Case Report Coexistence of Helicobacter pylori and Giardia duodenalis causes severe iron deficiency anaemia in an adult male: a case report

Introduction: Iron deficiency anaemia (IDA), the most prevalent type of anaemia, is recognised as a significant global health concern that affects individuals of all ages. Case Presentation: Herein, we present a case involving an adult male coinfected with Helicobacter pylori and Giardia duodenalis , which precipitated severe IDA. Results: A 24-year-old male presented with symptoms including fatigue, dizziness, headache, abdominal pain, and diarrhoea persisting for four weeks. Thorough blood tests, including complete blood counts, blood film, and iron studies, conclusively established the presence of severe IDA. Furthermore, his faecal sample was collected and subjected to analysis of common bacterial and parasitic gastrointestinal infections. Examination of upper and lower gastrointestinal pathogens indicated that the severe IDA was most likely a result of coinfection with H. pylori and G. duodenalis . The patient received treatment involving antibiotics and iron replacement therapy, which resulted in an improvement in both his symptoms and laboratory results. Conclusions: The present report provides crucial insights into the synergistic effect of concurrent H. pylori and G. duodenalis infections, highlighting their potential to induce severe IDA in infected patients.


Introduction
Iron deficiency anaemia (IDA), the most prevalent type of anaemia, constitutes a global health concern that impacts individuals of all ages, affecting approximately 30% of the world's population [1].Decreased iron levels in the body perturb haemoglobin synthesis, leading to the ineffective production of red blood cells (RBCs).The diagnostic criteria for IDA can be listed as follows: (a) Haemoglobin levels are less than 12 g/dL for women and less than 13 g/dL for men; (b) serum ferritin is less than 30 ng/mL; (c) transferrin saturation is less than 20%; (d) Mean corpuscular volume (MCV) and mean corpuscular haemoglobin concentration (MCHC) are less than 80 fL and 32 g/dL, respectively; and (e) microcytic hypochromic RBCs evident in the morphology of peripheral blood smear [1].Common causes of IDA include inadequate iron intake, gastrointestinal bleeding, malabsorption, menstruation in women, heightened iron requirements, or gastrointestinal infections [1,2].
Helicobacter pylori is a gram-negative gastrointestinal bacterium that colonises the gastric mucosa [2].H. pylori is a pervasive bacterial infection in developing nations, afflicting about 50% of the global population [2].H. pylori can give rise to various gastrointestinal complications, such as chronic gastritis, malabsorption, peptic ulcers, and gastric cancer [2].H. pylori infection can facilitate the colonisation of other infections in the gastric mucosa by increasing stomach pH, among them being giardiasis [2,3].Giardiasis is a parasitic infection caused by Giardia duodenalis, also known as G. lamblia or G. intestinalis, which commonly infects children, travellers, and individuals with impaired immune systems [4,5].The primary mode of G. duodenalis transmission from one person to another is the faecal-oral route [4,5].G. duodenalis stands as one of the most widespread intestinal parasitic infections globally, affecting around 250 million individuals yearly [4,5].This parasite can cause malnutrition, abdominal pain, vomiting, flatulence, diarrhoea, anorexia, nausea, and weight loss [4,5].While both H. pylori and G. duodenalis can individually contribute to IDA by affecting iron absorption in the gastrointestinal tract [2,3], limited knowledge exists regarding the synergistic impacts of H. pylori and G. lamblia coinfection on the blood picture of these patients.In this context, we present a case of an adult male suffering from severe IDA due to H. pylori and G. duodenalis coinfection.

Case Presentation
A 24-year-old man presented to an internal medicine clinic with a chief complaint of headache, fatigue, dizziness, and diarrhoea persisting for four weeks.The physical examination revealed low blood pressure, abdominal pain, and skin pallor.The patient denied any history of gastrointestinal disorders such as Crohn's disease and celiac disease.Table 1 provides a summary of the patient's laboratory results.The analysis showed microcytic hypochromic anaemia with low levels of red blood cell (RBC) count (4.07 × 10 6 /μL), haemoglobin (Hb) at 9.4 g/dL, haematocrit at 29.8%, mean cell volume (MCV) of 73.2 fL, and mean cell haemoglobin concentration (MCHC) at 31.1 g/dL.The white blood cell (WBC) count was slightly high at 12.3 × 10 3 /μL with remarkable granulocytosis, and the platelet count was high at 554 × 10 3 /μL.An elevated RBC distribution width (RDW) was also observed.Results for thalassemia and haemolysis, including Hb electrophoresis, bilirubin, and lactate dehydrogenase (LDH), were unremarkable.Iron studies indicated severe iron deficiency, with serum iron and ferritin levels measuring 23.60 μg/dL and 3.25 ng/mL, respectively.A faecal occult blood test was performed and showed a positive result.Based on the patient's laboratory findings and symptoms, the investigation primarily focused on screening for the most common bacterial and parasitic gastrointestinal infections.No abnormal bacteria or other organisms were found in the stool culture.The patient's faecal sample was subsequently analysed for Helicobacter pylori, Giardia duodenalis, Entamoeba histolytica, and Cryptosporidium utilising direct wet mount preparation, immune chromatographic rapid test, and enzyme-linked immunosorbent assay (ELISA).The analysis of upper and lower gastrointestinal pathogens confirmed the presence of H. pylori and G. duodenalis, while E. histolytica and Cryptosporidium were not detected.Therefore, the most likely cause of the patient's IDA was the coinfection of H. pylori and G. duodenalis.The treatment regimen included the administration of clarithromycin, metronidazole, omeprazole, and ferrous sulfate, which led to an amelioration of the patient's symptoms and positive changes in his laboratory results.During the four-month follow-up, the patient's haemoglobin and haematocrit levels were measured at 13.9 g/dL and 43.1%, respectively.

Discussion
The case presented in this study is remarkably unique since the patient suffered from severe iron deficiency anaemia (IDA) due to H. pylori and G. duodenalis coinfection.The patient showed all the classic symptoms and laboratory findings of IDA, such as headache, fatigue, dizziness, skin pallor, microcytic hypochromic anaemia, anisocytosis, low haemoglobin, low mean corpuscular volume (MCV), high RBC distribution width (RDW), low serum iron, and low ferritin.Considering the potential of occult gastrointestinal bleeding to trigger the onset of IDA accompanied by reactive thrombocytosis [6], the present case prominently featured H. pylori infection as the causal agent in the formation of a peptic ulcer, As mentioned above, H. pylori counteracts stomach acidity by producing urease enzyme, which generates ammonia from stomach lumen urea, leading to decreased levels of stomach acid.This creates an environment in which certain intestinal parasites have a better chance of surviving in the stomach.One of these parasites, which can cross the gastric acidity and colonise the duodenum, jejunum, ileum, and colon, is G. duodenalis [3,4].Several reports from different parts of the world have investigated the presence of G. duodenalis infection among patients infected with H. pylori.For instance, the frequency of G. duodenalis in H. pylori-infected patients in Ethiopia, Egypt, Iran, Venezuela, Uganda, Turkey, and Mexico was 26.3%, 52.5%, 41.4%, 70.8%, 30.2%,45.8%, and 50.0%, respectively [4,[9][10][11][12][13][14].G. duodenalis can cause intestinal malabsorption due to impaired epithelial tight junctions, shortening of the epithelial brush border microvilli, and increased enterocyte apoptosis [3,5].The presence of H. pylori and G. duodenalis together may exert a synergistic effect on the host by modulating its immune response, resulting in severe epithelial cell damage and malabsorption [3].It is possible, therefore, that the presence of both pathogens together may suggest another pathogenic mechanism of IDA.

Conclusions
This report provides crucial insights into the synergistic effect of H. pylori and G. duodenalis when present together, causing severe IDA in infected patients.Thus, IDA patients with upper gastrointestinal symptoms should be investigated for both H. pylori and G. duodenalis to properly manage their clinical consequences.Further research with a larger sample size should be done to explore the prevalence and precise mechanism of this potential microbial interaction in IDA patients.Good hygiene and sanitation are indispensable for preventing the spread of these infections.

Table 1 .
The patient's laboratory results.