Pertechnetate thyroid scan in Marine-Lenhart syndrome.

Sir,

Marine-Lenhart syndrome is a variant of Graves’ disease with incidentally functioning nodule(s) which are responsive to thyroid stimulating hormone but are not responsive to thyroid stimulating immunoglobulins. Here we present a classic case of Marine-Lenhart syndrome. A 65-year-old female, with hyperthyroidism diagnosed 6 years ago, was subjected to Tc-99m pertechnetate thyroid scan prior to I-131 ablation. At presentation, the patient was receiving propranolol and she stopped methimazole 10 days back. She was clinically hyperthyroid and complained of palpitations, tremors and loose motions. On clinical examination, a left-sided thyroid nodule was palpated. Thyroid functions tests were as follows: Thyrotropin (TSH) ≤0.01 uIU/mL (range, 0.27-4.20); free thyroxine (T4) ≥5.4 ng/dL (range, 0.7-1.6); triiodothyronine (T3) =4.6 ng/mL (range, 0.8-2.0). On ultrasound, the thyroid gland was asymmetrically enlarged with an isoechoic nodule surrounded by halo in the left lobe. There was no cervical lymphadenopathy. Tc-99m pertecnetate thyroid scan [Figure 1] showed diffuse homogeneously increased uptake throughout the gland with cold area in the infero-lateral part of the left lobe corresponding to the palpable nodule. Fine needle aspiration from thyroid nodule revealed features of colloid nodule. At that time the patient underwent successful ablation with 10 mCi of radioiodine-131.

Figure 1

Tc-99m pertechnetate thyroid scan showing diffuse homogeneously increased uptake throughout the gland with cold area in the infero-lateral part of the left lobe corresponding to the palpable nodule. Fine needle aspiration from thyroid nodule revealed features of colloid nodule

Marine-Lenhart syndrome, also known as nodular Graves’ disease, is the coincidence of Graves’ disease with TSH-sensitive functioning nodules. The syndrome was initially described in 1911 by Marine and Lenhart and is now considered a distinct sub entity of Graves’ disease.[1] Marine-Lenhart syndrome has been described as a variant of Graves’ disease with the following criteria: (i) The thyroid scan shows an enlarged gland and 1 or 2 poorly functioning nodules; (ii) the nodule is TSH dependent and the paranodular tissue is TSH independent; (iii) after endogenous or exogenous TSH stimulation, the return of function in the nodule can be demonstrated; and (iv) the nodule is histologically benign.[2] It is reported to be quite rare with a prevalence of 2.7-4.1% in patients with Graves’ disease.[34] Graves’ disease is an autoimmune disease in which stimulatory auto antibodies bind to TSH receptor and activate gland function, leading to hyperthyroidism. 25-30% patients of Graves’ disease are reported to harbour thyroid nodules.[567] Mostly these nodules are cold, benign and multiple,[8] but 1-2.5% are associated with hot autonomous nodules.[3] Thyroid scintigraphy shows the typical finding of increased activity with a decreased background, but with one or more cold nodules (suppressed by TSH). Following therapy with anti-thyroid drugs or I-131 radioablation, the nodules may accumulate radiotracer and appear like hot nodules as TSH level starts to rise.