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clinmed/2000010004v1 (March 21, 2000)
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Introduction
Disorders of thyroid are second in frequency to diabetes mellitus in our endocrine services. We report a man with primary hypothyroidism who developed diabetes mellitus, and who then went on to spontaneously become thyrotoxic.
Case report
A 39-year-old man presented with diabetes mellitus, diagnosed six months ago. He was on a schedule of diet and exercise, and glipizide tablet 2.5 mg a day. On inquiry as part of our computerized symptom checklist he admitted to weakness, weight loss, difficulty in falling asleep and body pains. He was not hypertensive nor did he have coronary heart disease. He neither smoked cigarettes nor consumed alcoholic beverages. There was family history of adult onset diabetes mellitus.
He was diagnosed to have primary hypothyroidism three years ago. The clinical features of weight gain, weakness, excessive daytime somnolence, constipation were consistent with lab investigations (Table 1). He was started on thyroxine replacement with which he improved clinically, and the thyroid hormone levels were normalized (Table 1).
On examination he had a pulse rate of 100 beats a minute. Blood pressure was 130/80 mm Hg right upper limb when sitting and 140/90 mm Hg when standing. He weighed 61.05 kg and had a body mass index of 22.15. He had grade 1 goiter (30 gm) and was clinically euthyroid. Laboratory investigations for diabetes mellitus were normal (Table 1).
The clinical diagnosis was adult onset diabetes mellitus, with primary hypothyroidism, on adequate replacement with thyroxine. He was prescribed a schedule of diet and exercise, asked to stop the oral hypoglycemic agent, and continue thyroxine in a dose of 150 ug a day.
Ten months later his postprandial blood glucose was normal, but he had lost weight (58.95 kg). He was advised to increase the caloric intake and follow the same line of treatment. Seven months later he weighed 59.55 kg and had clinical signs and symptoms of thyrotoxicosis (Table 1).
He was started on carbimazole (30 mg/day) with which he became euthyroid. On stopping carbimazole, thyrotoxicosis recurred.
He continues to be euthyroid three and a half years later, with carbimazole, 15 mg a day. His thyroid microsomal antibody is positive at a dilution of 1:25,600. Antithyroglobulin antibodies are negative (1:40).
Discussion
Diabetes mellitus (DM) is the most common group of disorders presenting to our endocrine services, followed by thyroid disorders (8225 consecutive persons with DM, 1777 with thyroid disorders). The association of autoimmune thyroid disorders with type 1 diabetes mellitus is well known (1), whereas thyroid disorders were present in 6.9% of a randomly selected group of adult diabetic patients in Edinburgh (2). Type 2 diabetes was seen in 7.6% of 747 patients with Grave’s thyrotoxicosis in Japan.
In our own prospective computerized database of individuals with endocrine diseases, among 8225 persons with diabetes mellitus, 73 had thyroid disorders (0.89%): 65 had hypothyroidism (65/73;89%), and eight thyrotoxicosis (8/73;11%). Out of 1777 persons with thyroid disorders 31 had diabetes mellitus (1.74%). Among these 31 with diabetes, 16 had hypothyroidism (51.6%), eight thyrotoxicosis (25.8%) and seven other conditions (subclinical hypothyroidism, multinodular goiter and euthyroid goiter).
There are anecdotal case reports of thyroid disorders in adults with diabetes being associated with Klinefelters syndrome (4), mitochondrial myopathy (5) and hypoparathyroidism (6). A variety of changes in pancreas and in carbohydrate metabolism are reported in thyroid disorders (7,8,9).
What could be responsible for the occurrence of thyroid dysfunction in type 2 diabetes? Primarily the association appears to be unexplained. Factors such as increasing age, when the prevalence of thyroid diseases increases, as well as some type 2 diabetic patients actually being slow-onset type 1 diabetic were implicated (2). There is some preliminary evidence for consanguinity being responsible for the coexistence of adult onset diabetes with other autoimmune disorders (10). Earlier we had shown that consanguinity was present in 23% of 321 individuals (n: 74) with diabetes mellitus (11).
The natural history of thyrotoxicosis going into hypothyroidism is logical and not unexpected. However the reverse process is unusual, and is likely due to the switch of blocking antibodies causing hypothyroidism, being replaced by stimulatory antibodies to TSH and resultant hyperthyroidism (12).
In summary an adult with primary hypothyroidism developed diabetes mellitus, and then went on to spontaneously become thyrotoxic.
References:
Table 1
Date Weight Investigations Treatment
(day/mo/y) (kg)
23-9-91 - T3:0.68 ng/ml[0.7-2] Thyroxine:100 ug
T4: undetectable
TSH: 96 miu/ml[0.25-4.3]
7-12-93 - T3 1 ng/ml[0.8-1.6] Thyroxine:100 ug
T4:6 ug/dl[5-11.5]
22-9-94 61.05 Fasting BS:94/dl;PPBS:97 Add: Diet+exercs
Cholesterol 121 mg/dl, trigly-
cerides 90 mg/dl
13-7-95 58.95 PPBS: 112 mg/dl Do
16-1-96 - PPBS: 212 mg/dl Do
26-2-96 59.55 T3:7.05 ng/ml Add
T4:27.28 ug/dl Carbmzl 25 mg/d
19-4-96 62.35 - Do
26-7-96 63.9 FBS: 101 mg/dl Do
PPBS: 183 mg/dl
20-12-96 67.2 FBS: 85 mg/dl Do
Chol: 135 mg/dl
Triglyc:118 mg/dl
15-9-97 65.0 FBS: 99 mg/dl Do
Chol: 135 mg/dl
Triglyc:92 mg/dl
T4:12.14 ug/dl
23-1-98 66.55 FBS: 96 mg/dl Carbimazole
Chol: 125 mg/dl 15 mg/d
Triglyc:85 mg/dl
Thyroid microsomal
antibodies: (+)
1:25,600
6-5-98 65.85 FBS 89 mg/dl Carbimazole
Chol 134 mg/dl 20 mg/d
T4:9.61 ug/dl
TSH: 0.5 uu/ml Chicken pox+
16/10/98 67.25 T4:11.21 ug/dl Carbimazole
TSH: 0.25 uu/ml 10 mg/dl
FBS: 120 mg/dl
20-3-99 67.1 FBS: 152 mg/dl Carbimazole
T4:16.7 ug/dl 20 mg/dl
18-9-99 69.65 FBS:104 mg/dl Carbimazole
T4:12.21 ug/dl[Aug 99] 20 mg/dl
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