Does Marine Lenhart Syndrome really exist?

Primary hyperthyroidism is the result of overproduction of thyroid hormone resulting in the classic symptoms of tachycardia, weight loss, diaphoresis, and hyperdefecation. There are multiple common causes to include Graves’ disease, toxic multinodular goiter, and solitary toxic adenomas. Marine Lenhart Syndrome (MLS) is a rare cause of hyperthyroidism, caused by a coexistence of constitutively active thyroid nodules and Graves’ disease. In the original document of Marine and Lenhart, there is no distinction made between the autoimmune phenomenon of Graves’ disease and the solitary toxic nodule of Plummer’s disease. Rather they are both considered to be the manifestation of the same disease. However, in the current era of radionuclide technology, a clear distinction of MLS can be seen with diffuse uptake in the thyroid gland and focused enhancement in the toxic nodules. Therefore what was previously described as one entity is now distinct as Graves’ disease and Plummer’s disease. It is also becoming increasingly clear within the literature that there is also a new phenomenon of post-radioiodine immunogenic hyperthyroidism in patients with toxic nodules and elevated autoantibodies. Therefore in order to properly treat and manage patients, a new definition of MLS may need to be proposed.

Improving treatment outcomes for Graves’ disease patients with inactive forms of Graves’ orbitopathy through an increased dose of radioiodine therapy

Introduction While surgical treatment is preferred for Graves’ disease with active forms of GO, there are various concepts for treating inactive forms of GO. The goal of radioiodine therapy is to resolve immunogenic hyperthyroidism by damaging the thyroid cells.The effects of the radioiodine dose on an associated inactive GO remain unclear, however. Methodology We conducted a retrospective analysis of 536 patients who received first-time radioiodine therapy to treat Graves’ hyperthyroidism. Patients without GO always received 200 Gy of iodine-131. Before the introduction of a differentiated treatment concept, patients with GO also received 200 Gy, while afterwards they received 300 Gy. For further analysis, we formed three patient groups based on GO diagnosis and administered radiation dose and compared their results. The main research question focused on the effect of an increased dose on Graves’ orbitopathy. The sub-questions addressed the resolution rate achieved with the higher dose as well as the development of GO in patients who received radioiodine therapy. Results The results show that GO symptoms were improved after radioiodine treatment in 68.5 % of patients treated with 300 Gy but only in 47.5 % of the patients treated with 200 Gy (p = 0.003). While in the 300 Gy group, hyperthyroidism was resolved in 93.2 % of patients, this was achieved in only 68.8 % of patients in the 200 Gy group (p </= 0.001). Discussion Especially with an inactive form of GO profit from their hyperthyroidism being quickly and sufficiently resolved. This is achieved significantly better by administering 300 Gy instead of 200 Gy. For this reason, data analysis supports a differentiated dose concept that provides 300 Gy for patients with GO and 200 Gy for patients without GO.

Változások a pajzsmirigybetegségek radiojódkezelésében

Radioiodine therapy for benign and malignant thyroid diseases was introduced about 70 years ago, however, there is still a lack of consensus regarding indications, doses and procedure. This review covers treatment results in immunogenic hyperthyroidism including the problem of orbitopathy. Radioiodine therapy for toxic and non-toxic multinodular goiter is also discussed with striking possibility of enhanching the radioiodine uptake. In this respect the recombinant human thyrotropin should be mentioned. Thyroid cancer treatment protocol has changed, too, due to ineffectivity in low-risk patients. More attention is needed to the carcinogenecity of radioiodine. The numerous problems mentioned above require large and well-designed prospective trials to resolve the fundamental questions. The author emphasizes that radioiodine dose should be administered in doses as low as reasonably achievable. Orv. Hetil., 2016, 157(3), 83–88.

Separation of Autonomous Function from Cell Density in Non-Immunogenic Hyperthyroidism

SummaryRegional autonomous cell mass (Q: cell density ratio) and function (T: toxicity index) were compared by double isotope parametric thyroid scintigraphy (Als et al., Nucl. Med. 1995; 34) in 53 patients with non-immunogenic hyperthyroidism before and after radioiodine therapy (aRIT) and showed a break-down (medians) of Q: 4.3→1.0 (toxic adenomas: TA), 2→1.1 (multifocal functional autonomies: MFA) (p <0.0001) as of T: 96→1.7 (TA), 15→1.1 (MFA) (p <0.001). Five functional aRIT patterns resulted: euthyroidism (n = 37, 70%), at half with scarred/non-scarred autonomous areas (low/higher T, respectively), primary hypothyroidism (n = 4), residual hyperthyroidism (n = 7), secondary hyperthyroidism (n = 5). The last two groups with persistent subnormal TSH values were clearly separated by divergent T, thyroxine and triiodothyronine levels. A resulting T >1 may represent a clinically sub-critical mass of residual autonomous tissue. This new technique facilitates individual prethera-peutic evaluations and aRIT quality control.

Separation of Autonomous Function from Cell Density in Non-Immunogenic Hyperthyroidism

SummaryA new quantitative subtraction method of thyroid scans is proposed which shows that regional function (F) by far exceeds regional cellularity or cell density (C) in potentially toxic thyroidal areas of non-immunogenic hyperthyroidism (NIH). Methods: A multistep processing of radioiodine and MIBI thyroid scans of patients with non-immunogenic hyperthyroidism led to normalized images of regional function excess and of perinodular enhancement. Two numeric factors were derived from regions of interest: Q (cell density ratio) comparing MIBI uptake in autonomous and suppressed areas and T (toxicity index): the maximal F/C contrast. Results: Q never exceeded 61; T, however, expanded toxicity levels over a range of 6-8735 with toxic adenomas (median = 165) and with hot areas of multifocal functional autonomy (median = 15). T was weakly correlated to serum TT3 (r = 0.41), but not to autonomous tissue mass, ultrasonographic or cytologic criteria. Conclusions: T is governed by inherent features of autonomous tissue and the response of the imbedded thyroid tissue to TSH stimulation. This standardized technique consolidates experiences from visual analysis; the huge T range mirrors the natural evolution from compensated autonomy towards hyperthyroid, decompensated stages.

Immunogenic and Non-Immunogenic Hyperthyroidism

SummaryAnnual occurrences of immunogenic (IH) and non-immunogenic hyperthyroidism (NIH) between Berne (1976, 1982, 1991) and Szczecin (1973, 1980, 1991) were compared. Out of 21,025 patients referred for thyroid examinations, 10.1% (average) were hyperthyroid. In Berne (former endemic goiter region) and Szczecin (without goiter endemicity) IH occurred in 41% and 68%, NIH in 59% and 32% of hyperthyroid patients, respectively. Within a stable incidence of NIH in Berne, toxic adenomas (TA) decreased from 41% (1976) to 17% (1991) (p <0.005). In Szczecin, where iodine deficiency is in an early stage, the TA frequency did not change significantly: from 24% (1973) to 28% (1991). Increases of TA or of multifocal functional autonomy apparently “mark” incipient or, respectively, decreasing deficiencies in nutritious iodine. Hyperthyroid patients in Berne compared to Szczecin were older, both with IH (54 versus 45 y) and NIH (65 versus 52 y). Age at diagnosis was stable in Berne but increasing (p <0.05) in Szczecin (from 43 to 52 y).