Background: An association between Graves’ disease (GD) and the gut microbiome has been identified, but the causal effect between them remains unclear.Methods: Bidirectional two-sample Mendelian randomization (MR) analysis was used to detect the causal effect between GD and the gut microbiome. Gut microbiome data were derived from samples from a range of different ethnicities (18,340 samples) and data on GD were obtained from samples of Asian ethnicity (212,453 samples). Single nucleotide polymorphisms (SNPs) were selected as instrumental variables according to different criteria. They were used to evaluate the causal effect between exposures and outcomes through inverse-variance weighting (IVW), weighted median, weighted mode, MR-Egger, and simple mode methods. F-statistics and sensitivity analyses were performed to evaluate bias and reliability.Results: In total, 1,560 instrumental variables were extracted from the gut microbiome data (p< 1 × 10⁵). The classes Deltaproteobacteria [odds ratio (OR) = 3.603] and Mollicutes, as well as the genera Ruminococcus torques group, Oxalobacter, and Ruminococcaceae UCG 011 were identified as risk factors for GD. The family Peptococcaceae and the genus Anaerostipes (OR = 0.489) were protective factors for GD. In addition, 13 instrumental variables were extracted from GD (p< 1 × 10^–8), causing one family and eight genera to be regulated. The genus Clostridium innocuum group (p = 0.024, OR = 0.918) and Anaerofilum (p = 0.049, OR = 1.584) had the greatest probability of being regulated. Significant bias, heterogeneity, and horizontal pleiotropy were not detected.Conclusion: A causal effect relationship exists between GD and the gut microbiome, demonstrating regulatory activity and interactions, and thus providing evidence supporting the involvement of a thyroid–gut axis.

Graves' orbitopathy (GO), the common extrathyroidal complication of Graves' disease (GD), is characterized by orbital fibroblast stimulation, adipogenesis, and hyaluronan production. Recently, gut microbiota and its metabolites have garnered attention for their possible involvement in GO. This study utilized an animal model of GO and examined the effects of butyrate treatment on orbital fibroblast cells and gut microbiota. Ex vivo experiments were performed using orbital fibroblasts derived from healthy patients' and patients' with GO orbital tissue to evaluate vitality, activation, and adipogenesis in response to butyrate treatment. Gut microbiota diversity was also analyzed in butyrate-treated and untreated GO mice. In human orbital fibroblasts, butyrate treatment dramatically decreased the vitality of GO-derived fibroblasts without harming normal fibroblasts. Butyrate prevented activation and fibrotic processes induced by transforming growth factor beta 1 (TGF-β1) in GO and normal fibroblasts. Additionally, butyrate reduced lipid droplet formation and downregulated lipogenic markers in GO and normal orbital fibroblasts, inhibiting adipogenesis. In the GO mouse model, butyrate therapy improved orbital histological abnormalities and normalized serum thyroid hormone and antibody levels. The intestinal microbiome of butyrate-treated GO mice also changed significantly, with a reduction in certain bacteria (Bifidobacterium, GCA-900066575, and Parabacteroides) and an increase in others (Bacteroides and Rikenellaceae_RC9). Butyrate ameliorates several of the symptoms of GO, lowering GO orbital fibroblast viability, adipogenesis, and TGF-β1-induced fibrosis without damaging normal fibroblasts. Butyrate normalizes thyroid function in a GO mouse model, improves histopathological alterations, and transforms gut microbiota populations, proving its potential in treating GO through the gut-thyroid axis.

Parasitic infections of the eye are a major cause of ocular-surface diseases globally. While most infections are treatable, parasites can cause varying levels of damage mostly due to late diagnosis or misdiagnosis as a result of doctors' unfamiliarity with their characteristics of latency and crypsis, as well as lack of awareness by the patients. In this study, we present three cases of phthiriasis palpebrarum, thelaziasis, and ophthalmomyiasis, respectively. Two of the cases were treated at the clinic and did not recur. One patient refused treatment and was lost to follow-up. By evaluating the natural histories, morphology, symptoms, clinical findings, and treatment of these parasitic diseases, we systematically analyzed several distinct and unique parasite characteristics, especially latency and crypsis. Furthermore, we have proposed specific examination techniques and methods as well as prevention and treatment strategies from these specific perspectives, aiming to prompt timely diagnoses and early interventions for these diseases by health care workers and improve the public's awareness of parasitic infections. Parasitosis on the ocular surface is a global infectious disease, and prevention strategies include maintaining personal and environmental hygiene and limiting contact with animals. We recommend that health care workers should enhance their ability to detect and diagnose these diseases while promoting the public's awareness of them in the context of our new perspectives.

Bone wax is the most widely used hemostatic bone sealant because of its availability, ease of use, immediate action, and minimal adverse effects. Several complications have been reported to be associated with the use of bone wax, such as infection, osteohypertrophy, pain, granuloma formation, allergic reaction, and thrombosis. Here, we present a rare complication, namely, bone wax migration, which developed after a craniotomy on a patient who had a frontal sinus abnormality. A 51-year-old woman complained of pain and swelling in her left eye accompanied by difficulty opening the left eyelid after undergoing a craniotomy. An examination revealed left eye proptosis with ptosis, eyelid swelling, and increases in intraorbital pressure and intraocular pressure (IOP). According to a CT and an MRI of the orbit, we found that the intraoperative bone wax had migrated to the orbit, thereby causing compression. We also found that the basal frontal sinus of the patient was congenitally defective, which may have induced the migration of the bone wax. Given that the patient recently underwent a craniotomy and given the risks associated with orbital surgery, she refused to undergo a surgery to remove the bone wax. Thus, the patient was administered mannitol intravenously daily, accompanied by topical Timolol, to reduce the intraorbital pressure and IOP. This treatment led to a gradual decrease in IOP and intraorbital pressure, and these parameters remained stable after treatment ended. During the 6-month follow-up, the best corrected visual acuity improved, and ptosis and restricted eye movements also improved significantly. We report a case of bone wax migration that developed after a craniotomy on a patient who had a congenital defect in the basal frontal sinus. Extra caution should be taken when using bone wax, and a comprehensive understanding of the patient’s intracranial anatomy is important for decreasing the incidence of bone wax migration. Additionally, when a patient presents with symptoms of ocular compression, bone wax migration should be considered in addition to typical radiological changes.