Letter to the Editor Acta Medica Anatolia Volume 2 Issue 3 2014

Graves‘ Disease Associated with Severe Hypoalbuminemia

Hacer Sen1, Emine Binnetoglu1, Fahri Günes1, Gökhan Erbag1, Mehmet Asık2, Neslihan Bozkurt1, Erdem Akbal3 1 Department of Internal Medicine, Canakkale Onsekiz Mart University Faculty of Medicine, Canakkale, Turkey. 2 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.

Received: 10.02.2014 Accepted: 26.02.2014 Acta Medica Anatolia Dear Editor,

Thyrotoxicosis is a common disorder and generally operatively. Levels of total protein and albumin caused by Graves’ disease, thyroiditis, and toxic returned to normal in the follow-up. nodule goiter while hyperthyroidism especially refers to increased thyroid hormone synthesis and secretion Hyperthyroidism is a condition where glucose (1). A number of diverse organ systems are affected by turnover, energy expenditure, lipolysis, and protein the excess of thyroid hormone. The basal metabolism turnover are all higher than normal (2). The more acceleration can result in abnormalities of such protein turnover goes up, the more protein biochemical parameters as glucose, lipid and protein. breakdown in all parts of the body and muscle protein We report a rare case of severe hypoalbuminemia breakdown increase (2). Increased rates of proteolysis with thyroid storm. As far as we know, this is the first with stable protein synthesis rates have been reported case of severe hypoalbuminemia due to thyrotoxicosis in experimental hyperthyroidism (3). in the literature. Liver functions are affected in thyrotoxicosis and there 41 years old female patient with the diagnosis of are changes in liver function tests in serum. Liver Graves’ disease had been followed up for 16 years. failure in hyperthyroidism was first reported by However she didn’t have a regular control and drug Haberson in 1874 (4). Hyperthyroidism affects use in the last one year. She referred to hospital with histology and metabolism of the liver (5). Elias RM et palpitation, dyspnea and complaints of discomfort. al.(6) reviewed 40 patients with acute thyrotoxicosis. Her temperature was 38.3 °C, arterial blood pressure Albumin and international normalized ratio (INR) was 178/88mmHg, irregular heart rate was values were examined in order to evaluate liver 140beats/min, respiratory rate was 22 breaths/min synthesis function. In the records of the patients with during the examination. Blood analysis revealed TSH thyrotoxic crisis, decrease in albumin was detected in of 0.005 IU/ ml (normal ranges 0.2 to 4.4), FT3 of 10.9 11 out of 40 patients, the lowest value was 2.9 g/dL. pg/ml ( normal ranges 2 to 4.4), FT4 of 3.5 pg/ml ( Abnormal values of liver function tests returned to normal range 0.9 to 1.7) , A-TPO of 600 IU/ml, A-TG of normal in the patients following treatment. As it 4000 IU/ ml.) The other routine examinations revealed comes to etiology of liver abnormalities in patients, it postprandial blood glucose 158 mg/dl, ALT: 16 U/L, can be stated that patients with acute thyrotoxicosis AST: 23 U/L, total-protein: 4.7 g/dl, albumin: 1.8 g/dl, suffer from direct thyroid hormone-mediated urea: 49 mg / dl, creatinine: 0.6mg/dl. The patient was hepatocyte damage (6). hospitalized with the diagnosis of thyrotoxic crisis. No proteinuria was detected in 24-hour urine analysis. Severe hypoalbuminemia (albumin: 1.8 g/dl) was Acute-phase reactant levels were normal. Anti- detected in our patient who has thyrotoxicosis in her endomysium and antigliadin antibodies were negative. history for a long time. No pathology was detected Upper gastrointestinal endoscopy revealed normal other than hepatocyte damage when we investigated mucosal findings. She was treated with large doses of the etiology of hypoalbuminemia. This was also propylthiouracil, propranolol, lithium, Lugol's solution supported by albumin values which returned normal and dexamethasone. On the fourth day of treatment, range following treatment. TSH of 0.005 IU/ml, fT3 of 2,97 pg/ml, fT4 of 1.98 In conclusion, severe hypoalbuminemia can occur in pg/ml and lithium of 1.02 mmol/L. After total many diseases. Long term progress of thyrotoxicosis is thyroidectomy, L-thyroxine was started 10 days post- a rare cause of hypoalbuminemia. So we suggested

Correspondence: Emine Binnetoglu MD, Canakkale Onsekiz Mart University Faculty Of Medicine, Canakkale, Turkey. 111 [email protected]

Letter to the Editor Sen H et al.

that patients with acute thyrotoxicosis should be hepatocyte damage which can result with severe evaluated for direct thyroid hormone-mediated hypoalbuminemia.

References

1. Franklyn JA, Boelaert K. Thyrotoxicosis. Lancet. 2012 Mar basal muscle protein breakdown.AmJ Physiol Endocrinol 24;379(9821):1155-66. Metab 2005 288:E1067–E1073 2. Riis AL, Jørgensen JO, Ivarsen P, Frystyk J, Weeke J, 4. Habershon S. Guy's Hospital. Exophthalmic goitre, heart Møller N. Increased Protein Turnover and Proteolysis Is an disease, jaundice, death. The Lancet. 1874;103(2641):p. Early and Primary Feature of Short-Term Experimental 510. Hyperthyroidism in Healthy Women. J Clin Endocrinol 5. Piper J, Poulsen E. Liver biopsy in thyrotoxicosis. Acta Metab. 2008 Oct;93(10):3999-4005. Medica Scandinavica. 1947;127(5):439–447. 3. Riis AL, Jørgensen JO, Gjedde S, Nørrelund H, Jurik AG, 6. Elias RM, Dean DS, Barsness GW. Hepatic dysfunction in Nair KS et al. Whole body and forearm substrate hospitalized patients with acute thyrotoxicosis: a decade of metabolism in hyperthyroidism: evidence of increased experience. Endocrinol. 2012;2012:325092.

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