Parkinson’s disease (PD) is characterized by alpha-synuclein misfolding with subsequent intraneuronal amyloid formation and accumulation, low grade neuroinflammatory changes, and selective neurodegeneration. Available evidence suggests that the pathology usually begins in the gut and olfactory mucosa, spreading to the brain via the vagus and olfactory nerves, by a prion-like mechanism. A causal relationship has not been established, but gut dysbiosis is prevalent in PD and may lead to intestinal inflammation and barrier dysfunction. Additionally, epidemiological data indicate a link between inflammatory bowel diseases and PD. Calprotectin and zonulin are markers of intestinal inflammation and barrier permeability, respectively. We evaluated their serum and fecal levels in 22 patients with sporadic PD and 16 unmatched healthy controls. Mean calprotectin was higher in PD, both in serum (14.26 mcg/ml ± 4.50 vs. 5.94 mcg/ml ± 3.80, p = 0.0125) and stool (164.54 mcg/g ± 54.19 vs. 56.19 mcg/g ± 35.88, p = 0.0048). Mean zonulin was also higher in PD serum (26.69 ng/ml ± 3.55 vs. 19.43 ng/ml ± 2.56, p = 0.0046) and stool (100.19 ng/ml ± 28.25 vs. 37.3 ng/ml ± 13.26, p = 0.0012). Calprotectin was above the upper reference limit in 19 PD serums and 6 controls (OR = 10.56, 95% CI = 2.17–51.42, p = 0.0025) and in 20 PD stool samples and 4 controls (OR = 30, 95% CI = 4.75–189.30, p = 0.000045). Increased zonulin was found only in the stool samples of 8 PD patients. Despite the small sample size, our findings are robust, complementing and supporting other recently published results. The relation between serum and fecal calprotectin and zonulin levels and sporadic PD warrants further investigation in larger cohorts.

Increasing evidence suggests that the gut microbiota and the brain are closely connected via the so-called gut–brain axis. Small intestinal bacterial overgrowth (SIBO) is a gut dysbiosis in which the small intestine is abundantly colonized by bacteria that are typically found in the colon. Though not a disease, it may result in intestinal symptoms caused by the accumulation of microbial gases in the intestine. Intestinal inflammation, malabsorption and vitamin imbalances may also develop. SIBO can be eradicated by one or several courses of antibiotics but reappears if the predisposing condition persists. Parkinson’s disease (PD) is a common neurodegenerative proteinopathy for which disease modifying interventions are not available. Sporadic forms may start in the gut years before the development of clinical features. Increased gastrointestinal transit time is present in most people with PD early during the course of the disease, predisposing to gut dysbiosis, including SIBO. The role that gut dysbiosis may play in the etiopathogenesis of PD is not fully understood yet. Here, we discuss the possibility that SIBO could contribute to the progression of PD, by promoting or preventing neurodegeneration, thus being a potential target for treatments aiming at slowing down the progression of PD. The direct symptomatic impact of SIBO and its impact on symptomatic medication are also briefly discussed.

Background and Objectives: Parkinson’s disease (PD) is a prevalent neurodegenerative condition responsible for progressive motor and non-motor symptoms. Currently, no prophylactic or disease-modifying interventions are available. Uric acid (UA) is a potent endogenous antioxidant, resulting from purine metabolism. It is responsible for about half of the antioxidant capacity of the plasma. Increasing evidence suggests that lower serum UA levels are associated with an increased risk of developing PD and with faster disease progression. Materials and Methods: We conducted an electronic medical record database study to investigate the associations between UA levels and different characteristics of PD. Results: Out of 274 datasets from distinct patients with PD, 49 complied with the predefined inclusion and exclusion criteria. Lower UA levels were significantly associated with the severity of parkinsonism according to the Hoehn and Yahr stage (rs = 0.488, p = 0.002), with the motor complications of long-term dopaminergic treatment (r = 0.333, p = 0.027), and with the presence of neurocognitive impairment (r = 0.346, p = 0.021). Conclusion: Oxidative stress is considered a key player in the etiopathogenesis of PD, therefore the involvement of lower UA levels in the development and progression of PD is plausible. Data on the potential therapeutic roles of elevating serum UA (e.g., by precursor administration or diet manipulation) are scarce, but considering the accumulating epidemiological evidence, the topic warrants further research.

Introduction Heart failure (HF) affects platelet activation, function, as well as the production of platelets from megakaryocytes. Low platelet counts have been described in HF patients, however without clear distinction whether this is a consequence of HF severity or an independent comorbidity contributing to worse outcomes. Aim Our purpose was to assess the prognostic role of thrombocytopenia in HF patients. Methods Patients with HF admitted to our Cardiology Department were included in this study, after excluding acute coronary syndromes, pulmonary embolisms, infections, malignancy and hepatic cirrhosis. Thrombocytopenia was defined as a platelet number below 15ehz747.0353/uL and classified as severe below 5ehz747.0353/uL and moderate between 5ehz747.0353–1ehz747.03530/uL. Patients with a left ventricular ejection fraction (LVEF) <40% were classified as HF with reduced EF (HFrEF), those with a LVEF between 40 and 49% as HF with mid-range EF (HFmrEF) and the rest as HF with preserved EF (HFpEF). All-cause mortality was assessed after a mean follow-up of 5.5 years. Results We included 1142 patients, with a mean age of 72.45±10.53 and 51.6% female. 121 (10.6%) patients had thrombocytopenia, of which 3 had severe thrombocytopenia and 21 had moderate thrombocytopenia. All-cause long-term mortality was 43.8%. Patients with acute decompensated heart failure had similar prevalence of thrombocytopenia as those with stable heart failure (12.3% vs 9.5%, p=0.22). Patients with thrombocytopenia had a higher risk ratio for all-cause mortality compared to patients with normal platelet counts (RR 1.35, 95% CI 1.14–1.60, p=0.002). Patients with severe thrombocytopenia had a risk ratio of 2.29 (95% CI 2.14–2.45, p=0.049), those with moderate thrombocytopenia had a risk ratio of 1.80 (95% CI 1.39–2.33, p=0.006) and those with mild thrombocytopenia had a risk ratio of 1.23 (95% CI 1.01–1.51, p=0.06) of all-cause long-term mortality, compared to patients with normal platelet counts. Patients with thrombocytopenia and HFpEF (RR 1.66, 95% CI 1.16–2.37, p=0.021) or HFrEF (RR 1.35, 95% CI 1.09–1.68, p=0.03) had higher risk of all-cause long-term mortality, but not those with HFmrEF and thrombocytopenia (RR 1.09, 95% CI 0.67–1.76, p=0.73), possibly due to the predominance of mild thrombocytopenia (80.9%). In multiple regression analysis, after adjusting for age and sex, alongside NT-proBNP levels and left ventricular ejection fraction, moderate thrombocytopenia (p=0.031) was an independent predictor of all-cause long-term mortality, but not mild thrombocytopenia (p=0.415). Due to the very low number of patients, no multiple regression analysis could be computed with severe thrombocytopenia. Conclusions Thrombocytopenia is an independent predictor of mortality in HF patients, especially platelet counts below 1ehz747.03530/uL. In both patients with HFrEF and HFpEF this biomarker should be assessed for prognosis.

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Neuromyelitis optica spectrum disorders (NMOSD) are a heterogeneous group of potentially disabling central nervous system inflammatory disorders. Association with other organ-specific or multisystem autoimmune disorders is commonly encountered. We report the case of a Caucasian woman with AQP4-IgG positive NMOSD and primary Sjögren syndrome - previously reported as a poster at the 14th Congress of the Romanian Society of Neurology (abstract published in ROJN, Vol. XV, Suppl). The clinical onset followed the successful treatment of chronic hepatitis C with interferon alpha and ribavirin. To the best of our knowledge, similar clinical presentations have not been described. The etiopathogenic treatment included high dose methylprednisolone, immune suppression with cyclophosphamide, and periodic plasma exchanges. In spite of an active disease with very high baseline AQP4-IgG titres, during the four years of treatment the patient has had only one relapse and has no residual disability.