR infants. During the second half of the first postnatal day, a significant rise in serum GH occurred in all infants regardless of their size or gestational age; this rise may be the result of the stimulating effect of early milk feedings. GH deficiency does not appear to contribute to either the small size or hypoglycemic tendency of FSGA newborn infants.


2013 ◽  
Vol 17 (4) ◽  
pp. 770
Author(s):  
ShariqRashid Masoodi ◽  
ShahnazAhmad Mir ◽  
KhalidJamal Farooqui ◽  
AbdulRashid Bhat ◽  
ArshadIqbal Wani ◽  
...  

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