The Usefulness of Reduced Anion Gap and the Possibility of Pupillary Findings in the Treatment of Acute Bromvalerylurea Intoxication.

Bromvalerylurea is found as an over-the-counter analgesic and hypnotic drug in Japan and can be purchased at drugstores or over the Internet. Therefore, both acute poisoning due to large doses taken in suicide attempts and chronic poisoning due to continuous use for chronic pain have been observed. We report a case of acute BVU poisoning due to the use of an over-the-counter hypnotic sedative for a suicide attempt. A 34-year-old woman was referred to our ICU with unexplained disturbance of consciousness, respiratory failure, and shock. During ICU management, when her pupil diameter was measured with an automatic pupillometer to confirm her conscious state, the right pupil diameter was larger than the left, but one hour later, the left pupil diameter was larger than the right. The difference between right and left fluctuated with the time of day. After awakening, it was found that the patient had taken 108 tablets of Utt, an over-the-counter hypnotic sedative, and the possibility of acute poisoning by its component, BVU, was raised. Because a blood gas analysis at the time of admission showed metabolic acidosis with anion gap ≤1, a diagnosis of acute BVU poisoning was made. The patient's general condition stabilized, and she was transferred to the psychiatric ward. Symptoms of acute BVU poisoning include impaired consciousness and respiratory and circulatory depression, which may make it impossible to obtain a medical interview. When treating a patient with suspected drug intoxication who is unable to communicate, the clinician needs to include BVU poisoning in the differential when a reduced anion gap is observed. The clinician should also know that BVU poisoning can cause ocular manifestations such as anisocoria. This may lead to early diagnosis and therapeutic intervention.

Endogenous endophthalmitis caused by Streptococcus mitis: A case report.

RATIONALE: Endogenous endophthalmitis is a rare disease caused by hematogenous intraocular metastasis of bacteria from an infectious source. Diagnosing endogenous endophthalmitis is challenging for non-ophthalmologists. However, ophthalmic diseases can cause irreversible vision loss, making prompt diagnosis and treatment critical. Here we present a rare case of endogenous endophthalmitis initially misdiagnosed as a cataract. PATIENT CONCERNS: An 84-year-old Japanese man presented to the emergency department with fever and dysmotility. The patient was aware of a left subconjunctival hemorrhage and cloudy cornea upon arrival at the hospital, but he misunderstood it as a fall-induced subconjunctival hemorrhage and age-related cataracts. DIAGNOSES: On the day following admission, petechial hemorrhage on the eyelid conjunctiva and the detection of Streptococcus mitis in the blood culture results led us to suspect endophthalmitis rather than cataracts. A definitive diagnosis of endophthalmitis was made through ophthalmologic examinations, and endophthalmitis was considered secondary to endocarditis. INTERVENTIONS: Subsequently, antimicrobial treatment was continued. OUTCOMES: However, the patient developed myocardial infarction and died on the ninth day of hospitalization. LESSONS: Two important lessons were learned from the examination of this case of endogenous endophthalmitis caused by S mitis. First, endophthalmitis and cataracts can be misdiagnosed. Because the symptoms of endophthalmitis and cataracts, such as decreased vision, photophobia, and blurred vision, are similar, the eye must be cautiously examined. Second, endocarditis caused by S mitis may lead to endogenous endophthalmitis. Although S mitis is not pathogenic, endogenous endophthalmitis may occur in patients with certain risk factors, such as older age, cancer, and immunosuppression.

Cytosine arabinoside induces phosphorylation of histone H2AX in hippocampal neurons via a noncanonical pathway.

Cytosine arabinoside (Ara-C), an anticancer drug, is known to inhibit DNA replication in mitotic cells. Ara-C is also considered to induce DNA damage, leading to neuronal cell death. To identify the mechanism by which Ara-C kills neurons, we assessed the levels of phosphorylated histone H2AX (γ-H2AX), a marker for DNA double-strand breaks (DSBs), in hippocampal neurons cultured for 48 h with Ara-C. There was a time-dependent increase in the percentage of cells accumulating γ-H2AX, but TUNEL staining did not indicate the formation of DSBs. The nuclear spread of γ-H2AX remained after Ara-C was withdrawn. These features of Ara-C-induced γ-H2AX formation were quite distinct from those observed in proliferating pheochromocytoma cells. Furthermore, Ara-C-induced γ-H2AX formation appeared to utilize cyclin-dependent kinase 7, but not ataxia telangiectasia mutated (ATM) or ATM and Rad3 related, which are well-known kinases in γ-H2AX formation. Taken together, our findings indicated that Ara-C stimulated γ-H2AX formation in neurons without DSB formation and utilization of canonical kinases, leading to neuronal cell death.