Is there a connection between neurocognitive profile in treatment naïve non-cirrhotic HCV patients and level of systemic inflammation?

Hepatitis C virus (HCV) infection is a progressive, systemic disease which leads to the development of end-stage liver disease. In 70% of patients, HCV infection is followed by the development of extrahepatic manifestations (EHM). A common EHM is HCV associated neurocognitive disorder (HCV-AND), characterized by neuropsychological changes in attention, working memory, psychomotor speed, executive function, verbal learning, and recall. The aim of this study is to examine the correlation between the neurocognitive profile and routine, available laboratory parameters of inflammation, liver function tests, grade of liver fibrosis, and clinical and laboratory parameters of mixed cryoglobulinemia in treatment naïve non-cirrhotic HCV patients. This is a single-center exploratory study in which we examined 38 HCV + treatment naïve patients. The complete blood count and hematological parameters of systemic inflammation, liver function tests, biopsy confirmed grade of liver fibrosis, and clinical and laboratory parameters of mixed cryoglobulinemia caused by chronic HCV infection were observed. In the study, we used a battery of neuropsychological tests assessing multiple cognitive domains: executive functions, verbal fluency, delayed memory, working memory and learning, and one measure for visuo-constructive performance. Before the Bonferroni correction for multiple comparisons, the results show significant correlations between the scores in the neurocognitive variables and the single measures of inflammation, liver function parameters, and mixed cryoglobulinemia. It has not found a statistically significant correlation between systemic inflammation and neurocognitive variables. After the Bonferroni adjustment, no correlations remained significant. Certainly, the obtained results can be a recommendation for additional validation through future research.

Patients with neuropathic pain from lumbosacral radiculopathy demonstrate similar pressure pain thresholds and conditioned pain modulation to those with fibromyalgia.

OBJECTIVE: The purpose of the study was to evaluate pain thresholds, impairment of the endogenous pain modulatory system, and self-reported cognitive-emotional and central sensitization-related symptoms among three subject groups: a rarely studied patient cohort with neuropathic pain from lumbosacral radiculopathy (NPLSR), patients with fibromyalgia (FM) and healthy controls (HC). METHODS: Patient-reported pain-related symptomology was evaluated with psychometricallyvalidated questionnaires. Pressure pain threshold (PPT), heat pain threshold (HPT), and cold pain threshold (CPT) were assessed in the low back and contralateral forearm. Conditioned pain modulation (CPM) was evaluated with a recently introduced methodology that accounts for a standard error of measurement. RESULTS: Compared to the HC subjects, the FM and NPLSR subjects had significantly lower pain thresholds and more CPM impairment. No significant differences in PPT and CPM were observed between the FM and NPLSR groups. Significant group differences were found in self-reported symptoms of depression, anxiety, stress, and central sensitization. Self-reported symptom severity increased in a stair-step fashion, with the HC group scoring lowest and FM group scoring highest. CONCLUSION: The NPLSR group manifested CPM dysfunction and pressure hyperalgesia at similar levels to the FM group, indicating that these two chronic pain syndromes, likely based on different pathophysiological mechanisms, in fact share some common pain processing features. However, though both patient groups demonstrated similarities in pain processing, self-reported cognitive-emotional and central sensitization-related symptom severity was significantly higher in the FM cohort, which distinguished them from the chronic NPLSR cohort.

Relation of Steatosis to Neurocognitive Function in People Living with HIV.

BACKGROUND: In HIV negative population metabolic syndrome and steatosis are related to poorer neurocognitive (NC) performance. We investigated if similar relation exists in people living with HIV (PLWH). METHODS: We included male PLWH aged 20-65, with undetectable viral load for at least 6 months. Data on levels of education, anthropometric measurements, CD4 levels, ART, markers of metabolic syndrome, smoking and concurrent treatment were collected from database. Concentrations of TNF-α and IL-6 were measured. An ultrasound was used to establish the presence of steatosis, visceral fat thickness and carotid intima media thickness. An extensive NC assessment was done by an experienced neuropsychologist. Cognitive domains were defined as executive functions, divergent reasoning, visuo-constructional abilities, delayed recall and working memory and learning and were measured using a battery of 12 tests. RESULTS: 88 PLWH were included (mean age 39,9 years), 51% on PIs, 46% on NNRTI; 20,4% had metabolic syndrome, 42% patients had steatosis. Weak but statistically significant negative correlations were found between the presence of metabolic syndrome, steatosis and VFT and cognitive domains (divergent reasoning, delayed recall and working memory). Poorer perfomrance in the domains of divergent reasoning and in the working memory were found in participants with steatosis (p=0,048 and 0,033 respectively). CONCLUSION: Although the sample size was relatively small, our results show consistent correlations between the observed neurocognitive variables and metabolic parameters. As central obesity is one of the contributors to NCI, it would be one of the modifiable factors to prevent further neurocognitive decline.