Peptic ulcer disease among dyspeptic patients at endoscopy unit, University of Gondar hospital, Northwest Ethiopia

Dyspepsia is a common complaint in upper gastrointestinal disorders. It is described as predominant epigastric pain lasting for at least one month [1, 2]. It can manifest as postprandial fullness, early satiety, or epigastric burning or pain. Globally, dyspepsia occurs in 10–20% of adults, and accounts for 3% of medical office visits. Dyspepsia has an impact on the quality of life of patients and the expenses to the health care service [1, 2]. According to previous studies, peptic ulcer disease (PUD) occurred in 2.4–3.5% of the Western populace, 12–15% of Asian inhabitants, and 24–28% of sub-Saharan African dwellers [3‐8]. Helicobacter pylori (H. pylori) infection and non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin (ASA) use are the major culprits for causing gastroduodenal mucosal injuries [9‐14]. H. pylori is widely known to cause gastritis and peptic ulcer disease. Also, H. pylori is attributed to gastric cancer and gastric B-cell lymphoma, and is categorized as a class I carcinogen by the International Agency for Research on Cancer (IARC), a division of the World Health Organization (WHO) [9‐12]. Use of NSAIDs is recognized to cause erosive gastritis and peptic ulcer disease. Prevalence of PUD was documented to be 14–25% among NSAIDs/ASA users [13‐15]. Other less frequently implicated risk factors for PUD include genetics, stress, diet, smoking and alcohol [16, 17]. Global reports indicated that H. pylori infection rate among PUD patients was 14–21% in the United States, 60–70% in Asia, and 70–90 in sub-Saharan Africa [4, 5, 7, 18‐23]. There was no recent document on H. pylori infection rate among PUD patients in Ethiopia. There are several invasive and non-invasive diagnostic tests to detect H. pylori infection. Invasive tests include endoscopic biopsy specimen for histology, culture and rapid urease test (RUT) and polymerase chain reaction (PCR). Non-invasive tests consist of urea breath test (UBT), serum antibody test, stool antigen test, saliva antibody test and urinary antibody test [24, 25]. The choice of diagnostic tests is based on the prevalence of H. pylori infection, the availability and cost of the diagnostic tests, and patient-related characteristics [19‐23]. This study used fecal H. pylori antigen test to document active H. pylori infection, which has optimal diagnostic accuracy. The study aimed to determine the magnitude, H. pylori infection rate, and associated factors of PUD among dyspeptic patients at the University of Gondar hospital, Northwest Ethiopia. The study would give valuable information on the approach to treating dyspepsia in the setting and similar institutions.

Among a total of 218 dyspeptic patients, active H. pylori infection was documented in 49% (95% CI 42.4–56.2) of study subjects. Likewise, the H. pylori infection rate among PUD patients was 71% (95% CI 66.7–77.5). These findings were congruent with hospital-based sub-Saharan African (SSA) reports. The African reports verified that 40–65% of dyspeptic and 65–90% PUD patients were positive for H. pylori infection [7, 8, 19, 20, 23, 24]. The Ethiopian pooled prevalence of H. pylori infection was 52.2% (95% CI 45.8–58.6) in a recent hospital-based meta-analysis [30]. The global magnitude of H. pylori infection was 34% in Western Europe, 37% in Northern America, 55% in Asia, and 70% in Africa [31]. The global difference in the magnitude of the H. pylori infection rate could be explained by the difference in socio-economic status, environmental sanitation, living conditions, and personal hygiene. In this study, PUD (35%) was the commonly observed abnormal endoscopic lesion, followed by gastritis/duodenitis (19%) and gastric mass (6%). More than one-third (36%) had functional dyspepsia. Recent Nigerian study reported that gastritis/duodenitis (27%) and PUD (28%) were the frequently documented abnormal endoscopic findings. Gastric cancer (2.3%) was less frequently reported [7]. Studies in Tanzania and Ethiopia reported that gastritis/duodenitis (80–98%) followed by PUD (25–32%) were the commonly observed endoscopic pathologies. Gastric cancer was detected in 3–7% of dyspeptic patients [8, 19]. PUD (62%) followed by gastric cancer (12%) was the frequently detected endoscopic finding in Ghanaian study [23]. While, studies in Nigeria and Kenya witnessed gastritis/duodenitis (72–79%) was the commonest endoscopic finding. PUD (6.5–13%) and gastric cancer (1.4–2.3%) were less frequently reported [20, 24]. The difference in the type of gastro duodenal lesions among dyspeptic patients in African reports could be explained by differences in patient-related characteristics (age, genetics), H. pylori virulence strain, NSAIDs/ASA exposure rate, lifestyle preferences (smoking, alcohol), and other environmental factors [19, 20, 23, 24]. This study revealed that nearly forty percent (39.5%) of dyspeptic patients had a history of NSAIDs/ASA use, and more than half (55%) of NSAIDs/ASA users developed PUD. Western literature reviews documented that dyspepsia occurred in up to half (50–60%) of patients taking NSAIDs/ASA and up to a third (15–30%) of patients using NSAIDs/ASA developed PUD [13‐15]. On multivariable logistic regression analysis, odds of developing PUD was sixfold higher among dyspeptic patients with H. pylori infections than those with negative H. pylori infections (AOR = 6.298, 95% CI 2.965–13.378, P value <  0.001). It was confirmed that H. pylori establishes prolonged gastro duodenal mucosal infection, and leads to chronic active gastritis and PUD [9‐12, 19, 20, 23, 24]. Dyspeptic patients who use NSAIDs/ASA had sixfold increased risk of developing PUD as compared to non-NSAIDs/ASA users (AOR = 6.252, 95% CI 2.925–13.362, P value  <  0.001). NSAIDs/ASA interferes with the cyclo-oxygenase (COX) pathway and depletes biosynthesis of gastric prostaglandins. In addition, NSAIDs/ASA are weak acids which cause direct gastric mucosal toxic injury [9, 10, 13‐17]. Study subjects with non-married status were 60% protected from developing PUD as compared to their counter parts (AOR = 0.367, 95% CI = 0.154–0.887, P value = 0.024). Reduced family size and non-crowded living condition among non-married subjects might contribute to reduced H. pylori infection rate and occurrence of PUD.

The study subjects were referred patients to the hospital, which was more likely to be the severely ill study candidates. In addition, the convenience sampling method might introduce selection bias.

H. pylori infection was often detected in dyspeptic patients. Majority of PUD patients were diagnosed to have H. pylori infection. Dyspeptic patients with H. pylori infection and NSAIDs/ASA use were at risk of developing PUD.

Medical treatment of PUD should target treatment of H. pylori infection and cautious use of NSAIDs/ASA. Community-based study is required to conclude the actual findings in the target population.