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Helicobacter pylori infection (Hp-I) is a prevalent disorder identified in the majority of the population in many countries around the world and is responsible for substantial gastrointestinal morbidity. Likewise, neurodegenerative diseases such as Alzheimer's disease, Parkinson's diseases, multiple sclerosis or glaucoma defined as ocular Alzheimer's disease, are associated with a large public health burden and are among the leading causes of disability. Emerging evidences suggest that Hp-I may be associated with neurodegenerative conditions. Moreover, Hp-I could be a predictor of metabolic syndrome (MetS). Hp-I and its related MetS may induce gastrointestinal tract dys-motility disorders with systemic complications possibly including central nervous system neurodegenerative pathologies. We hereby explore the emerging role of Hprelated metabolic gastrointestinal dys-motilities on the molecular pathophysiology of Hprelated neurodegenerative and gastrointestinal disorders. Improving understanding of such Hp-I pathophysiology in brain pathologies may offer benefits by application of new relative therapeutic strategies including novel opportunities toward enhancing Hp eradication.

Context Limited clinical data suggest Helicobacter pylori (Hp) infection may contribute to nonalcoholic fatty liver disease (NAFLD) pathogenesis. Objectives The effect of Hp eradication on hepatic steatosis (magnetic resonance imaging), nonalcoholic fatty liver disease fibrosis score and HSENSI (Homocysteine, serum glutamic oxaloacetic transaminase, Erythrocyte sedimentation rate, nonalcoholic steatohepatitis Index) in nonalcoholic steatohepatitis patients. Methods Thirteen adult patients with biopsy-proven nonalcoholic steatohepatitis, asymptomatic for gastrointestinal disease, underwent 13C urea breath test; Hp positive patients received eradication therapy until repeat test become negative. Hepatic fat fraction, standard biochemical tests and calculation of nonalcoholic fatty liver disease fibrosis score and HSENSI were performed at baseline and month 12. Results Hepatic fat fraction was similar for between and within group comparisons. Nonalcoholic fatty liver disease fibrosis score showed a non-significant trend towards decrease in Hp(+) [-0.34 (-1.39-0.29) at baseline and -0.24 (-0.99-0.71) at month 12; P = 0.116], whereas increase in Hp(-) group [-0.38 (-1.72-0.11) and -0.56 (-1.43-0.46), respectively; P = 0.249]. HSENSI was significantly decreased only in Hp(+) group [1.0 (1.0-2.0) at baseline and 1.0 (0-1.0) at month 12; P = 0.048]. Conclusions Hp eradication had no long-term effect on hepatic steatosis, but showed a trend towards improvement in nonalcoholic fatty liver disease fibrosis score and HSENSI. These results warrant larger studies with paired biopsies.

Helicobacter pylori (H. pylori) induces reactive oxygen species (ROS) production that contribute to pathogenesis of a variety of H. pylori-related gastric diseases, as shown in animal and human studies. Helicobacter pylori infection is also associated with variety of systemic extragastric diseases in which H. pylori-related ROS production might also be involved in the pathogenesis of these systemic conditions. We proposed that Hp-related ROS may play a crucial role in the pathophysiology of Hp-related systemic diseases including Alzheimer's disease, multiple sclerosis, glaucoma and other relative neurodegenerative diseases, thereby suggesting introduction of relative ROS scavengers as therapeutic strategies against these diseases which are among the leading causes of disability and are associated with a large public health global burden. Moreover, we postulated that H. pylori-related ROS might also be involved in the pathogenesis of extragastric common malignancies, thereby suggesting that H. pylori eradication might inhibit the development or delay the progression of aforementioned diseases. However, large-scale future studies are warranted to elucidate the proposed pathophysiological mechanisms, including H. pylori-related ROS, involved in H. pylori-associated systemic and malignant conditions.

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We present a case of previously healthy, immunocompetent, 41-year-old woman who developed systemic inflammatory response syndrome secondary to Neisseria gonorrhoeae bacteremia. Clinical course was complicated by the simultaneous formation of multiple muscular abscesses, epidural abscess, and septic spondylodiscitis. The patient responded well to prolonged ceftriaxone treatment and was released 10 weeks after initial admission. Spinal lesions and/or pyomyositis individually constitute rare complications of disseminated gonococcal infection. This case, combining both manifestations, is to our knowledge unique. Apropos, diversity of the clinical presentation, and therapeutic challenges for this historical disease are discussed for the practicing physician.

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