(1) Introduction: The main way of spreading the herpes simplex virus 1 (HSV-1) is through direct contact, as the virus enters the host via mucous membranes. Ocular infection can occur as a primary infection or as a recurrent one. The movement of HSV-1 along the ophthalmic branch of the fifth cranial nerve from its latency phase in the trigeminal ganglion and its activation represent a process influenced by various symbiotic factors, such as environmental conditions and the host’s genetic characteristics. The aim of this study was to assess the frequency of IL28 (rs12980275) and (rs8099917) in recurrent ocular HSV infections. (2) Materials and methods: The study included 60 patients aged over 18, of both sexes, all of whom had a history of herpes simplex labialis (HSL). Patients were tested for HSV-1-specific IgG antibodies, and seropositive individuals were genotyped for single nucleotide polymorphisms (SNPs) rs12980275 and rs8099917. A total of 57 seropositive patients were included in the study. (3) Results: A statistically significant association was found between recurrent HSV keratitis (HSK) and heterozygous GT rs8099917 and homozygous TT rs8099917, as well as heterozygous AG rs12980275 and homozygous AA rs12980275 (p < 0.01). Interestingly, patients with homozygous GG polymorphism for both genotypes GG rs8099917 and GG rs12980275 did not develop recurrent HSV keratitis. (4) Conclusion: The most frequent SNP variations in patients with recurrent HSV disease were heterozygous AG rs12980275 (61.40%) and heterozygous GT rs8099917 (52.63%). Patients with recurrent HSV keratitis lacked the homozygous GG polymorphism in both GG rs8099917 and GG rs12980275 genotypes, suggesting that HSV-seropositive individuals expressing these genotypes may have lower predisposition to develop recurrent stromal HSV keratitis.

Introduction: Anorexia nervosa (AN) is a severe chronic psychiatric disorder with often underestimated prevalence. Patients suffering from anorexia nervosa can die from natural causes, such as severe heart problems, organ failure, or malnutrition, as well as from unnatural causes, such as suicide. However, the mechanism of death in anorexia nervosa is poorly understood. Patient review: Our paper describes a case of sudden death in a 22-year-old woman suffering from anorexia nervosa. The autopsy showed severe malnutrition. Upon opening the abdominal cavity, extremely dilated stomach (without signs of wall necrosis or rupture) was noted. Biochemical findings showed that the vitreous chloride, sodium and potassium levels were markedly low, suggesting ante-mortem significant hypokalemia. There were no biochemical signs of severe hypoglycemia and dehydration. As cardiac disease is a significant cause of death in AN, aggravation caused by concurrent biochemical derangement must be taken into account. It is possible that gastric dilatation has a role in the occurrence of death, but this remains questionable. Conclusion: In this case, the possible mechanism of death could have been a disruption of heart rhythm in an arrhythmogenic state due to an electrolyte imbalance or vagal activation related to gastric dilatation.