Efek hp pada mirobota gaster sepenuhnya belum diketahui, namun densitas dari hp

meningkat sesuai onset dari gastritis

The seroprevalence of Helicobacter pylori among 111 dyspepsia patients in Kalibaru village
was 22.5% (95% CI 14.8% - 30.2%). This result was lower than studies conducted by Yim et
al10 in South Korea and Chen et al7 in South China. Both studies also showed a decline in
prevalence caused by improvement of socio-economic condition and eradication therapy In
this study, mean age of patients with positive Helicobacter pylori infection were younger than
patients with negative results. By age group, the proportion of Helicobacter pylori infection
was increased according to age groupa nd decreased when eaching age of >60 years. There
was no significant relationship between age and Helicobacter pylori infection statistically.
Results of this study were consistent with similar studies in Indonesia. Research conducted by
Syam in Jakarta also found no relation between age and Helicobacter pylori.23 Another
studyin five major islands in Indonesia also obtained similar results with Kalibaru which was
higher proportion of Helicobacter pylori were in two age groups, under 29 years old and 50-
59 years old group.20 Study abroad showed different results.In South Korea, the older the
age, the higher the seroprevalence of Helicobacter pylori until it reach the age of 60 years and
then there was a decline.10 This difference may be caused by low socioeconomic level,
education levels as well as low hygiene level.

Prevalensi hp pada 111 pasien dispepsia di Kalibaru Jakarta berjumlah 22,5%. Hasil ini lebih
rendah dari pada penelitian di Korea Selatan dan China. Pada penelitian di Jakarta
menunjukkan tidak ada hubungan yang signifikan antara usia dan infeksi hp. Namun
beberapa penelitian di 5 pulau Indoneisa menunjukkan bahwa infeksi hp tertinggi terdapat
pada 2 kelompok usia yaitu <29 tahun dan kelompok usia 50-59 group. Pada penelitian di
Korea Selatan juga menunjukkan angka infeksi hp tertinggi dimula pada usia muda dan terus
meningkat sesuai dengan usia, dan menurun ketika usia> 60 tahun. Adanya perbedaan ini
disebabkan oleh tingkat sosial ekonomi yang berbeda, tingkat pendidikan dan tingat
kebersihan yang rendah.

Darnindro N, Syam AF, Fauzi A, Rumende CM. Seroprevalence and socio-demographic

factors of Helicobcater pylori infection in patients with dyspepsia in Kalibaru primary
health care north Jakarta. Acta Med Indones. 2015;47(4):297–303.

Helicobacter pylori is a Gram-negative spiral bacterium that colonizes the gastric mucous of
human, causing chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucous-
associated lymphoma. Despite the development of strong immune responses against Hp
infection in human, the bacteria are rarely eliminated from the stomach and infection is
usually lifelong.9,10 Infection of Helicobacter pylori induces strong local immune responses
in the gastric mucous of infected host. It is characterized by the recruitment of neutrophils, T
and B lymphocytes, plasma cells, macrophages and dendritic cells (DCs), together with
epithelial cell damage.11 Innate immune system is the first-line defense against invading Hp.
Toll-like reseptor-2 (TLR2) is a major innate receptor for the recognition of Hp infection and
may cause inflammation. Activation of these innate receptors led to activation of NF-κB,
caspase, and interferon pathways that result in production of pro-inflammatory cytokines
such as IL-1β, TNF-α, IL-6, MCP-1 and IFN-β. These cytokines attract acute inflammatory
mediators such as neutrophils as well as lymphocytes leading to activation of the adaptive
immune response

Helicobacter pylori berkoloni di mukosa gaster dan menyebabkan gastritis, ulkus peptikum,
adenokarsinoma gaster. Infeksi H-pylori cenderung menetap dan seumur hidup. Infeksi Hp
akan menginduksi sel imunitas yaitu neutrofil, limfosit B dan T, sel plasma, makrofag, dan
sel dendritik. Aktivasi dari sel imun bawaan tersebut akan menginduksi interferon untuk
memproduksi sitokin yang akan menarik mediator inflamasi akut dan menyebabkan aktivasi
respon imun adaptif.

Darwin E, Murni AW, Nurdin AE. The Effect of Psychological Stress on Mucosal IL-6
and Helicobacter pylori Activity in Functional Dyspepsia. Acta Medica Indones. April
2017;49(2):99–104.

Helicobacter pylori causes chronic gastritis in virtually all infected individuals.14 Such
inflammation in H. pylori carriers leads to a 3-fold to 10-fold increase in risk of peptic ulcer
disease as compared with H. pylori-negative subjects.15,16 During long-term follow-up,
peptic ulcers and the related complications occur in 10–15% of H. pylori carriers.16 When a
peptic ulcer is present, almost 100% of duodenal ulcers and approximately 80% of gastric
ulcers have H. pylori infection in the absence of other risk factors, such as NSAID use or
Zollinger–Ellison syndrome.17 Moreover, the cause-and-effect relationship between H.
Pylori infection and peptic ulcers is supported by the substantial benefit of H. pylori
eradication in terms of the healing of active ulcers18 and decrease in ulcer recurrence.19–21
A summary of 12 Randomized controlled trials (RCTs) showed that eradication therapy
significantly reduced the risk of gastric ulcer by 69% compared with no eradication
therapy.22 In two meta-analyses including five and seven RCTs, significant reductions of
57% and 50% were found, respectively, in the prevention of peptic ulcers among NSAID
users following H. pylori eradication.23,24

Mahachai V, Vilaichone R, Pittayanon R, Rojborwonwitaya J, Leelakusolvong S,

Maneerattanaporn M, dkk. Helicobacter pylori management in ASEAN: The Bangkok
consensus report: Helicobacter pylori management. J Gastroenterol Hepatol. Januari
2018;33(1):37–56.
Inflamasi pada antrum akan mensti-mulasi sekresi gastrin yang selanjutnya a-kan merangsang
sel parietal untuk mening-katkan sekresi asam lambung. Infeksi heli-cobacter pilory
meningkatkan kadar gastrin terutama yang berasal dari mukosa antrum. Selain itu
peningkatan sekresi gastrin juga terjadi akibat menurunnya kadar somatosta-tin dalam
mukosa antrum yang berasal dari sel D. Dalam hal ini, secara fisiologis so-matostatin atau sel
D berfungsi sebagai acid brake, yang menekan fungsi sel G dan sekresi asam lambung oleh
sel parietal

Permatasari L, Wangko S. PERAN SEL GASTRIN (SEL G) DALAM SALURAN

PENCERNAAN. J BIOMEDIK. 2011;3(3)

The most common GI symptoms associated with HP infection are vomiting, burning
sensation, passing gas, bloating, bad breath, nausea, belching, loss of appetite, gnawing pain,
heartburn, indigestion, stomach growls, gurgling, grumbling and groaning, indigestion
(dyspepsia), and gastritis.8,30–32 Kusters et al established that the first phase of HP
colonization might be associated with dyspeptic symptoms such as fullness, nausea,
vomiting, inflammation of the proximal and distal mucosa, or pan-gastritis

Fase pertama dari kolonisasi Helicobacter pylori berhubungan dengan gejala dispepsia
seperti mual,muntah, dan perut terasa penuh.

Pada penelitian di United States pada ras putih, hitam, Hispanik, Asian, dan Amerika
ditemukan resiko tertinggi infeksi Hp berhubungan dengan usia, dimana terjadi pada
kelompok usia 41-50 tahun dan 51-65 tahun.

In our study, the highest risk for HP infection associated with age was found in the age
groups of 41–50 and 51–65 years, for all racial/ethnic populations. In the US, HP infection
mainly affects older adults (~50% of those aged >60 years compared to 20% of those aged
<40 years), particularly those with low economic resources

Using the demographic variables, the prevalence ratios give the risk of the infection in
reference to a determined demographic characteristic. For example, for the gender variable,
the risk of HP infection when the patients were females (using the male gender as the
reference group) was determined. Using the variable “age,” the risk of infection associated
with belonging to some age group was determined, using the younger age group (21–30
years) as a reference group.

Pada penelitian di United States ditemukan resiko infeksi Hp lebih tinggi terjadi pada jenis
kelamin perempuan

Table 1 presents the RR of HP infection based on sex and age among the ethnic/race
populations studied. The risk of HP infection was higher in females than in males among the
white, black, and Hispanic groups. Females also had a higher frequency of the infection
compared to males (63.8% vs 36.2%; 66.0% vs 33.99%; 63.8% vs 36.2%; 62.5% vs 37.5%;
and 56.8% vs 43.2% for white, black, Hispanic, API, and AN/NA, populations, respectively).
The distribution of patients by age showed that except for Hispanics (21.2%), patients who
were 51–65 years old had the highest frequency of HP (35.3%, 33.01%, 30.94%, and 27.4%
for white, black, API, and NA/AN patients, respectively). The frequencies for the groups of
41–50 and 31–40 years old were 23.5%, 26.8%, 23.63%, 24.3%, and 22% and 19.3%, 20.4%,
28.11%, 25.7%, and 23.96% for white, black, Hispanic, APIs, and NA/ANs, respectively.
Young adults aged 21–30 years had the lowest frequencies of infection (21.9%, 19.81%,
27.1%, 19.1%, and 26.7% for white, black, Hispanic, API, and NA/AN populations,
respectively). Table 1 also shows that compared to patients from the other age groups, black,
Hispanic, and API patients above the age of 40 had the highest RR of HP infection.

Budzyński and Kłopocka6 established that HP infection is the cause of the most common
form of chronic gastritis and contributes to the pathogenesis of functional dyspepsia and
gastritis symptoms, particularly in patients who live in stressful conditions (mental stress can
affect the mucosal immune response, increasing HP colonization)

Budzynski menyatakan bahwa infeksi Hp menyebabkan gatritis kronik, berkontribusi dalam

patogenesis dispepsia fungsional, dan gejala gastritis

Huerta-Franco M-R, Banderas JW, Allsworth J. Ethnic/racial differences in gastrointestinal symptoms

and diagnosis associated with the risk of Helicobacter pylori infection in the US. Clin Exp
Gastroenterol. Januari 2018;Volume 11:39–49.