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© Borgis - Postępy Nauk Medycznych 12/2017, s. 660-664 | DOI: 10.25121/PNM.2017.30.12.660
Agnieszka Majos1, Dorota Leszczyńska1, Jarosław Kozakowski2, Małgorzata Gietka-Czernel2
Marine-Lenhart syndrom
Zespół Marine-Lenharta
1Department of Endocrinology, Bielański Hospital, Warsaw
Head of Department: Professor Wojciech Zgliczyński, MD, PhD
2Department of Endocrinology, Centre Bielański Hospital of Postgraduate Medical Education, Warsaw
Head of Department: Professor Wojciech Zgliczyński, MD, PhD
Streszczenie
Nadczynność tarczycy dotyczy ok. 2% populacji. Najczęstszymi jej przyczynami, w zależności od podaży jodu, są choroba Gravesa i Basedowa oraz wole guzowate nadczynne. U pacjentów z chorobą Gravesa i Basedowa obserwuje się częstsze występowanie guzków tarczycy niż w populacji ogólnej, większość z nich stanowią guzki nieczynne hormonalnie. Do rzadkości należy współistnienie choroby Gravesa i Basedowa oraz pojedynczego lub mnogich guzków autonomicznych nazywane zespołem Marine-Lenharta – dotyczy jedynie 2,4-4,1% osób z chorobą Gravesa i Basedowa. Celem pracy jest prezentacja przypadku pacjentki z zespołem Marine-Lenharta oraz analiza podobnych przypadków dostępnych w bazie PubMed od 2000 roku.
Czterdzistoletnia kobieta ze zdiagnozowanym w przeszłości guzkiem autonomicznym tarczycy została przyjęta do Poradni przy Klinice Endokrynologii CMKP w Warszawie z objawami ciężkiej nadczynności tarczycy w przebiegu choroby Gravesa i Basedowa. W artykule przedstawiono i przedyskutowano kolejne kroki diagnostyczne i metody leczenia. Przeanalizowano także inne dostępne w piśmiennictwie przypadki zespołu Marine-Lenharta. Wskazują one na trudności diagnostyczne wynikające ze zmienności obrazu scyntygraficznego guzków oraz miąższu tarczycy. Dlatego dokładna obserwacja kliniczna w połączeniu z oceną stężenia przeciwciał przeciwko receptorowi dla TSH oraz metodami obrazowania tarczycy – ultrasonografią i scyntygrafią – są niezbędne do postawienia właściwego rozpoznania i wdrożenia właściwego leczenia.
Summary
Hyperthyroidism affects about 2% of adult population. The most common underlying causes are, dependant on dietary iodine supply, Graves’ disease and toxic nodular goiter. The occurrence of thyroid nodules in patients with Graves’ disease is greater than in general population and the majority of them are non-functioning ones. The coexistence of Graves’ disease and a solitary or multiple autonomous thyroid nodules is extremely rare and is called Marine-Lenhart syndrome. The aim of this paper is to present a case of Marine-Lenhart syndrome and to analyze similar cases reported in PubMed since 2000. A 40-year-old woman who was previously diagnosed to have autonomous thyroid nodule was admitted to the Outpatient Endocrinology Department of Medical Centre of Postgraduate Education after seven years with signs and symptoms of severe hyperthyroidism in the course of Graves’ disease. The following diagnostic steps and treatment strategy were presented and discussed. Other reported cases of Marine-Lenhart syndrome were also discussed. All analyzed cases showed that the diagnosis of the syndrome may be difficult due to fluctuating scintigrafical character of the nodules and thyroid parenchyma. Therefore, strict clinical follow-up as well as the assessment of serum anti-TSH receptor antibodies and thyroid imaging procedures: scintigraphy and ultrasonography are all necessary to make the right diagnosis and choose the appropriate treatment strategy.
Key words: hyperthyroidism,
INTRODUCTION
Hyperthyroidism affects about 2% of adults. The most common causes are Graves’ disease and toxic nodular goiter. The prevalence of these two disorders depends mainly on dietary iodine supply: Graves’ disease predominates in populations with adequate iodine intake, whereas toxic nodular goiter occurs more often in iodine-deficient areas. Poland like many European countries suffered from moderate to mild iodine deficiency but became iodine-sufficient from 1997 when iodine prophylaxis program was reestablished. Due to the long-lasting insufficient iodine supply toxic nodular goiter is responsible for 30-40% cases of hyperthyroidism in Poland and typically affects older population (1).
The above disorders lead to hyperthyroidism through different pathomechanisms. In Graves’ disease which has an autoimmune origin, the excessive production of thyroid hormones is caused by thyroid-stimulating immunoglobulins (TSI), while in toxic nodular goiter – by acquired activating mutation of TSH-receptor or protein G. The coexistence of both disorders, known as Marine-Lenhart syndrome, is extremely rare.
Herein we present a case of a 40-year-old woman with Marine-Lenhart syndrome who was admitted to the Outpatient Endocrinology Department of Medical Centre of Postgraduate Education. We also discuss similar cases reported in PubMed since 2000.
CASE PRESENTATION
A forty-year-old woman with a family history of autoimmune diseases (rheumatoid arthritis in mother, psoriasis in son) was admitted to the Outpatient Endocrinology Department of Medical Centre of Postgraduate Education in April 2016 with signs and symptoms of hyperthyroidism. Seven years before, based on the abnormal thyroid function tests (TFTs) (tab. 1), thyroid ultrasound and 99mTc thyroid scan (fig. 1) she was diagnosed to have subclinical hyperthyroidism due to a solitary autonomously-functioning nodule with diameter of 16 mm in the right thyroid lobe. The patient was feeling well and she abandoned the further medical surveillance until 2016 when she started to complain of progressive fatigue, muscles weakness, sweating, tremor, anxiety, heart palpitations, diarrhea and weight loss. TFTs established in February 2016 demonstrated the signs of severe hyperthyroidism (tab. 1) and treatment with thiamazole 30 mg daily and propranolol 60 mg daily was instituted. Two weeks later the allergic skin reaction to thiamazole had occurred, thus therapy was discontinued and propylthiouracil 300 mg daily was started. Then, ultrasound-guided fine-needle aspiration biopsy (FNAB) of the right thyroid lobe nodule was performed and showed benign cytology (category 2 according to the Bethesda System for Reporting Thyroid Cytopathology).
Tab. 1. Thyroid function tests
 March 2009February 2016Admission to Outpatient Clinic, April 2016June 2016
TSH, uIU/mL
n.: 0.35-4
0.0470.0160.003< 0.005
fT4, pmol/l
n.: 12-22
18> 10035.7415.31
fT3, pmol/l
n.: 3.95-6.8
5.63> 508.477.43
TRAb, IU/l
n.: < 1.8
  10.25 
a-TPO, IU/ml
n.: < 60
  > 1300 
a-Tg, IU/ml
n.: < 60
  116.1 
Fig. 1. Thyroid scintigraphy with 99m technetium in March 2009: a hot nodule in the lower pole of the right thyroid lobe (arrow)
At admission to the Outpatient Endocrinology Department in April 2016 physical examination of the patient revealed blood pressure of 140/80 mmHg, regular heart rate of 70 bpm, moist skin, enlarged thyroid gland with a palpable nodule in the bottom of the right lobe and vascular murmur over the whole thyroid gland. TFTs revealed overt hyperthyroidism and significant elevation of anti-thyroid autoantibodies: anti-peroxidase (a-TPO), anti-thyroglobulin (a-Tg) and thyrotropin receptor antibodies (TRAbs) (tab. 1). The ultrasound scans showed thyroid enlargement (thyroid right lobe volume 27 ml, thyroid left lobe volume 21.2 ml), heterogenic echotexture with small hypoechogenic areas, diffusely increased vascularity on Color-Doppler examination. In the lower part of right thyroid lobe there was a mixed partially solid and cystic nodule, soft on elastography, with diameter of 23 mm and volume of 4.8 ml (fig. 2a-c). Thyroid 131I scintigraphy revealed increased iodine uptake (T24131I – 71.2%) with a cold area corresponding to the right lobe nodule and intensive iodine accumulation in the rest of thyroid parenchyma (fig. 3). At admission the patient was treated with propylthiouracil 250 mg daily and propranolol 60 mg daily, both in 3 divided doses. Then propylthiouracil was reduced to 150 mg daily and one month later a significant decrease in thyroid hormones levels was observed (tab. 1). Eventually surgical treatment was performed after euthyroidism was obtained and levothyroxine substitution was started afterwards. Histopathological examination revealed hyperplastic thyroid epithelium with moderate lymphocytic infiltration characteristic to Graves’ disease and hyperplastic thyroid nodule of the right thyroid lobe.
Fig. 2a-c. Thyroid ultrasound scans in April 2016. Heterogenic echotexture of parenchyma with small hypoechogenic areas (a), diffusely increased vascularity on Color-Doppler examination (c), complex solid and cystic lesion in the right thyroid lobe with a peripheral-central flow pattern (a, b)
Fig. 3. Thyroid scintigraphy with 131I in April 2016: a cold nodule in the lower pole of the right thyroid lobe (arrow)
DISCUSSION

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otrzymano: 2017-11-10
zaakceptowano do druku: 2017-11-30

Adres do korespondencji:
*Agnieszka Majos
Klinika Endokrynologii Szpital Bielański
ul. Cegłowska 80, 01-809 Warszawa
tel. +48 (22) 569-05-09
klinendo@cmkp.edu.pl

Postępy Nauk Medycznych 12/2017
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