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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 14  |  Issue : 3  |  Page : 127-129

Recurrent hypoglycemia: An unusual finding of hypothyroidism


1 Department of Medicine, PGIMS, Rohtak, Haryana, India
2 Department of Obstetrics and Gynecology, PGIMS, Rohtak, Haryana, India

Date of Web Publication9-Oct-2017

Correspondence Address:
Jaikrit Bhutani
121-B, Model Town, Karnal, Haryana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/trp.trp_35_17

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  Abstract 

Hypothyroidism is one of the most prevalent endocrine disorders in the world, with a sharp rising incidence. The evaluation of recurrent hypoglycemia in the light of hypothyroidism still remains a major diagnostic challenge for most clinicians. We report a rare case of hypothyroidism presenting as recurrent hypoglycemia with relative adrenal insufficiency. Blunting of hypophyseal–pituitary–adrenal axis, pituitary dysfunction, delayed gastric emptying, decreased production and effect of glucagon on hepatocytes, reduced insulin clearance, gluconeogenesis, and glycogenolysis in patients with hypothyroidism may be the plausible mechanisms of hypoglycemia in such individuals. This will enable clinicians to consider thyroid dysfunction while evaluating causes of hypoglycemia in individuals without diabetes mellitus or treating unexplained hypoglycemic episodes in individuals with diabetes.

Keywords: Low blood glucose, relative adrenal insufficiency, thyroid disorders


How to cite this article:
Yadav TC, Bhutani J, Upadhyay M, Raghunandan S K. Recurrent hypoglycemia: An unusual finding of hypothyroidism. Thyroid Res Pract 2017;14:127-9

How to cite this URL:
Yadav TC, Bhutani J, Upadhyay M, Raghunandan S K. Recurrent hypoglycemia: An unusual finding of hypothyroidism. Thyroid Res Pract [serial online] 2017 [cited 2019 Sep 18];14:127-9. Available from: http://www.thetrp.net/text.asp?2017/14/3/127/216212


  Introduction Top


Hypothyroidism is one of the most prevalent endocrine disorders in the world, with a sharp rising incidence.[1] Hypoglycemia has not been described as a typical presenting feature of hypothyroidism in most existing literature, including major thyroidology textbooks.[2] Recent reviewers have emphasized hypothyroidism to be an endocrinopathy responsible for hypoglycemia.[3] This concept has also been rejected by other researchers, who continue to believe that should hypoglycemia exist in the setting of hypothyroidism, it is a manifestation of panhypopituitarism instead of primary thyroid pathology.[4] There have been case reports earlier that link hypoglycemia with congenital hypothyroidism and editorials highlighting the importance of screening for hypothyroidism in hypoglycemic participants.[5] However, the evaluation of recurrent hypoglycemia in the light of hypothyroidism still remains a major diagnostic challenge for most clinicians.

We report a rare case of hypothyroidism presenting as recurrent hypoglycemia with relative adrenal insufficiency.


  Case Report Top


A 32-year-old female, not a known case of any chronic illness, presented to the emergency service of the Department of Medicine, PGIMS Rohtak, with complaints of generalized fatigue, weakness, and repeated episodes of palpitation and sweating, at intervals of 6–8 h, for 2 weeks. Further enquiring the history, she reported amenorrhea for the past 3 months. There was no other significant history pertaining to hypoglycemia. On examination, her general condition and vitals were stable, and all systemic examination was within normal limits.

Baseline electrocardiogram and chest skiagram were obtained and were normal. Her random plasma glucose was found to be 24 mg/dL. A simultaneous venous sample collected in sodium fluoride vial, processed immediately revealed blood glucose to be 20 mg/dL. Immediate correction of hypoglycemia was done with 25% dextrose solution, and strict glucose monitoring was initiated. After relief of symptoms, she was further evaluated for further causes of hypoglycemia. Pharmacological or toxicological screens for causes of hypoglycemia returned negative. The patient developed similar episode of hypoglycemia (blood glucose level – 37 mg/dL) 6 h later and was corrected as before. These episodes continued to recur at intervals of 6 h. During one of these episodes, blood samples were drawn for serum insulin and C-peptide levels. A low plasma insulin and C-peptide level measured by immunochemiluminometric assay ruled out exogenous insulin administration or presence of an insulinoma or islet cell hypertrophy. To rule out nonislet cell tumors causing hypoglycemia, a contrast-enhanced computed tomography (CECT) of the abdomen was done, which did not reveal any abnormal pathology.

Further, while evaluating for abnormalities in hypothalamic–pituitary–adrenal (HPA) axis as a cause of hypoglycemia, basal morning 8 am cortisol and adrenocorticotropic hormone (ACTH) tests were done. While cortisol levels were markedly reduced, ACTH levels were borderline and on the higher end. A high-dose ACTH stimulation test revealed adequate rise in ACTH levels; however, cortisol remained markedly low. The presence of very long-chain fatty acids and antibodies against 21-hydroxylase in serum returned negative, thus eliminating autoimmune causes and adrenoleukodystrophy. For ruling out other adrenal pathologies, a repeat CECT abdomen was done focusing on adrenals which turned out to be normal. Since the patient had no hypotensive crisis or other symptoms of acute adrenal insufficiency, a provisional diagnosis of relative primary adrenal insufficiency (PAI) was considered.

Treatment was initiated for relative PAI, with 6 hourly 100 mg hydrocortisone. Despite therapy, hypoglycemic episodes continued to occur at similar intervals. After unsuccessful 1 week of therapy with hydrocortisone, a thyroid profile, follicle-stimulating hormone, luteinizing hormone levels, and magnetic resonance imaging of the brain was ordered for the completeness of workup of adrenal insufficiency. Everything returned normal except thyroid profile which revealed thyroid-stimulating hormone (TSH) to be elevated (40.75 μIU/ml), and total T3 (0.34 ng/ml) and total T4 (1.40 mcg/dL) were reduced. Thyroid replacement was initiated at a dose of 50 mcg/day, appropriate to the patient's body weight. Within 1 week, the patient improved symptomatically and hypoglycemic episodes reduced to twice a day. Hydrocortisone was tapered off as no hypoglycemia occurred, and the patient was discharged on only 50 mcg of thyroxine.

The patient visited for follow-up after 6 weeks in the outpatient department and was symptom free. Basal cortisol, ACTH, TSH, T3, and T4 levels were repeated and were within normal range. The reported laboratory values before and after thyroid replacement are summarized in [Table 1].
Table 1: Laboratory parameters before and after thyroid replacement

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  Discussion Top


Hypoglycemia is a common presenting complaint in the endocrine clinic. Although harmful, it is an unavoidable part of treatment of both type 1 and type 2 diabetes mellitus, irrespective of the use of insulin, or oral glucose-lowering drugs.[1] Another common endocrine disorder, hypothyroidism, is linked with numerous neurohormonal, metabolic, and nervous derangements which may lead to hypoglycemia.

Blunting of HPA axis in hypothyroid people has been well demonstrated. These patients are susceptible to develop relative adrenal insufficiency, if not primary adrenal failure.[6] Counter regulatory release of cortisol in response to insulin-induced hypoglycemia is also blunted in such cases leading to further worsening. Furthermore, it has been shown that pituitary dysfunction leading to rather thyroid dysfunction may actually be a consequence of primary hypothyroidism. It has been shown that hypothyroidism leads to reduction in both basal and stimulated growth hormone by acting on both hypothalamus and pituitary.[7] A similar hypothesis can explain the low basal and stimulated cortisol levels in our case. The process of gluconeogenesis and glycogenolysis is also impaired in hypothyroidism, both in skeletal muscle and in adipose tissue.[8]

Other less significant metabolic abnormalities in hypothyroidism include reduced glucagon production and its action on hepatocytes [9] and reduced insulin clearance.[10] The gastrointestinal system is also affected, with delayed gastric emptying, decreased intestinal glucose absorption, and portal venous flow.[11] These biochemical disturbances together may be responsible for hypoglycemia in hypothyroid persons.

Thus, it maybe clinically relevant for all patients with or without diabetes, and hypoglycemia to undergo screening for hypothyroidism, and vice versa as these metabolic disorders may coexist and affect the treatment strategy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Unnikrishnan AG, Menon UV. Thyroid disorders in India: An epidemiological perspective. Indian J Endocrinol Metab 2011;15 Suppl 2:S78-81.  Back to cited text no. 1
    
2.
McDermott MT. Overview of the clinical manifestations of hypothyroidism. In: Braverman LE, Cooper DS, editors. Werner and Ingbar's The Thyroid: A Fundamental and Clinical Text. 10th ed. New Delhi, Philadelphia: Lippincott William and Wilkins; 2013.  Back to cited text no. 2
    
3.
Samaan NA. Hypoglycemia secondary to endocrine deficiencies. Endocrinol Metab Clin North Am 1989;18:145-54.  Back to cited text no. 3
    
4.
Saleh M, Grunberger G. Hypoglycemia: An excuse for poor glycemic control? Clin Diabetes 2001;19:161-7.  Back to cited text no. 4
    
5.
Shibutani Y, Yokota T. A case of acetohexamide-induced hypoglycemia: The influence of hypothyroidism on the metabolism of acetohexamide. Nihon Naibunpi Gakkai Zasshi 1991;67:42-9.  Back to cited text no. 5
    
6.
Kamilaris TC, DeBold CR, Pavlou SN, Island DP, Hoursanidis A, Orth DN. Effect of altered thyroid hormone levels on hypothalamic-pituitary-adrenal function. J Clin Endocrinol Metab 1987;65:994-9.  Back to cited text no. 6
    
7.
Katz HP, Youlton R, Kaplan SL, Grumbach MM. Growth and growth hormone 3. Growth hormone release in children with primary hypothyroidism and thyrotoxicosis. J Clin Endocrinol Metab 1969;29:346-51.  Back to cited text no. 7
    
8.
McCulloch AJ, Johnston DG, Baylis PH, Kendall-Taylor P, Clark F, Young ET, et al. Evidence that thyroid hormones regulate gluconeogenesis from glycerol in man. Clin Endocrinol (Oxf) 1983;19:67-76.  Back to cited text no. 8
    
9.
Clausen N, Lins PE, Adamson U, Hamberger B, Efendic S. Counterregulation of insulin-induced hypoglycaemia in primary hypothyroidism. Acta Endocrinol (Copenh) 1986;111:516-21.  Back to cited text no. 9
    
10.
Shah JH, Motto GS, Papagiannes E, Williams GA. Insulin metabolism in hypothyroidism. Diabetes 1975;24:922-5.  Back to cited text no. 10
    
11.
Holdsworth CD, Besser GM. Influence of gastric emptying-rate and of insulin response on oral glucose tolerance in thyroid disease. Lancet 1968;2:700-2.  Back to cited text no. 11
    



 
 
    Tables

  [Table 1]


This article has been cited by
1 Refractory hypoglycemia in an infant with isolated severe primary hypothyroidism
Shreya Sharma,Sudha Rao Chandrashekhar
Hormones. 2019;
[Pubmed] | [DOI]



 

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