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Introduction: Helicobacter pylori (H. pylori) infection is a global healthcare challenge. In its course of infection, Helicobacter pylori infection leads to a systemic increase of post-inflammatory cytokines and can have extra gastric manifestations, affecting the worsening of metabolic and cardiovascular diseases and endangering normal liver function, especially when liver cirrhosis is present. Aim: The aim of this study was to examine the frequency of H. pylori infection in patients with cirrhosis of the liver in stage AD or ACLF. The frequency of antibiotic resistance to clarithromycin and fluoroquinolones was also investigated. Material and methods: A prospective study with 45 patients was conducted which included both sexes. Samples of gastric mucosa were taken from all patients included in the study during the upper endoscopy and were sent to the Institute of Microbiology of the Faculty of Medicine University of Belgrade. A molecular method, Polymerase chain reaction (PCR) was used to detect H. pylori and mutations responsible for resistance to clarithromycin and fluoroquinolones. Results: The presence of H. pylori infection was registered in 15 decompensated patients (33.33%), while 30 (66.67%) were negative. In H. pylori positive patients, PCR detection of genotypes responsible for antibiotic resistance revealed clarithromycin resistance in 11 patients (73.33%), while fluoroquinolone resistance was detected in 7 patients (46.66%). In 6 patients (40.0%), an associated resistance to clarithromycin and fluoroquinolones was found. Conclusion: The H. pylori infection in cirrhotic patients with acute decompensation or ACLF has no significant effect on the severity of the clinical condition, elevated laboratory parameters and survival. Resistance rates to fluoroquinolones and clarithromycin or both antibiotics are high in decompensated patients with cirrhosis. There is a need to increase awareness of the rational use of antibiotics based on further investigations.

Introduction: Schizophrenia is a chronic mental illness that affects 1% of the world's population. The phencyclidine animal model of schizophrenia is based on the glutamate theory of the development of schizophrenia. Enkephalin is a neuropeptide with a role in the development of schizophrenia symptoms via the modulatory effect of neurotransmission. Aim: This study aimed to elucidate whether the long-term treatment with haloperidol and risperidone causes the difference in the appearance of enkephalin-immunoreactive neurons (EIN) in the brain of rats perinatally treated with phencyclidine (PCP). Material and methods: Experimental Wistar rats were treated on postnatal days 2 (PN2), 6, 9, and 12 with either PCP (10mg/kg) or saline. From PN35 to PN100 haloperidol (3mg/kg) and risperidone (1mg/kg) were administrated orally in drinking water. Animals were divided into six groups. The control group received saline and drinking water, PCP group received PCP and drinking water. Hal group received saline and haloperidol, PCP-Hal group PCP and haloperidol, while Ris group and PCP-Ris received saline or PCP and risperidone. All animals were sacrificed at PN100 and the cortex, hippocampus, striatum, and septal area were used to analyze the presence of EIN by immunohistochemistry. Results: In the hippocampus, the number of EIN was significantly higher in the PCP group than in the control group. Antipsychotics had a potent effect in the septal area, where both of them decreased the area covered by the EIN compared to the control group. In the striatum, only haloperidol changed the level of EIN by increasing the area covered with these neurons compared to the covered area in the control group. Conclusion: Long-term administration of antipsychotics caused the region-specific change in the distribution of enkephalin-immunoreactive neurons in the brain of a rat, perinatally treated with PCP.

Antibiotics are among the most common causes of drug-induced liver injury worldwide. Amoxicillin/clavulanic acid and nitrofurantoin are the most common culprits while tetracyclines are a rare cause of liver injury. Among tetracyclines, minocycline has been reported more frequently than doxycycline, which is an extremely rare cause of drug-induced liver injury. We present a healthy 28-year-old male patient from rural United States who was taking doxycycline for Lyme disease. After five days of therapy, he developed nausea, vomiting, fatigue, and significant transaminitis consistent with a hepatocellular pattern of liver injury. After a thorough workup which ruled out other causes such as infection, autoimmune diseases, liver malignancy, and vascular, structural, and metabolic disorders, his liver injury was attributed to doxycycline. We reached the diagnosis also by demonstrating a consistent temporal association between doxycycline intake and liver injury and the patient recovered completely with the cessation of doxycycline. Recognition of doxycycline as a cause of drug-induced liver injury should be considered in patients utilizing this antibiotic. Doxycycline, unlike minocycline, has a short latency period. Early recognition and discontinuation of doxycycline in our patient resulted in the complete resolution of symptoms and transaminitis preventing further morbidity and mortality., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Nikolajevic et al.)