The SARS-CoV-2 vaccines have had an overwhelming success in curbing the COVID-19 global pandemic, accounting for countless lives saved. Adverse reactions are inevitable, given the vast scale of vaccination required to mitigate future surges of COVID-19. Hyperthyroid disorders have been reported as potential adverse reactions to SARS-CoV-2 vaccines in two patients with Graves’ disease and a group of adults with subacute thyroiditis occurring in young women healthcare workers. We report a case of clinical Graves’ disease in a woman with a previously stable multinodular goitre that occurred 14 days following her second dose of Pfizer-BioNTech SARS-CoV-2 vaccine.
A 69-year-old Caucasian woman presented with chronic lymphocytic leukaemia (CLL; stage 1-Rai System), significant oropharyngeal lymphoid enlargement, snoring and fatigue. Overnight polysomnography revealed moderately severe obstructive sleep apnoea (OSA), which was managed successfully with oral appliance therapy with resolution of snoring and daytime fatigue. Structural abnormalities of the upper airways are known to cause OSA. Airway narrowing can result from bony structural abnormalities, nasopharyngeal growth, soft tissue redundancy, macroglossia, malignant and benign growth of the upper aero-digestive tract, and adenotonsilar enlargement. Clinicians should be encouraged to consider a diagnosis of OSA in patients with CLL when they present with symptoms of worsening fatigue.
BackgroundObstructive Sleep Apnea (OSA) is prevalent throughout the world. However, there are currently limited data concerning the prevalence of OSA in populations that originate from developing countries; the prevalence of OSA is expected to rise in these countries. OSA is poorly characterized amongst Ethiopians, and our study is the first to describe clinical characteristics of OSA among Ethiopians.MethodsWe conducted a retrospective study of primarily Ethiopian patients at an internal medicine clinic in Rockville, Maryland. All patients (n=24) were evaluated for daytime sleepiness using the Epworth Sleepiness Scale (ESS) and received physical examinations and polysomnograms (PSG) by either portable monitoring (Itamar WatchPAT 200 device) or in-lab. Statistical analyses were performed in R.ResultsLinear regression model of Body-Mass Index (BMI) and Apnea-Hypopnea Index (AHI) indicated that for every 1-unit increase in BMI, there was a 0.8657-unit increase in AHI (p<0.05). Pearson's correlation coefficient indicateda positive linear relationship between BMI and AHI (0.47) (p<0.05). Adjusted linear regression model for AHI and oxygen saturation indicated that for every 1-unit increase of AHI, there was a 0.8452-unit decrease in nocturnal oxygen saturation (p<0.05). Pearson's correlation coefficient did not demonstrate significance between AHI and oxygen desaturation (p=0.062). Patients received either continuous positive airway pressure (CPAP) (n=15) or oral appliance therapy (n=3).ConclusionAll patients who complied with therapy reported improved sleep quality, snoring resolution, and improved daytime alertness. Practitioners in developing countries should suspect OSA in the right clinical setting and offer diagnostic and therapeutic services when available.
BACKGROUND፡ Gilbert syndrome is a well-recognized condition causing unconjugated hyperbilirubinemia with otherwise normal transaminases and liver function tests. CASE: A 21 year old male patient presented with recurrent episodes of jaundice over four years. The episodes were preceded by stressful conditions and intercurrent illnesses. All laboratory prameters were normal except an unconjugated hyperbilirubinemia. A diagnosis of Gilbert syndrome was made after careful clinical evaluation.CONCLUSION: Recognizing Gilbert syndrome has important clinical implicaitions by avoiding uncessary and expensive workup of patients with jaundice. Mangement entails avoiding stressful conditions and prolonged fasting.
A middle-aged man of average weight presented to the sleep medicine clinic for multiple episodes of nocturnal eating during night-time awakenings for the past several months. His symptoms were more characteristic of night eating syndrome rather than sleep-related eating disorder because of his recollection of the eating episodes and intake of edible substances during these episodes. He was treated with a low dose of sertraline with an initial improvement of symptoms followed by a relapse that was controlled with an increased dose. A year after initiation of therapy, his symptoms have resolved.
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