Hypothyroidism and non-cardiogenic pulmonary edema: are we missing something here?

UNLABELLED: We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diagnosis from cardiogenic to non-cardiogenic pulmonary edema. Further questioning revealed a history of nocturnal snoring, frequent awakening, and daytime fatigue, suggesting a possible sleep apnea syndrome (SAS). In conclusion, we believe that SAS was the missing link between our patient's hypothyroidism and non-cardiogenic pulmonary edema. LEARNING POINTS: Always keep an open mind and look for a pathology that would explain the whole clinical scenario.The involvement of the respiratory system in hypothyroidism can range from SAS, pulmonary hypertension, hypoventilation, and severe respiratory failure.Hypothyroidism and SAS should be considered in the differential diagnosis of non-cardiogenic pulmonary edema.Patients should be instructed to take levothyroxine on an empty stomach 30-60 min before food to avoid erratic absorption of the hormone.

Temperature controlled radiofrequency ablation at different sites for treatment of obstructive sleep apnea syndrome: a systematic review and meta-analysis.

BACKGROUND: This study seeks to determine the efficacy of temperature controlled radiofrequency tissue ablation (TCRFTA) to alleviate symptoms of obstructive sleep apnea (OSA) and reduce polysomnographic measures of OSA in the first year post-treatment. METHODS: Systematic review and meta-analysis. Two independent searches of MEDLINE, EMBASE bibliographic databases, and Evidence Based Medicine Reviews to identify publications relevant to OSA and TCRFTA. Effectiveness of TCRFTA was measured separately for application of TCRFTA at the base of tongue and soft palate, and for multilevel intervention using the respiratory disturbance index (RDI), lowest oxygen saturation (LSAT), Epworth sleepiness scale (ESS), and bed partner's rating of snoring using a visual analogue scale (VAS snoring). The most recent search was conducted in April 2013. Statistical analysis was performed using Review Manager Version 5.2 using a relative measure of effect, i.e., ratio of means (RoM). RESULTS: Our initial search resulted in 29 eligible studies, and subsequently, 20 studies were included in the meta-analysis. Substantial and consistent improvement in PSG and subjective outcomes were observed post-TCRFTA in the base of tongue (BOT) and multilevel surgery groups only. Application of TCRFTA at the BOT was associated with a significant reduction in RDI (RoM 0.60, CI 0.47-0.76), ESS (RoM 0.59, CI 0.51-0.67), and VAS snoring (RoM 0.48, CI 0.37-0.62) and increase in lowest oxygen saturation (RoM 1.05, CI 1.01-1.10). Similarly, a significant reduction in RDI (RoM 0.61, CI 0.47-0.80) and ESS (RoM 0.79, CI -0.71 to 0.88) was observed after multilevel TCRFTA, but substantial heterogeneity between these studies was observed. CONCLUSION: TCRFTA is clinically effective in reducing RDI levels and symptoms of sleepiness in patients with OSA syndrome when directed at the base of tongue or as a multilevel procedure.

[¹8F]FDOPA uptake in the raphe nuclei complex reflects serotonin transporter availability. A combined [¹8F]FDOPA and [¹¹C]DASB PET study in Parkinson's disease.

Brain uptake of [(18)F]FDOPA, measured with PET, reflects the activity of aromatic amino acid decarboxylase, an enzyme largely expressed in monoaminergic nerve terminals. This enzyme catalyzes a number of decarboxylation reactions including conversion of l-dopa into dopamine and 5-hydroxytryptophan into serotonin. For more than 20years [(18)F]FDOPA PET has been used to assess dopaminergic nigrostriatal dysfunction in patients with Parkinson's disease (PD). More recently, however, [(18)F]FDOPA PET has also been employed as a marker of serotoninergic and noradrenergic function in PD patients. In this study, we provide further evidence in support of the view that [(18)F]FDOPA PET can be used to evaluate the distribution and the function of serotoninergic systems in the brain. Eighteen patients with PD were investigated with both [(18)F]FDOPA and [(11)C]DASB PET, the latter being a marker of serotonin transport (SERT) availability. We then assessed the relationship between measurements of the two tracers within brain serotoninergic structures. [(18)F]FDOPA uptake in the median raphe nuclei complex of PD patients was significantly correlated with SERT availability in the same structure. Trends towards significant correlations between [(18)F]FDOPA Ki values and [(11)C]DASB binding values were also observed in the hypothalamus and the anterior cingulate cortex, suggesting a serotoninergic contribution to [(18)F]FDOPA uptake in these regions. Conversely, no correlations were found in brain structures with mixed dopaminergic, serotoninergic and noradrenergic innervations, or with predominant dopaminergic innervation. These findings provide evidence that [(18)F]FDOPA PET represents a valid marker of raphe serotoninergic function in PD and supports previous studies where [(18)F]FDOPA PET has been used to assess serotoninergic function in PD.

Nature and variants of idiopathic restless legs syndrome: observations from 152 patients referred to secondary care in the UK.

BACKGROUND: Heterogeneity in clinical presentation and daytime somnolence in restless legs syndrome (RLS) have been poorly explored in the UK. MATERIAL AND METHODS: Analysis of database of 152 cases of primary RLS compiled from clinical consultation using a structured questionnaire administration and clinical examination, spanning six years of referral. Standard evaluations included use of the Epworth Sleepiness Scale (ESS). Secondary RLS was excluded and polysomnography performed in some when clinically indicated. RESULTS: The mean duration of RLS before appropriate treatment initiation was 12.7 years (age range of patients 26-90 years). 79% of patients had insomnia while 30% had excessive daytime sleepiness (EDS). Severe pain, restless arms and paroxysmal RLS causing lifestyle alterations also occurred. CONCLUSIONS: This study suggests that there is considerable delay before appropriate therapy in RLS. A large number have EDS and insomnia among others, is the commonest presenting feature. Phenotypic heterogeneity may cause diagnostic difficulty.