A 58-year-old male with a history of hypertension, hypercholesterolemia, hyperuricemia, smoker of 40 cigarettes a day for 33 years, drinker of 25-30 units of alcohol a week for 3 years, paroxysmal atrial fibrillation.
The last review of her cardiological condition, five months before, showed that all complementary tests were within normal ranges (including thyroid hormones).
At the time of consultation, she was treated with enalapril 20 mg/day, chlorthalidone 25 mg/day, atorvastatin 10 mg/day, acetylsalicylic acid 200 mg/day and amiodarone 400 mg/day, except for
The patient began three weeks earlier with a constitutional condition dominated by significant asthenia and loss of appetite with weight loss of 8 kilograms (representing 10% of his body weight).
In addition, the patient reported significant weakness in the scapular and pelvic girdles, more striking in the first.
Another noteworthy finding was that the patient complained of insomnia with nervousness.
One week before the consultation she had a self-limited episode of diarrhea consisting of three liquid stools a day without pathological products or abdominal pain.
On physical examination, we found a patient with good general condition and good constants (TA 120/70 mm Hg, Ta 36.5 oC and 78 bpm, weight 74 kg), eupneic, well-nourished, and not eating.
Cardiopulmonary auscultation revealed no abnormalities.
In the abdomen, the liver was palpable 1.5 cm from the costal margin, with soft consistency and no other findings.
He had a mild bilateral pretibial oedema that left fovea under pressure with symmetrical preserved peripheral pulses.
platelet count: 4,640 leukocytes/ mm3 with normal count, 4.17 million with intact formula, HC/ mm3, Hb 12.7g/dl, H0.5to 233.
VSG 23 mm/h.
Biochemistry: glucose 83 mg/dl, creatinine 0.7 mg/dl, bilirubin 54 mg/dl, alkaline triglycerides transferrin 7.10 mg/dl, GGT 91 mg/dl, bilirubin 148 mg/dl Ferrat cholesterol 140 mg/dl
Chest radiography showed no significant changes.
Hepatitis serology: Ac HVC (-), Ac HB core (-), AcHBs (- ) and HAV Ig M (-) Serology of CMV : Ig M (-) and Ig G
Tumor Markers: alpha-fetoprotein, anti-cancer agent and pro-specific antigen total negative.
Abdominal ultrasound: diffuse alteration of hepatic echogenicity compatible with steatosis without space occupying lesions or other findings.
Colonoscopy up to the cecal pole showed no abnormalities.
Horizontal thyroid hormones: TSH 0.01 mIU/l (0.20-5.00), free T4 9.86 ng/dl (0.85-2.1).
DISCUSSION We are faced with a patient with a constitutional syndrome and impaired liver function tests.
It should be borne in mind that an increase in transaminase levels is a nonspecific phenomenon, which can occur in a large number of pathological situations and not always translates into liver disease.
The assessment and interpretation of hypertransaminasemia must always be made within the clinical context of the patient and the quantitative importance of its elevation as well as the time during which the anomaly persists must always be taken into account.
The high prevalence of viral enolism and hepatitis in our environment makes these etiologies to be ruled out.
We started the study with the confirmation of biochemical alterations since the first step should always be to repeat laboratory tests3 to rule out any errors.
We then carried out an exhaustive study where we found a history of moderate alcohol consumption (without stenosis for justifying alcoholic liver disease), use of atorvastatin can increase trans-signal risk without complete interest, liver disease, transfusion data.
With serology (first of hepatitis virus and later of other hepatotropic viruses such as cytomegalovirus and Epnstein virus in unlikely context), the possibility of viral hepatitis and others seemed unlikely.
Abdominal ultrasound shows an echogenic alteration of the liver compatible with hepatic steatosis (we should not forget that our patient has hypercholesterolemia and alcohol consumption) that, although it could justify the hepatic impairment, does not seem to justify the whole.
1.
Due to the age of the patient, the alteration of the intestinal habit and the elevation of ferritin, another diagnostic option that is raised is the tumoral etiology, although with ultrasound we had ruled out the presence of space occupying lesions, and
Another possibility would be hemochromatosis, but there are no other suggestive data (articular, myocardial, gonadal, cutaneous, etc.) or family history suggestive of the disease, and transferrin saturation should not support the diagnosis.
Before resorting to other more complex and costly studies, it was decided to repeat the determination of thyroid hormones, despite having a rigorously normal study five months before, because the patient continued on treatment with amiodarone.
The results were compatible with the diagnosis of hyperthyroidism in a patient treated with amiodarone.
The attitude we followed was to withdraw the drug and start treatment with methimazole and beta-blockers to control their arrhythmia.
1.
Amiodarone is a class III antiarrhythmic whose molecular structure is very similar to triiodothyronine.
It contains two iodine atoms, which confers 2% iodine weight.
This means that with a maintenance dose of 200 to 600 mg, 75 to 225 mg/day of iodine are administered.
This excess of iodine may have consequences on thyroid physiology.
On the other hand, we must bear in mind that it is a very lipophilic molecule, which gives it a very long half-life (22-55 days), being detected in plasma up to 9 months after drug withdrawal.
Treatment with amiodarone causes a series of changes in thyroid hormones consisting of an increase in total and free T4 and of rT3, a decrease in total T3 tends to be normal at an early stage and TSH persists after an initial increase.
These changes occur in more than 50% of patients treated with amiodarone, with no clinical relevance (euthyroid status).
The incidence of thyroid dysfunction ranges from 2 to 24%.
In our environment the incidence of amiodarone thyrotoxicosis is around 1.5% and is more frequent in iodine deficient areas.
Two different pathophysiological mechanisms have been described6: Type I: it occurs on thyroid with underlying pathology with an alteration in the self-regulating mechanism of iodine uptake that would lead to increased synthesis of thyroid hormone.
Type II: it occurs on apparently normal glands, without goiter and with negative antithyroid antibodies and TSH receptor.
The mechanism would be a cytotoxicity induced by amiodarone or iodine.
The most common clinical manifestation in these cases is usually a worsening of the underlying heart disease, although classical symptoms of hyperthyroidism may exist.
Sometimes the course of the disease is self-limiting, resolving the situation after withdrawal of amiodarone and without additional treatment, although generally after long periods of time.
The resolution of the condition is earlier when there is no underlying pathology.
Treatment includes thionamides that may be associated with potassium perchlorate to achieve a rapid discharge of intrathyroid iodine increasing its efficacy, corticosteroids, plasmapheresis in cases of thyrotoxic crisis in the host.
Bartalena has proposed specific treatment according to type.
In type I, in which there is an increased thyroid hormone synthesis, the treatment of choice would be antithyroid drugs together with potassium perchlorate, while corticosteroids would have a limited role.
However, in type II, in which the fundamental mechanism is tissue destruction, the treatment of choice would be corticoids in high doses, because of their anti-inflammatory and stabilizer membrane effects.
Surgery is indicated in severe cases with potentially lethal arrhythmias for patients requiring rapid solution, when amiodarone cannot be withdrawn and when resistance to medical treatment has been demonstrated.
Total or near-total thyroidectomy should be performed especially in patients who are going to follow amiodarone treatment.
BACKGROUND: Carmen G. Suárez Álvarez Hospitalization Unit to Home Fundación Jiménez Díaz Avda.
Reyes Catolic, 2 28040 Madrid
