SESSION TYPE: Critical Care Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Viral pericardial effusions, have not been reported to cause airway compression possibly as the fluid does not create a mass effect. In young children, external compression of the bronchi may be seen more frequently due to the softer cartilage of these airways. (1)

CASE PRESENTATION:

A 5-month-old white female with an insignificant past medical history was admitted to an outside hospital with a low- grade fever of 10 days, labored breathing, and decreased appetite and urinary output. Upon day one evaluation by chest x-ray, the patient had an enlarged cardiothymic silhouette with diffuse hazy infiltrate in the left lung. Treatment was started for possible pneumonia. (Figure 2. A) The patient deteriorated with respiratory distress; on day three, a CT scan was ordered. CT scan was interpreted by radiology as: very large rounded mass involving the anterior mediastinum with airway compression. (Figure 2. C) The referring hospital transferred the patient. Upon arrival to the Batson Children's PICU, a bedside echocardiogram was performed immediately due to clinical exam findings. Massive pericardial effusion with tamponade physiology was confirmed. (Figure 1. A) Emergency pericardiocentesis was performed under local 2% lidocaine with sterile precautions. After pericardiocentesis, the patient's condition improved markedly with resolution of respiratory distress. Echocardiogram, chest x-ray, and repeat CT scan were ordered upon completion of the procedure, which showed no compression of the primary bronchi and there was no impression of a mediastinal mass. (Figure2. B&D, Figure 1.B). Pericardial fluid was sent for analysis and revealed to be non- malignant. Viral studies, enterovirus and flu PCR, respiratory cultures, antinuclear antibodies, rheumatoid factor, TSH, and T4 were ordered to investigate etiology. All tests returned negative, except a stool swab positive for adenovirus.

DISCUSSION:

In pediatric patients, massive pericardial effusion is often not linked to a causative agent; approximately 37% of cases of pericardial effusion are ultimately categorized as idiopathic disease. (2) We suspect the cause of our patient's massive pericardial effusion was viral in etiology due to a stool swab positive for Adenovirus. We believe this is the first case report of a viral pericardial effusion in a previously healthy infant presenting as a mediastinal mass causing airway compression.

CONCLUSIONS:

We suggest that when a diagnosis of mediastinal mass is made by chest X-ray or CT scan a possibility of pericardial effusion and cardiac tamponade should be investigated by obtaining an emergency echocardiogram in children.1) Awad WI, Graves TD, White VC, Wong K, Airway Obstruction Complicating Mediastinal Tuberculosis: A Life-Threatening Presentation, Annals of Thoracic Surgery 2002; 74: 261-2632) Kuhn B, Peters J, Marx GR, Breitbart RE, Etiology, Management and Outcome of Pediatric Pericardial Effusions, Pediatric Cardiology 2008; 29: 90-94DISCLOSURE: The following authors have nothing to disclose: Ashley Meekin Johnson, Najmul Salman, Charles Gaymes, Andrew RivardNo Product/Research Disclosure InformationUniversity of Mississippi Medical Center School of Medicine, Jackson, MS.

SESSION TYPE: ILD Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Interstitial lung diseases associated with collagen vascular diseases are diverse. Among these, there is a low prevalence of bronchiolitis. We present a case with sudden onset of symptoms and significant advanced disease at the time of diagnosis.

CASE PRESENTATION:

This is the case of a 49 y/o female with Systemic Lupus Erythematosus (SLE) who presented complaining of exertional chest pain, shortness of breath, dry cough, and orthopnea for two weeks. The physical exam is unremarkable except for oxygen desaturation with exertion and obesity. Cardiopulmonary exam is normal. A Ct angiogram demonstrated no pulmonary embolus but was significant for diffuse thin walled cystic lung disease with interstitial fibrosis and areas of ground glass alveolitis. ANA positive C3 105 C4 13 TSH 2.23 IgG 3137mg/dl, IgA 621mg/dL, IgM 291mg/dL. Pulmonary function test showed restriction (FVC 1.64 64% FEV1 1.41 59% ratio 91) and decreased DLCO 55. Patient underwent VATS with wedge resection of Right Middle Lobe which showed follicular bronchiolitis with vague granulomatous features and multiple meningothelial-like nodules. Patient was started on prednisone, pantoprazole and albuterol. She had improvement of dyspnea and ground glass alveolitis. Fibrosis and innumerable cysts persisted.

DISCUSSION:

Follicular bronchiolitis is defined by the presence of hyper plastic lymphoid follicles with reactive germinal centers distributed along bronchovascular bundles. Follicular bronchiolitis results from antigenic stimulation of the bronchial associated lymphoid tissue and polyclonal lymphoid hyperplasia. Follicular bronchiolitis has been associated with numerous diseases including collagen vascular disease (most commonly Sjogren's and Rheumatoid Arthritis), immunodeficiency states, and hypogammaglobulinemias. The typical presenting symptom is progressive breathlessness and cough although some patients may have fever. Variable pulmonary function abnormalities have been reported, including obstructive, restrictive, and mixed patterns. Patients with follicular bronchiolitis typically have a favorable prognosis. Treatment is directed at the underlying disease or may consist of steroids. Macrolides may reduce inflammation and cytokine production, improving symptoms and lung function. This data has been extrapolated from patients with diffuse panbronchiolitis and requires further investigation.

CONCLUSIONS:

Thought follicular bronchiolitis is less commonly associated with SLE it should be considered as a cause of dyspnea. Early detection of follicular bronchiolitis is necessary for initiation of treatment prior to progression to fibrosis. The role of macrolides and immunomodulators need further investigation.1) W D Travis, et a.l Non-neoplastic pulmonary lymphoid lesions. Thorax 2001;56:964-9712) S Howling, et al. Follicular Bronchiolitis: Thin section CT and histological findings. Radiology 1999;212:637-423) J.H.Ruy et al. Brochiolar disorder. Am J Respir Crit Care 2003;168:1277-92DISCLOSURE: The following authors have nothing to disclose: Lymaris Garcia, Keren Bakal, Ezra DweckNo Product/Research Disclosure InformationNYU School of Medicine, New York, NY.

Abstract During space missions, radiation represents a major hazard for human health and involves all body organs and tissues. Regarding thyroid function, it has been shown that ultraviolet radiation (UVC) has dose-dependent apoptotic effects on FRTL-5 cells, a normal strain of rat thyrocytes. We examined the effects of a sublethal dose of UVC on FRTL-5 cell growth and gene expression. Cells exposed to 10 J/m(2) UVC showed no differences in viability compared to control cells after 24 h, but the BrdU incorporation was reduced, indicating a cytostatic effect. Quantitative RT-PCR carried out at 24 and 48 h after irradiation demonstrated that the mRNA levels of thyroglobulin (Tg), thyroperoxidase (Tpo), and sodium/iodide symporter (Nis) were transiently decreased at 24 h in treated cells, while the mRNAs of the thyroid transcription factors TTF1, Foxe1, and Pax8 were not affected. In cells cultured with TSH-free medium, the basal transcription of Tg, Tpo, and Nis genes was equally impaired by radiation and no longer stimulated by TSH. Overall, the results demonstrate that a sub-apoptotic dose of UVC compromises not only thyrocyte proliferation but also the expression of genes involved in thyroid hormone production. These findings might contribute to explaining the histological, biochemical, and clinical features of hypothyroidism observed in both animals and humans during spaceflight, and suggest that free thyroxine levels of astronauts during prolonged space missions should be monitored. Key Words: Thyrocyte-Thyroglobulin-Thyroperoxidase-Sodium/iodide symporter-Ultraviolet radiation-Spaceflight. Astrobiology 13, xxx-xxx.

There is no consensus on the optimal treatment of multinodular goiter (MNG), but in the past few years, the use of radioiodine has increased. This study's objective was to evaluate adjuvant methimazole (MMI) therapy to increase and standardize radioiodine uptake (RAIU) with a fixed therapeutic (131)I dose of 1110 MBq (30 mCi).Our study included 5 women with MNG treated with MMI, 10 - 15 mg/day for 2 to 4 months, prior to the administration of 1110 MBq (131)I (30 mCi); none of the patients developed hypothyroidism during MMI therapy and had average basal TSH levels of 0.32 ± 0.39 mIU/L that increased to 2.6 ± 0.9 mIU/L (P = 0.07).RAIU increased from 25.6 ± 8.7% to 49.2 ± 8.3% (P = 0.003). All patients were followed for 12 months: median thyroid volume (TV) decreased from 77.2 mL (32.9 - 124.2) to 48.8 ml (12.4 - 68.9) with an average decrease of 46.4 ± 14.8% (P = 0.01). All patients developed hypothyroidism during the first 6 months after radioiodine therapy.This new therapeutic protocol using MMI as adjuvant therapy is effective in increasing RAIU as well as the deleterious effects of (131)I, without increasing the required dose, but leading to thyroid volume decreases similar to those reported with the use of recombinant human thyrotropin (rhTSH) or higher radioiodine doses.

We aimed to study uterine and ovarian morphology, hormonal levels, and pituitary height in prepubertal girls with pituitary hyperplasia secondary to primary hypothyroidism (PH) before and after thyroid hormone replacement therapy. We investigated 24 prepubertal girls with severe PH who were divided into 2 groups: secondary pituitary hyperplasia (group A, n=18), without pituitary hyperplasia (group B, n=6). Serum levels of free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH), follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), testosterone (T) and prolactin (PRL), pituitary height, uterine volume (UV), ovarian volume (OV), follicular diameter (FD), and follicular number (FN) in group A were measured before and 3-month after levothyroxine therapy. Age-matched healthy prepubertal girls (control group, n=30) were also enrolled in the study. The levels of FT3 and FT4 were significantly lower and the values of TSH, FSH, E2, PRL, pituitary height, UV, OV, and FD were significantly higher in group A than in the control group (all p<0.05). In group B, FT4 levels were significantly lower and TSH levels were significantly higher than in the control group (both p<0.05); the values of FSH, E2, PRL, UV, OV, and FD tended to be higher than those in the control group; there were no statistically significant differences (all p>0.05). After 3-month of therapy, hormonal levels regressed and imaging abnormalities decreased. Our results indicate that PH patients with pituitary hyperplasia have enlarged uterus, ovaries and follicles, as well as high values of FSH, E2, PRL, and pituitary height, which are improved after levothyroxine therapy.

Our previous study reported that thyroid-stimulating hormone (TSH) promotes cholesterol synthesis via the cyclic adenosine monophosphate/protein kinase A/cAMP regulatory element-binding protein (cAMP/PKA/CREB) pathway after binding to TSH receptors in the liver. The hepatic cAMP/PKA/CREB pathway also plays an important role in maintaining fasting glucose homeostasis. These findings implied a possible role for TSH in hepatic glucose metabolism. In this study, we used TSH receptor knockout mice (Tshr-ko mice) to clarify the effect of Tshr deletion on hepatic glucose metabolism, and investigated whether the effects of TSH directly regulate hepatic gluconeogenesis in HepG2 cells. Tshr-ko mice exhibited decreased fasting blood glucose levels, increased insulin sensitivity but normal level of fasting plasma insulin. Tshr deletion impaired hepatic glucose production by down-regulating the expression of glucose-6-phosphatase (G6P) and phosphoenolpyruvate pyruvate carboxylase (PEPCK) mRNA, two rate-limiting enzymes in hepatic gluconeogenesis, and enhancing the abundance of hepatic glucokinase (GK), the first enzyme regulating glycogen synthesis. Moreover, Tshr deletion inhibited the protein expression of hepatic phospho-CREB and increased the protein expression of hepatic phospho-AMP-activated protein kinase (p-AMPK), two up-stream regulators of PEPCK and G6P mRNA. In HepG2 cells, TSH increased the expression of G6P and PEPCK at mRNA level. These results indicated the simulative effects of TSH on hepatic glucose production in vivo and in vitro, suggesting a novel role for TSH in hepatic glucose metabolism.

Objective.

Hyperthyroidism has been described as elevated serum free T3 and/or free T4 levels with decreased thyrotropin (TSH) concentrations. The main causes are related to autoimmune and neoplastic pathology. However, it might be caused due to a long-term topical exposure (iodine solution dressing) or by intravenous administration of iodine-containing substances. Both clinical and laboratory features might be presented. The main management is based on interruption of all exposures with iodine solutions and also antithyroid medicine in case of severe laboratory and clinical disturbances. Data Sources. We present a case of iodine-induced hyperthyroidism in a critically ill ICU patient caused by excessive iodine containing antiseptic solution washes and contrast agent administration. The patient was successfully treated by discontinuing iodine exposure and beta-blocker administration.

Conclusions.

In patients with underlying thyroid gland pathology, thyroid-function tests and clinical observation in the ICU are of critical importance.

Introduction: L-thyroxine replacement therapy is the treatment of choice for hypothyroidism. Recently, several studies suggested to complete it with l-triiodothyronine in acquired hypothyroidism.

Aim:

To study the role of combined l-thyroxine and l-triiodothyronine therapy in special cases with congenital hypothyroidism. Method: Data of 16 patients (age: 11.9±6.3 years; mean±SD) are presented who had high serum free thyroxine values or even above the upper limit of reference range (21.16±2.5 pmol/l) together with nonsuppressed TSH levels (15.7±5.7 mIU/l), and therefore received l-triiodothyronine in completion (0.18±0.09 μg/kg) once a day.

Results:

The combined replacement therapy resulted in a rapid improvement of the hormone parameters (TSH: 4.2±3.15 mIU/l; free thyroxine: 16.55±2.4 and free triiodothyronine: 7.4±1.8 pmol/l). The efficiency of this combined therapy proved to be more evident (TSH: 4.33±3.2 mIU/l; free thyroxine: 16.85±3.1 and free triiodothyronine: 6.4±0.85 pmol/l) in 10 patients treated for a longer period of time (duration of treatment: 2.9±2.0 years). The dose of thyroxine substitution decreased from 2.6±0.9 to 2.18±0.6 μg/kg/day), the ratio of these hormones was between 5:1 and 19:1 and the quotient of free fractions was normalized (3.8±0.4→2.6±0.3) during the replacement therapy.

Conclusions:

According to the observation of the authors a serious disturbance of feed-back mechanism may develop in some (>5%) children with congenital hypothyroidism (increased TSH release despite elevated free thyroxine level) after normal function of the feed-back system for years. Hormone parameters of these patients improve, then become normal on combined therapy supporting the rationale for this treatment method. Orv. Hetil., 2013, 154, 738-744.

Benign and malignant thyroid nodules are more prevalent in females than in men. Experimental data suggest that the proliferative effect of oestrogen rather than polymorphisms is responsible for this gender difference. This study analysed whether both differentiated thyroid cells and thyroid stem and progenitor cells are a target of oestrogen action. In thyroid stem/progenitor cells derived from nodular goitres the ability of 17beta-oestradiol to induce thyrosphere formation, the expression of oestrogen receptors and the effect of 17beta-oestradiol on growth, expression of marker of stem cells and thyroid differentiation (TSH receptor, thyroperoxidase, thyroglobulin, sodium iodide symporter expression) were analysed. 17beta-oestradiol induced thyrosphere formation, albeit to lower extent than other growth factors. Thyroid stem and progenitor cells expressed oestrogen receptor alpha and beta with an 8 time higher expression level of oestrogen receptor alpha mRNA compared to differentiated thyrocytes. 17beta-oestradiol was a potent stimulator of thyroid stem/ progenitor cell growth. In contrast, TSH-induced differentiation of progenitor cells, in particular the expression of the sodium iodide symporter, was significantly inhibited by 17beta-oestradiol.In conclusion, oestrogen stimulated growth and simultaneously inhibited differentiation of thyroid nodules derived stem/progenitor cells. From these data and based on the concept of cellular heterogeneity, we hypothesize a supportive role of oestrogen in the propagation of thyroid stem/progenitor cells leading to a selection of a progeny of growth-prone cells with a decreased differentiation. These cells may be the origin of hypo- or non-functioning thyroid nodules in females.

Objective In cross-sectional studies, TSH levels within the reference range have been positively associated with blood pressure and adverse serum lipid levels. In a prospective study, we aimed to find out if differences in TSH within the reference range are associated with future levels of blood pressure and lipids.Design Prospective population-based study.Methods Among 9709 women and 4644 men without previous thyroid disease who had a baseline TSH of 0.45-4.5 mU/l, we studied the associations of baseline TSH with blood pressure and lipid levels at follow-up 11 years later.Results Higher TSH at baseline was associated with higher systolic (P=0.002 in women) and diastolic (P=0.03 in women) blood pressure, non-HDL cholesterol (P=0.01 in men), and triglycerides (P=0.008 in men), and lower HDL cholesterol (P<0.001 in women and men) at follow-up, but the associations were very modest and not consistent between sexes. Among people who remained free of thyroid disease, changes in TSH during follow-up were associated with concomitant changes in systolic and diastolic blood pressure, non-HDL cholesterol, and triglyceride levels (all P<0.001), with similar results for women and men. Thus, blood pressure and lipid levels increased among people with increase in TSH, and decreased among people with a decrease in TSH, compared to people with no change in TSH.Conclusions High TSH levels within the reference range may be associated with modestly higher future levels of blood pressure and adverse serum lipids. TSH may co-vary with blood pressure and lipid levels among people with apparently normal thyroid function.