Iron deficiency anemia, but not getting better after iron supplementation? It turned out to be this thing infected

A variety of causes can lead to anemia in children, of which iron deficiency anemia can be quickly alleviated by iron supplementation, the case we are talking about today is also a child with iron deficiency anemia, but its anemia has not improved after iron supplementation, what is the cause? Let's take a look.

Case profile

Male, 13 years old, fatigue, slightly pale lips about 2 months in the clinic.

Present medical history: During outpatient visits at local county hospitals, blood routine examination shows: hemoglobin (Hb): 82 g/L, average volume of red blood cells (MCV): 72fl, mean amount of hemoglobin (MCHC): 21 pg, mean hemoglobin concentration (MCH): 0.27, serum ferritin (SF): 11 μg/L. Outpatient doctors have been giving dextran iron orally for more than a month, and the blood routine is shown on review: Hb: 85g/L. Unbiased food, local residents.

Physical examination: clear, mental, slightly pale conjunctiva of both eyes, slightly pale lips, negative heart and lungs, mild tenderness under the sword process, free movement of limbs, negative nervous system.

Follow up on the medical history: no bone pain, occasional abdominal pain, mostly under the sword process, uncertain time, normal bowel and urine.

Relevant tests are given:

Liver and kidney function is normal, abdominal ultrasound: no abnormalities in the hepatobiliary pancreas and spleen, no abnormalities in the urinary system, multiple mesenteric lymph nodes can be seen, the maximum is 15 mm×5 mm.

Helicobacter pylori (Hp) 7 tests: positive for HpI, negative for HpII., positive for cytotoxicity-associated gene protein (CagA) (116KD), positive for vacuolar toxin A (VacA) (95KD), positive for vacuolar toxin A (VacA) (91KD), positive for urease (Ure) A(30KD), positive for urease (Ure)B(66KD).

Further gastroscopy was recommended, but parents refused.

At this point, the diagnosis of the child: Helicobacter pylori infection, iron deficiency anemia.

Why does Helicobacter pylori infection lead to iron deficiency anemia?

What are the characteristics of Helicobacter pylori?

Helicobacter pylori is a unipolar, multi-flagellar, blunt-rounded, spiral-curved gram-negative, microaerobic bacterium that lives in various areas of the stomach and duodenum. This is shown in Figure 1 below.

Fig. 1 Helicobacter pylori morphology

In 1983, Australian scientists Barry J. Marshall and J. Robin Warren was successfully isolated for the first time from gastric mucosal biopsy tissue in patients with chronic active gastritis.

In 1994, it was listed by the World Health Organization (WHO) as a category I (i.e., affirmative) biological carcinogen.

In 2005, Australian scientists Barry J. Marshall and J. Robin Warren won the Nobel Prize in Physiology or Medicine for his discovery of Helicobacter pylori.

Characteristics of Helicobacter pylori infection: high infectivity, high infection rate, large number of infected people, and more disease-inducing diseases.

Humans are the only source of infection for Helicobacter pylori, and the route of transmission is the digestive tract, which can be transmitted by mouth-to-mouth (shared tableware, water cups, etc.), gastric-oral transmission (gastric reflux to the mouth), fecal-oral transmission (Helicobacter pylori can be excreted with stool). Therefore, in some cases, you may be infected with Helicobacter pylori, such as eating water or food contaminated with Helicobacter pylori, eating together without using chopsticks, kissing with a Person infected with Helicobacter pylori, breastfeeding of a Helicobacter pylori infection mother, and so on.

High infection and familial clustering in children are prominent features of Hp infection, and intra-family transmission may be the main route of Hp infection.

Why Helicobacter pylori causes it

What about iron deficiency anemia?

In childhood, there is a sharp increase in Helicobacter pylori infection, which increases at a rate of 3% to 10% per year, and the infection rate is about 40% to 60% in the teenage years, that is, most of them are infected in childhood. Once infected, Helicobacter pylori persists in the body for decades, with little natural eradication.

Helicobacter pylori is not only associated with the onset of gastrointestinal diseases, but may also be associated with extragastric disorders such as cardiovascular, skin, nerve, immune, blood, liver, gallbladder, respiratory, endocrine, and metabolic disorders [1].

Epidemiological studies in recent years have shown that Hp is one of the main risk factors for the development of digestive diseases, such as: functional dyspepsia, constipation, esophagitis, gastritis, peptic ulcer, chronic gastritis, etc. Helicobacter pylori is also one of the high risk factors for gastric cancer.

So how does Helicobacter pylori cause iron deficiency anemia? There are mainly the following reasons[2]:

This results in a decrease in the body's absorption of iron

Non-heme iron is the main form of daily dietary intake of iron. Both ascorbic acid and gastric acid in gastric juice are promoters of non-heme iron absorption, and Hp infection can cause a decrease in the level of both in gastric juice, resulting in decreased absorption of non-heme iron. Hp infection also often causes atrophic gastritis (ABG), often accompanied by too little stomach acid and alopecia, which reduces iron absorption. The main sites of iron absorption are the duodenum and proximal jejunum, and Hp infection can easily lead to duodenal damage, causing iron malabsorption disorders.

Hp increases the body's demand for iron

Hp infection can increase the content of human lactoferrin (HLF) in the tissues of the stomach and duodenal mucosa, and Hp can take more iron from HLF, which in turn promotes hp proliferation, resulting in a vicious cycle.

Increased loss of iron

Hp can cause erosive hemorrhagic gastritis, such as chronic gastritis and peptic ulcer, leading to overt or occult blood loss in patients, and long-term neglect can lead to the occurrence of iron deficiency anemia [3]. Sometimes although gastroscopy does not have any bleeding foci, Hp can cause epithelial cell dysfunction, resulting in the loss of elemental iron and iron-containing proteins from the mucosa of the human stomach and duodenum.

Prevention in everyday life

Because most of the infections of Helicobacter pylori are carried out from the digestive tract, the prevention focus is on the digestive tract. Pay attention to oral hygiene, regularly change toothbrushes, disinfect dishes and chopsticks, divide meals, apply public chopsticks at home, especially in the family of parents and children's tableware should be used separately, but also to abandon the mouth-to-mouth way to feed infants and young children or chewed food to children after feeding bad habits.

Patients after radical treatment should still pay attention to preventing re-infection, especially parents need to treat together, which is the key to avoid mutual infection and re-infection.

In the children mentioned above, after 14 days of anti-Helicobacter pylori treatment, continued oral dextran iron, hemoglobin recovered to 128 g/L after one month. Inform the child's mother to continue oral iron to ensure that the body's iron is sufficient. The child's mother was overjoyed and thanked her.

【Reference】

Wang Jiajing, Gu Haiying.Genotyping techniques and applications of Helicobacter pylori. Journal of Zhejiang University(Medical Scienc),2018,47(1):97-103.

Lin Xi,Chen Xiaobing,Wu Bin. Effects of Helicobacter pylori infection on iron nutrition, growth and development in children[J].Foreign Medicine (Pediatrics Division),2001,28(6):305-307.

Yang Xuewen, Wang Liwen, Chen Yunfeng, Miao Jieping, Chen Yajun. Helicobacter pylori v acA genotyping and cag A gene detection. Chinese Journal of Health Inspection,2000,10(4):391-394.]

[4] Editorial Board of Chinese Journal of Pediatrics, Gastroenterology Group, Science Branch of Chinese Medical Association. Expert consensus on the diagnosis and treatment of Helicobacter pylori infection in children. Chin J Pediatrics,2015,53(7):496-498.

Source: Pediatrics Channel of the Medical Professions

Editor: Ren Mileage Reviewer: Xiao Ran