Latent autoimmune diabetes in adults (LADA) and Graves disease (GD) may coexist due to shared autoimmune mechanisms and genetic susceptibility. We report a 39-year-old woman with class III obesity who presented with palpitations, blurry vision, and hypertension. Evaluation revealed new-onset diabetes (hemoglobin A1c 8.3% [SI: 67 mmol/mol]; reference range, 4.6-6.4% [SI: 27-46 mmol/mol]) and hyperthyroidism with suppressed thyroid stimulating hormone and elevated free thyroxine (free T4), along with positive thyroid peroxidase and thyrotropin receptor antibodies, confirming GD. Further testing demonstrated markedly elevated glutamic acid decarboxylase-65, zinc transporter 8, and insulinoma-associated antigen-2 antibodies. C-peptide was 2.34 ng/mL (SI: 0.78 nmol/L) (reference range, 0.80-3.85 ng/mL [SI: 0.26-1.27 nmol/L]) with a glucose of 92 mg/dL (SI: 5.1 mmol/L) (reference range, 70-99 mg/dL [SI: 3.9-5.5 mmol/L]), consistent with early LADA. She was treated with methimazole and metformin as she was quite averse to insulin therapy and was able to achieve good glycemic control. At 23 months, worsening hyperglycemia with declining C-peptide level, necessitated multiple daily insulin injections and continuous glucose monitoring. This case highlights the biphasic course of LADA and the importance of screening for additional autoimmune diseases, consistent with autoimmune polyglandular syndrome type 3.

Thyrotoxic periodic paralysis (TPP) is a rare but life-threatening cause of acute flaccid paralysis associated with hypokalemia. Although more common in males and individuals of Asian descent, it may present atypically in young females and be easily misdiagnosed. We report a case of a 30-year-old female who presented with acute quadriparesis. Extensive neuromuscular evaluation initially pointed toward Guillain-Barré syndrome (GBS), but subsequent investigations revealed profound hypokalemia. Further workup confirmed thyrotoxicosis as the underlying cause. Prompt potassium replacement and initiation of antithyroid therapy led to complete clinical recovery. This case highlights the importance of considering both endocrine disorders and electrolyte disturbances, such as hypokalemia, in the differential diagnosis of acute paralysis.

While Wernicke encephalopathy (WE) is well-recognized as a condition most frequently associated with chronic excessive alcohol consumption, non-alcoholic WE (NAWE) remain underrecognized despite their clinical importance. An 85-year-old nursing home resident was brought to the Emergency Department (ED) with impaired consciousness. She had been taking furosemide 40 mg and spironolactone 25 mg daily for chronic heart failure for five months prior to presentation. One month before admission, she began receiving parenteral nutrition without thiamine due to poor oral intake accompanied by vomiting. On arrival, her Glasgow Coma Scale score was 3, exhibiting flaccid quadriplegia and absent deep tendon and oculocephalic reflexes. Brain MRI demonstrated hyperintensities in the peri-central sulcus cortex as well as typical WE-related regions, including the periaqueductal gray and bilateral medial thalami, on diffusion-weighted imaging (DWI) and T2-weighted imaging. Intravenous high-dose thiamine therapy was initiated based on a clinical diagnosis of WE, subsequently confirmed by a thiamine level below the detection limit (<5 ng>/mL). Although follow-up MRI showed radiological improvement after seven days, neurological recovery remained minimal despite 35 days of treatment. Nonspecific clinical manifestation of NAWE makes early diagnosis difficult, often resulting in progression to more advanced stages with cortical lesions. To prevent irreversible and potentially fatal neurological sequelae, it is crucial to be aware of NAWE in its early stages, particularly in patients with known risk factors, such as malnutrition (poor nutritional intake), parenteral nutrition without thiamine, gastric bypass surgery, malabsorption, dialysis, diuretic use, infections/sepsis, and hyperthyroidism.

Fibroblasts are crucial in tissue engineering because of their ability to synthesize the extracellular matrix (ECM) and secrete growth factors. Orbital fibroblasts (OFs) from patients with thyroid eye disease (TED) exhibit enhanced fibroblastic properties, making them ideal candidates for regenerative medicine in ocular tissue. In the present study, we investigated the effect of nanoperlite on TED OFs. Nanoperlite, with its unique properties including high silica (SiO2) content, holds promise for enhancing fibroblast functions. Nanoperlite was prepared and characterized in terms of particle size and chemical composition. A sample of orbital adipose tissue was taken from a TED patient during orbital decompression surgery and OFs were expanded in vitro. The cells were then treated with nanoperlite at concentrations of 1 and 10 μg/mL for 24 h, and gene expression related to the fibrogenesis process was assessed using real-time PCR. Nanoperlite at 1 μg/mL significantly increased the expression of TGF-β, CD90, α-SMA, ZEB1, β-Catenin, and Snail genes in OFs. However, at 10 μg/mL, this effect was not observed. This study highlights nanoperlite's potential to enhance fibroblast activity specifically at the concentration of 1 μg/mL. This effect can potentially aid tissue engineering strategy for periorbital tissue repair and eyelid reconstruction. However, further research is needed to fully elucidate its therapeutic potential and safety profile.