Medical Hypotheses 82 (2014) 795–796

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Correspondence Helicobacter pylori infection, insulin resistance and nonalcoholic fatty liver disease

To the editor: We read with interest the case report by Abenavoli et al. [1], reporting improvement in insulin resistance (IR) and fatty liver indices after Helicobacter pylori (Hp) eradication therapy in an adult man, thereby providing further evidence for the interplay among Hp infection, IR and nonalcoholic fatty liver disease (NAFLD). In our previous systematic review, a trend towards a positive association between Hp infection and homeostatic model of assessment insulin resistance (HOMA-IR) was reported [2], despite a significant heterogeneity between studies regarding the diagnostic methods of Hp infection and the study populations. We have also shown that biopsy-proven NAFLD patients had higher anti-Hp IgG titers, together with lower circulating adiponectin and higher tumor necrosis factor (TNF)-a levels (which all contribute to NAFLD pathogenesis), compared to non-NAFLD individuals [3]. In the same series, the participants with history of Hp therapy and/or Hp seropositivity had significantly higher HOMA-IR and TNF-a levels compared with those without either history of Hp therapy or Hp seropositivity [3]. Moreover, the presence of 16S recombinant RNA of Hp spp. on liver samples of NAFLD patients was previously reported [4], although it remains unclear whether Hp was an incidental finding in these specimens or it affected the course of NAFLD. Other authors reported increased liver and spleen size in Hp-positive compared with Hpnegative individuals, and those with hepatic steatosis [5]. An association between Hp infection and NAFLD appears appealing, because Hp infection affects almost half of the world’s population, the prevalence of NAFLD is increasing worldwide and Hp eradication regimens might have therapeutic implications on NAFLD [2]. Since relative existing evidence is limited, further research is warranted. Conflict of interest statement The authors have no competing interests pertinent to this manuscript. Sources of funding No grant supported this study. Sources of support or grant None. References [1] Abenavoli L, Milic N, Masarone M, Persico M. Association between nonalcoholic fatty liver disease, insulin resistance and Helicobacter pylori. Med Hypotheses 2013;81(5):913–5.

[2] Polyzos SA, Kountouras J, Zavos C, Deretzi G. The association between Helicobacter pylori infection and insulin resistance: a systematic review. Helicobacter 2011;16(2):79–88. [3] Polyzos SA, Kountouras J, Papatheodorou A, et al. Helicobacter pylori infection in patients with nonalcoholic fatty liver disease. Metabolism 2013;62(1):121–6. [4] Pirouz T, Zounubi L, Keivani H, Rakhshani N, Hormazdi M. Detection of Helicobacter pylori in paraffin-embedded specimens from patients with chronic liver diseases, using the amplification method. Dig Dis Sci 2009;54(7):1456–9. [5] Dogan Z, Filik L, Ergul B, Sarikaya M, Akbal E. Association between Helicobacter pylori and liver-to-spleen ratio: a randomized-controlled single-blind study. Eur J Gastroenterol Hepatol 2013;25(1):107–10.



Stergios A. Polyzos Jannis Kountouras Christos Zavos Georgia Deretzi Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece ⇑ Corresponding author. Address: 13 Simou Lianidi, 551 34 Thessaloniki, Greece. Tel./fax: +30 2310424710. E-mail address: [email protected] (S.A. Polyzos) doi:http://dx.doi.org/10.1016/j.mehy.2014.03.003

Super ORS: Is calcium the key?

Oral rehydration solution (ORS) has remarkably reduced the death rate due to diarrhea in many developing countries [1]. However, recourse to intravenous fluid therapy is necessary in cases of severe diarrhea. Attempts to convert ORS into Super ORS in order to enhance its rehydrating capacity have met with varying degrees of success [2]. A consensus on their composition and use, has not been arrived at. WHO recommended ORS now contains 75 mM of glucose along with Sodium, Potassium, Chloride and Citrate giving an osmolarity of 245 mOsm [3]. It is thought that the intestinal cotransporter of glucose and sodium, SGLT which is functional even in severe diarrhea, transports these two substrates into the cell. Sodium is pumped out of the cell across the basolateral membrane to create an osmotic force that would draw water from the lumen into the capillaries in the gut wall [2]. The path the water takes- transcellular or paracellularhas not been defined. In recent years evidence has accumulated demonstrating the induction of another glucose transporter GLUT 2 into the brush border of epithelial cells when presented with large amounts (50– 100 mM) of glucose [4]. The sequence of events is reported to be as follows: High luminal glucose, Increased SGLT activity, Insertion of a nifedipine inhibitable calcium channel , Rise in intracellular calcium leading to insertion of GLUT 2 in apical membrane and rearrangement of cytoskeleton [5]. This rearrangement involves phosphorylation of myosin light chain (MLC) in the terminal web and the perijunctional actomyosin ring. Such cytoskeletal changes

Helicobacter pylori infection, insulin resistance and nonalcoholic fatty liver disease.

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