Unusual Toxoplasma infection of the eye and central nervous system in an HIV-positive patient.

OBJECTIVE: To report on a unique combination of cerebral toxoplasmosis and ocular toxoplasmosis in an HIV-positive patient in Slovakia. METHODS: A 35-year-old heterosexual patient who presented with headache and major seizures underwent computed tomography (CT) and magnetic resonance imaging (MRI). Based on clinical findings, serological tests for toxoplasmosis were performed on serum and ocular fluid specimens. PCR was also used to detect Toxoplasma gondii and cytomegalovirus DNA. Goldmann and Witmer coefficient calculation was applied to demonstrate the synthesis of intraocular IgG antibodies. RESULTS: CT and MRI revealed cystic lesions suspected of metastasis in the occipital and temporal regions, and we searched for the primary tumor. After vision loss in the left eye, which rapidly progressed to complete blindness, an eye examination detected macular edema. Anti-edema treatment was initiated. HIV positivity with a very low CD4 T-cell count (20/μL) was found, and the viral load was 100 400 HIV-RNA copies/ml. The serum was positive for anti-Toxoplasma IgG antibodies (> 200 IU/mL), IgM negative, and IgA borderline. As toxoplasmic encephalitis and retinitis were suspected, antitoxoplasmic therapy with pyrimethamine, spiramycin, and folinic acid was started. The ophthalmologist considered cytomegalovirus retinitis, which was not confirmed by serology or PCR. In contrast, the presence of IgG antibodies in ocular fluid and serum with the calculation of the Goldmann-Witmer coefficient (GW = 32) as well as PCR DNA positivity pointed to Toxoplasma gondii as the etiological agent. Follow-up MRI scan confirmed regression of the pathological lesions, neurological deficit also improved, CD4 T-lymphocytes increased above 200/μL, but blindness of the left eye persisted. CONCLUSION: CT and MRI scans offered no clue as to Toxoplasma etiology of the brain and eye involvement in an HIV-positive patient, which was only confirmed by laboratory tests. Due to the delay in the diagnosis of toxoplasmosis, time from the epileptic seizure to treatment initiation was 16 days, which assumedly caused irreversible blindness in the patient.

Non-steroidal anti-inflammatory drugs caused an outbreak of inflammation and oxidative stress with changes in the gut microbiota in rainbow trout (Oncorhynchus mykiss).

One of the main contributors to pharmaceutical pollution of surface waters are non-steroidal anti-inflammatory drugs (NSAIDs) that contaminate the food chain and affect non-target water species. As there are not many studies focusing on toxic effects of NSAIDs on freshwater fish species and specially effects after dietary exposure, we selected rainbow trout (Oncorhynchus mykiss) as the ideal model to examine the impact of two NSAIDs - diclofenac (DCF) and ibuprofen (IBP). The aim of our study was to test toxicity of environmentally relevant concentrations of these drugs together with exposure doses of 100× higher, including their mixture; and to deepen knowledge about the mechanism of toxicity of these drugs. This study revealed kidneys as the most affected organ with hyalinosis, an increase in oxidative stress markers, and changes in gene expression of heat shock protein 70 to be signs of renal toxicity. Furthermore, hepatotoxicity was confirmed by histopathological analysis (i.e. dystrophy, congestion, and inflammatory cell increase), change in biochemical markers, increase in heat shock protein 70 mRNA, and by oxidative stress analysis. The gills were locally deformed and showed signs of inflammatory processes and necrotic areas. Given the increase in oxidative stress markers and heat shock protein 70 mRNA, severe impairment of oxygen transport may be one of the toxic pathways of NSAIDs. Regarding the microbiota, an overgrowth of Gram-positive species was detected; in particular, significant dysbiosis in the Fusobacteria/Firmicutes ratio was observed. In conclusion, the changes observed after dietary exposure to NSAIDs can influence the organism homeostasis, induce ROS production, potentiate inflammations, and cause gut dysbiosis. Even the environmentally relevant concentration of NSAIDs pose a risk to the aquatic ecosystem as it changed O. mykiss health parameters and we assume that the toxicity of NSAIDs manifests itself at the level of mitochondria and proteins.

Intraprocedural complications of uterine fibroid embolisation and their impact on long-term clinical outcome.

OBJECTIVES: Authors evaluate the impact of intraprocedural complications on successful technical realisation and long-term clinical outcome of the uterine fibroid embolisation. BACKGROUND: The uterine artery embolisation (UAE) has become an accepted treatment method for uterine fibroids. In general, the unilateral embolisation is considered to be insufficient due to poor clinical effect. METHODS: Overall, 165 uterine artery embolisations were analysed (retrospectively-prospectively) in 163 female patients. Intraprocedural complications and their impact on the possibility to perform bilateral embolisationwere evaluated. In patients with unscheduled unilateral embolisation, short-term as well as long-term clinical effects were observed with mean follow-up period of 41 months. RESULTS: The bilateral uterine artery embolisation was possible in 95.7 % (95 %, CI 91.3-99.4 %) procedures. The unilateral embolisation was reported in 7 procedures (4.3 %, CI 1.2-8.3 %) and reasons were following: resistant arterial spasm in 4 patients (2.5 %, CI 0.7 %-5.3 %) and impossible catheterisation due to unfavourable anatomic situation in 3 patients (1.8 %, CI 0.3-4.1 %). Other complications, such as dissection and perforation, did not affect the successful technical realisation. The long-term clinical effect of unscheduled unilateral embolisation was reported in 5 patients. CONCLUSION: The results of our series of unscheduled unilateral uterine fibroid embolisation had high long-term clinical success rate. In way of unscheduled unilateral embolisation, we recommend MRI follow-up and reintervention only in way of persistence or recurrence of symptoms with concurrent MRI finding of residual fibroids(Tab. 5, Fig. 3, Ref. 12).