Josip Hanulak

Cerebral toxoplasmosis is a rare but potentially fatal opportunistic infection in renal transplant recipients receiving long-term immunosuppressive therapy. It may result from donor-derived transmission or reactivation of latent infection. We report the case of a 70-year-old female who underwent kidney transplantation from a deceased donor in 2004 for end-stage renal disease due to glomerulonephritis. She was maintained on cyclosporine, mycophenolate mofetil, and prednisone. In September 2024, she presented with headache, mood changes, and right-sided hemiparesis. Brain multislice computed tomography revealed a large temporoparietal lesion initially suspected to be glioblastoma. Craniotomy and histopathological analysis demonstrated encysted Toxoplasma gondii bradyzoites within gliotic tissue. Polymerase chain reaction testing confirmed the presence of T. gondii DNA, while human immunodeficiency virus testing was negative. The patient reported frequent contact with domestic cats. Treatment with pyrimethamine, sulfadiazine, and leucovorin, alongside adjustment of immunosuppressive therapy, led to marked neurological improvement and radiological regression of the lesion. However, nine months later, she succumbed to multidrug-resistant urosepsis. This case highlights the diagnostic challenges of cerebral toxoplasmosis in transplant recipients, as radiological findings are often nonspecific and can mimic neoplastic or lymphoproliferative lesions. Polymerase chain reaction and histopathological analysis remain essential for definitive diagnosis. Awareness of this rare complication is critical for early recognition and prompt initiation of anti-toxoplasma therapy, which can significantly improve outcomes. Although cerebral toxoplasmosis is uncommon after kidney transplantation, it should be considered in immunosuppressed patients presenting with neurological symptoms. Early detection and targeted therapy are key to reducing morbidity and mortality in this population.

Cerebral toxoplasmosis is a rare but potentially fatal opportunistic infection in renal transplant recipients receiving long-term immunosuppressive therapy. It may result from donor-derived transmission or reactivation of latent infection. We report the case of a 70-year-old female who underwent cadaveric kidney transplantation in 2004 for end-stage renal disease due to glomerulonephritis. She was maintained on cyclosporine, mycophenolate mofetil, and prednisone. In September 2024, she presented with headache, mood changes, and right-sided hemiparesis. Brain multislice computed tomography revealed a large temporoparietal lesion initially suspected to be glioblastoma. Craniotomy and histopathological analysis demonstrated encysted Toxoplasma gondii bradyzoites within gliotic tissue. Polymerase chain reaction testing confirmed the presence of T. gondii DNA, while human immunodeficiency virus testing was negative. The patient reported frequent contact with domestic cats. Treatment with pyrimethamine, sulfadiazine, and leucovorin, alongside adjustment of immunosuppressive therapy, led to marked neurological improvement and radiological regression of the lesion. However, nine months later, she succumbed to multidrug-resistant urosepsis. This case highlights the diagnostic challenges of cerebral toxoplasmosis in transplant recipients, as radiological findings are often nonspecific and can mimic neoplastic or lymphoproliferative lesions. Polymerase chain reaction and histopathological analysis remain essential for definitive diagnosis. Awareness of this rare complication is critical for early recognition and prompt initiation of anti-toxoplasma therapy, which can significantly improve outcomes. Although cerebral toxoplasmosis is uncommon after kidney transplantation, it should be considered in immunosuppressed patients presenting with neurological symptoms. Early detection and targeted therapy are key to reducing morbidity and mortality in this population.

Objective: The objective of this research is to examine hormonal levels of participants and their influence on male infertility, and to examine if there is a correlation between hormonal levels and levels of parameters of spermiogram. Study design: This study is designed as a cross-sectional study. Participants and methods: The study included patients who have been treated under diagnose of male infertility in the Department of Urology in Clinical Hospital Osijek in 2017. The data were collected in April 2018 from database of Department of Urology. Hormones examined in research are follicle-stimulating hormone, luteinizing hormone, prolactin, thyroid-stimulating hormone, testosterone, estradiol, triiodothyronine and thyroxine. Hormone levels were determined from blood samples by CMIA method. Variables of spermiogram in this research are volume, pH, concentration, number, vitality, motility and morphology of sperms and levels of zinc, fructose and citrates. Spermiogram was processed from ejaculate samples. Participants were classified in relation to reference values and then set in interrelations. Results: The study included 49 infertile males. 15 (31 %) of them were suspect for deviation of hormone levels. The median age of participants was 33 (interquartile range from 30 to 37 years) in range from 21 to 44 years. Values of follicle-stimulating hormone, thyroxine, thyroid-stimulating hormone and prolactin were in all cases in reference range. One participant had decreased level of testosterone, one decreased level of luteinizing hormone, two had decreased level of thyroid-stimulating hormone and two had increased level of estradiol. There was a negative correlation between luteinizing hormone and concentration, number and morphology of sperms, and there was also a negative correlation between testosterone and concentration, number, vitality and morphology of sperms. Conclusion: Deviations from reference values in hormonal levels are a factor in male infertility. The most significant are luteinizing hormone and testosterone with their negative correlation to certain parameters of spermiogram.