The mechanisms involved in the increase of orbital retro-ocular adipose tissue that occurs in Graves' ophthalmopathy (GO) are still unclear. In this condition, the orbital tissue shows glycosaminoglycans deposition produced by activated fibroblasts capable of undergoing adipocytic differentiation. Many genes are involved in adipogenic mechanisms including the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). We evaluated the level of expression of the PPAR-gamma gene in normal and GO orbital adipose/connective tissue specimens using a quantitative and sensitive reverse transcription (RT) competitive polymerase chain reaction (PCR) assay. Our results show that the expression of PPAR-gamma was significantly greater in adipose/connective tissue from patients in the active stage of GO than in controls (150.8 +/- 103.9 and 24.0 +/- 4.9 amol/micro g of total RNA respectively, p < 0.05), while there was no significant difference between patients with inactive GO (58.8 +/- 40.6 aM/microg total RNA) and controls. These results suggest that increased PPAR-gamma gene expression in the active stage of GO may be dependent on the inflammatory process in this disease. We speculate that the increased orbital fat tissue observed in GO may be a consequence of the anti-inflammatory PPAR-gamma action.

Objective: To report the use of sodium diclofenac, an antagonist of PPAR-gamma and cyclooxigenase-2 (COX-2) inhibitor in the treatment of mild to moderate Graves' ophthalmopathy. Subjects and methods: Thirteen patients with clinical activity score (CAS) 2 to 7 were treated during a period ranging from 3 to 12 months (mean 7.8 ± 3.4) with oral sodium diclofenac, 50 mg every 12 hours. Results: Extra-ocular muscle restriction and CAS improved significantly, p = 0.003 and = 0.004, respectively. Ocular pain and diplopia disappeared, except for one patient who reported improvement of these symptoms. No recurrence was found after interruption of treatment. Conclusions: Treatment of moderate Graves' ophthalmopathy with oral sodium diclofenac is a good, safe and less expensive therapeutic option. Like others new treatment trials, findings must be confirmed in a greater number of patients in a controlled study. Arq Bras Endocrinol Metab. 2011;55(9):692-5

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OBJETIVO: Descrição de 4 casos de desenvolvimento transitório de mamas em meninas pré-púberes tratadas com hormônio de crescimento recombinante humano (rhGH). CASUÍSTICA E MÉTODOS: Quatro meninas pré-púberes com baixa estatura, duas com síndrome de Turner (ST) e duas com deficiência de hormônio de crescimento (DGH). O desenvolvimento das mamas (Tanner II e III) ocorreu com idade cronológica (IC) de 5,6 e 7,7 anos e idade óssea (IO) de 5,7 a 6,9 anos, 2 a 60 meses após o inicio do tratamento com rhGH na dose de 0,1 -0,15U/kg/d. ABSTRACT ABSTRACTOBJECTIVE: Description of 4 cases of breast development in prepubertal girls treated with recombinant human growth hormone (rhGH). PATIENTS AND METH-ODS: Four prepubertal girls with short stature: 2 with Turner's syndrome (TS) and 2 with growth hormone deficiency (GHD). Breast development (Tanner II and III) was detected from ages 5.6 to 7.7 years and bone ages from 5.7 to 6.9 years, from 2 to 60 months after starting rhGH treatment doses of 0.1 -0.15U/kg/d. Breast development had disappeared 8 to 15 months after have been noted in all patients. Three patients were submitted to GnRH test that showed a prepubertal LH response. DISCUSSION: Prepubertal breast development has been reported in boys after rhGH treatment, but not in prepubertal girls. CONCLUSION: rhGH can induce transient breast development, even in girls, without activation of the hypothalamic-pituitary-gonadal axis and these patients do not need suppression of puberty. A GINECOMASTIA OCORRE EM ATÉ 70% dos meninos durante a puberdade (1), mas é rara no período pré-puberal (2). Na literatura, foram relatados casos de ginecomastia em meninos pré-púberes durante o tratamento com hormônio de crescimento recombinante humano (rhGH) (3). A fisiopatologia da ginecomastia induzida por rhGH ainda é desconhecida, mas aventa-se a possibilidade de ação direta do GH sobre o tecido mamário. O desenvolvimento mamário em meninas pré-púberes tratadas com rhGH não foi relatado na literatura. No sexo feminino, o desenvolviartigo original artigo original

Background Graves’ disease (GD) is an autoimmune thyroid disease usually associated with hyperthyroidism. There have been cases of patients switching from hyperthyroidism to hypothyroidism, and even rarer patients flipping from hypothyroidism to hyperthyroidism. However, a case of spontaneously alternating hyperthyroidism and hypothyroidism in GD is comparably an even rarer phenomenon. It is thought that the switching of stimulating TSH receptor antibodies (TSAb) and blocking TSH receptor antibodies (TBAb) has a role in alternating thyroid function. We present a case of spontaneously oscillating thyroid function, pretibial myxedema and achropachy in three months. CASE REPORT 50 y,m,active smoker(90 yr old), weight loss (12 kg),tremors, irritability,proptosis,bad sensation eyes and acropachy(FigE) hyperthyroidism and ophthalmopathy secondary GD,underwent irregular treatment with methimazole 1st y. After1y, Graves' ophthalmopathy was worsened CAS 9(FigAB),with stereotactic radiotherapy, 10sec, 20Gy,pulse methylprednisolone followed by oral prednisone and decompressive surgery, initially used methimazole 30mg/d with reduction to 10mg/d.After 3 months of corticotherapy the patient returns with complaints of intestinal constipation, asthenia, brittle nails, the appearance of pre-tibial myxedema (FigC), being confirmed hypothyroidism frankly associated with the increase of thyroid autoantibodies (tb1), thyroid USG showing parenchyma with diffuse and grossly heterogeneous ecotexture and reduced echogenicity, diffusely increased vascularization, total thyroid volume of 33.4 ml (FigD). Patient maintained ambulatory follow-up, maintaining hypothyroidism on remission with levothyroxine 6 months ago. DISCUSSION This's the first case presenting hyperthyroidism shift to abrupt hypothyroidism with myxedema and acropachy in patient with GO. GD spontaneous change from hyperthyroidism to hypothyroidism (without ablative radioactive iodine intervention or treatment with antithyroid drugs) can occur in two ways: by the unexpected development of TBI (TSH receptor blocking immunoglobulin); or by chronic lymphocytic thyroiditis surpassing the stimulatory effects of TSI (Immune Globulin stimulating TSH receptors). The shift from TSI to TBI, with changes in immunoglobulin concentration, affinity and potency, leading to TBI dominance, is usually associated with the use of DAT (antithyroid drugs) and immunosuppressive states. We describe a case of hyperthyroidism due to GD evolving with frank hypothyroidism probably related to the alternation of TSI to TBI, with a predominance of the TBI effect, with onset after immunosuppressive therapy with corticosteroids. CONCLUSION The occurrence of a shift of predominance of the stimulatory effect to the inhibitor on TSH receptors emphasizes the need for careful monitoring of patients with Graves' disease.