Letter to the Editor

Acta Medica Anatolia

Volume 2 Issue 3 2014

Graves Disease Associated with Severe Hypoalbuminemia

1

Hacer Sen , Emine Binnetoglu , Fahri Gnes , Gkhan Erbag , Mehmet Ask , Neslihan Bozkurt , Erdem Akbal
1

Department of Internal Medicine, Canakkale Onsekiz Mart University Faculty of Medicine, Canakkale, Turkey.
Department of Endocrinology, Canakkale Onsekiz Mart University Faculty of Medicine, Canakkale, Turkey.
3
Department of Gastroenterology, Canakkale Onsekiz Mart University Faculty of Medicine, Canakkale, Turkey.
2

Received: 10.02.2014

Accepted: 26.02.2014

Acta Medica Anatolia

Dear Editor,

Thyrotoxicosis is a common disorder and generally

caused by Graves disease, thyroiditis, and toxic
nodule goiter while hyperthyroidism especially refers
to increased thyroid hormone synthesis and secretion
(1). A number of diverse organ systems are affected by
the excess of thyroid hormone. The basal metabolism
acceleration can result in abnormalities of such
biochemical parameters as glucose, lipid and protein.
We report a rare case of severe hypoalbuminemia
with thyroid storm. As far as we know, this is the first
case of severe hypoalbuminemia due to thyrotoxicosis
in the literature.
41 years old female patient with the diagnosis of
Graves disease had been followed up for 16 years.
However she didnt have a regular control and drug
use in the last one year. She referred to hospital with
palpitation, dyspnea and complaints of discomfort.
Her temperature was 38.3 C, arterial blood pressure
was 178/88mmHg, irregular heart rate was
140beats/min, respiratory rate was 22 breaths/min
during the examination. Blood analysis revealed TSH
of 0.005 IU/ ml (normal ranges 0.2 to 4.4), FT3 of 10.9
pg/ml ( normal ranges 2 to 4.4), FT4 of 3.5 pg/ml (
normal range 0.9 to 1.7) , A-TPO of 600 IU/ml, A-TG of
4000 IU/ ml.) The other routine examinations revealed
postprandial blood glucose 158 mg/dl, ALT: 16 U/L,
AST: 23 U/L, total-protein: 4.7 g/dl, albumin: 1.8 g/dl,
urea: 49 mg / dl, creatinine: 0.6mg/dl. The patient was
hospitalized with the diagnosis of thyrotoxic crisis. No
proteinuria was detected in 24-hour urine analysis.
Acute-phase reactant levels were normal. Antiendomysium and antigliadin antibodies were negative.
Upper gastrointestinal endoscopy revealed normal
mucosal findings. She was treated with large doses of
propylthiouracil, propranolol, lithium, Lugol's solution
and dexamethasone. On the fourth day of treatment,
TSH of 0.005 IU/ml, fT3 of 2,97 pg/ml, fT4 of 1.98
pg/ml and lithium of 1.02 mmol/L. After total
thyroidectomy, L-thyroxine was started 10 days post-

operatively. Levels of total protein and albumin

returned to normal in the follow-up.
Hyperthyroidism is a condition where glucose
turnover, energy expenditure, lipolysis, and protein
turnover are all higher than normal (2). The more
protein turnover goes up, the more protein
breakdown in all parts of the body and muscle protein
breakdown increase (2). Increased rates of proteolysis
with stable protein synthesis rates have been reported
in experimental hyperthyroidism (3).
Liver functions are affected in thyrotoxicosis and there
are changes in liver function tests in serum. Liver
failure in hyperthyroidism was first reported by
Haberson in 1874 (4). Hyperthyroidism affects
histology and metabolism of the liver (5). Elias RM et
al.(6) reviewed 40 patients with acute thyrotoxicosis.
Albumin and international normalized ratio (INR)
values were examined in order to evaluate liver
synthesis function. In the records of the patients with
thyrotoxic crisis, decrease in albumin was detected in
11 out of 40 patients, the lowest value was 2.9 g/dL.
Abnormal values of liver function tests returned to
normal in the patients following treatment. As it
comes to etiology of liver abnormalities in patients, it
can be stated that patients with acute thyrotoxicosis
suffer from direct thyroid hormone-mediated
hepatocyte damage (6).
Severe hypoalbuminemia (albumin: 1.8 g/dl) was
detected in our patient who has thyrotoxicosis in her
history for a long time. No pathology was detected
other than hepatocyte damage when we investigated
the etiology of hypoalbuminemia. This was also
supported by albumin values which returned normal
range following treatment.
In conclusion, severe hypoalbuminemia can occur in
many diseases. Long term progress of thyrotoxicosis is
a rare cause of hypoalbuminemia. So we suggested

Correspondence: Emine Binnetoglu MD, Canakkale Onsekiz Mart University Faculty Of Medicine, Canakkale, Turkey.
edemirbas1@yahoo.com

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Letter to the Editor

that patients with acute thyrotoxicosis should be
evaluated for direct thyroid hormone-mediated

Sen H et al.
hepatocyte damage which can result with severe
hypoalbuminemia.

References
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2. Riis AL, Jrgensen JO, Ivarsen P, Frystyk J, Weeke J,

Mller N. Increased Protein Turnover and Proteolysis Is an
Early and Primary Feature of Short-Term Experimental
Hyperthyroidism in Healthy Women. J Clin Endocrinol
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4. Habershon S. Guy's Hospital. Exophthalmic goitre, heart

disease, jaundice, death. The Lancet. 1874;103(2641):p.
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3. Riis AL, Jrgensen JO, Gjedde S, Nrrelund H, Jurik AG,

Nair KS et al. Whole body and forearm substrate
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Acta Med Anatol 2014;2(3):111-112

5. Piper J, Poulsen E. Liver biopsy in thyrotoxicosis. Acta

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