Tag: Helicobacter pylori

Author(s) Details:

Abdullah M. Nasrat
Zaitona Medical Center, Medina, Saudi Arabia.

Rania Ashour
Al Hayat National Hospital, Medina, Saudi Arabia.

This section is a part of the chapter: An Approach for the Hematologic Challenges of Helicobacter pylori in Children: An Expensive Cost of Parents’ Misbehavior towards their Kids

Increasing evidences indicate that H. pylori is an important reason for causing gastric carcinoma and lymphoma (Andreoli, 2001; Baron, 2000). Gastric cancer is the world’s second leading cause of cancer-related mortality. H. pylori was classified as a type I (definitive) carcinogen, while prolonged residual MALT lymphoma could constitute an additional risk of gastric carcinoma (Farinha & Gascoyne 2005; Copie-Bergman et al., 2005).

It has been estimated that 1:30-1:60 of the UK population die from an H. Pylori related disease (Moayyedi & Axon 1998). All these reasons make H. Pylori eradication a necessary attempt (Nasrat et al., 2015).

How to Cite

Nasrat, A. M., & Ashour, R. (2025). An Approach for the Hematologic Challenges of Helicobacter pylori in Children: An Expensive Cost of Parents’ Misbehavior towards their Kids. Medical Science: Trends and Innovations Vol. 4, 20–26. https://doi.org/10.9734/bpi/msti/v4/4043

 

To Read the Complete Chapter See Here

Author(s) Details:

Abdullah M Nasrat
Department of Surgery, Balghsoon Clinic, Jeddah, Saudi Arabia.

Salwa AM Nasrat
Department of Physical Therapy, Cardiac Surgery Academy, Cairo, Egypt.

Randa M Nasrat
Department of Internal Medicine, Helwan General Hospital, Helwan, Egypt.

Mohammad M Nasrat
Department of Internal Medicine, Helwan General Hospital, Helwan, Egypt.

Sana Y Babiker
Faculty of Medicine, Elrazi University, Sudan.

This section is a part of the chapter: Helicobacter pylori and Hyperuricemia: Revisiting Gout Diagnosis in Young Adults with Normal Renal Function

Hyperuricemia could contribute to diabetes, hypertension and arteriosclerosis due to endothelial dysfunction triggered by vascular wall tissue inflammation because of urate crystal deposition. These reasons are sufficient to render physicians anxious in the immediate assessment and treatment of elevated serum uric acid levels. On the contrary, patients hesitate to accept the decision of their pre-gouty illness due to elevation of serum urate particularly if they are young and have perfect renal function. H. pylori could migrate or get forced to migrate to the colon leading to colonic re-absorptive error with excess accumulation of fluids and salts in the body; uric acid could be among these reabsorbed elements giving a picture of elevated serum uric acid levels that would have no relation to age of the individual or the integrity of his renal function. Furthermore, gout has been recently considered as one of the auto-inflammatory diseases, hence cytokines are the most common mediators of inflammation; therefore, the role played by the increased mucosal production of inflammatory mediators (cytokines) induced by H. pylori is supposed to contribute to the pathogenesis of gout. In this situation, hyperuricemia is not expected to be adequately or successfully improved by traditional urate-lowering measures regardless of the age of the patient or the state of his kidney function.

How to Cite

Nasrat, A. M., Nasrat, S. A., Nasrat, R. M., Nasrat, M. M., & Babiker, S. Y. (2025). Helicobacter pylori and Hyperuricemia: Revisiting Gout Diagnosis in Young Adults with Normal Renal Function. Medical Science: Trends and Innovations Vol. 4, 1–8. https://doi.org/10.9734/bpi/msti/v4/3641

To Read the Complete Chapter See Here