Thyrotoxicosis Due to Acute Suppurative Thyroiditis in a Pediatric Patient: A Case Report.

Acute suppurative thyroiditis is a rare and potentially life-threatening cause of thyroid inflammation requiring prompt recognition and management. There are few reported cases of thyrotoxicosis due to acute suppurative thyroiditis. We are reporting the case of a 9-year-old boy who presented to the emergency room with fevers, neck pain and swelling, night terrors, and emotional lability. He was hemodynamically stable with initial lab work remarkable for neutrophilia without leukocytosis, elevated inflammatory markers, and hyperthyroidism. Imaging of the neck revealed a heterogenous collection in the region of the left thyroid concerning for suppurative thyroiditis and adenitis. He was admitted to the hospital and initiated on intravenous antibiotics. Given lack of significant improvement in pain, he was taken to the operating room for drainage on hospital day 4 with remarkable clinical improvement in pain. He was discharged on oral antibiotics. Lab work obtained on postoperative day 15 showed resolution of hyperthyroidism and decreasing inflammatory markers. Subsequent imaging following resolution of the acute illness did not reveal any anatomic abnormality that may have predisposed him to developing acute suppurative thyroiditis. Thyrotoxicosis as a complication of acute suppurative thyroiditis is a rare occurrence, and is thought to be due to the release of preformed thyroid hormone from damaged thyroid follicles. The thyrotoxic state is often transient and resolves with appropriate management of acute suppurative thyroiditis. This complication is important to recognize, as failure to appropriately diagnose and treat acute suppurative thyroiditis can lead to poor outcomes, such as airway compromise and death.

A high-fat diet impacts memory and gene expression of the head in mated female Drosophila melanogaster.

Obesity predisposes humans to a range of life-threatening comorbidities, including type 2 diabetes and cardiovascular disease. Obesity also aggravates neural pathologies, such as Alzheimer's disease, but this class of comorbidity is less understood. When Drosophila melanogaster (flies) are exposed to high-fat diet (HFD) by supplementing a standard medium with coconut oil, they adopt an obese phenotype of decreased lifespan, increased triglyceride storage, and hindered climbing ability. The latter development has been previously regarded as a potential indicator of neurological decline in fly models of neurodegenerative disease. Our objective was to establish the obesity phenotype in Drosophila and identify a potential correlation, if any, between obesity and neurological decline through behavioral assays and gene expression microarray. We found that mated female w1118 flies exposed to HFD maintained an obese phenotype throughout adult life starting at 7 days, evidenced by increased triglyceride stores, diminished life span, and impeded climbing ability. While climbing ability worsened cumulatively between 7 and 14 days of exposure to HFD, there was no corresponding alteration in triglyceride content. Microarray analysis of the mated female w1118 fly head revealed HFD-induced changes in expression of genes with functions in memory, metabolism, olfaction, mitosis, cell signaling, and motor function. Meanwhile, an Aversive Phototaxis Suppression assay in mated female flies indicated reduced ability to recall an entrained memory 6 h after training. Overall, our results support the suitability of mated female flies for examining connections between diet-induced obesity and nervous or neurobehavioral pathology, and provide many directions for further investigation.