Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors.The diagnosis of Helicobacter pylori can be made by:

Urea breath test (noninvasive and does not require EGD);
Direct culture from an EGD biopsy specimen; this is difficult and can be expensive. Most labs are not set up to perform H. pylori cultures;
Direct detection of urease activity in a biopsy specimen by rapid urease test;
Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;
Stool antigen test;
Histological examination and staining of an EGD biopsy.The breath test uses radioactive carbon to detect H. pylori. To perform this exam, the person is asked to drink a tasteless liquid that contains the carbon as part of the substance that the bacteria breaks down. After an hour, the person is asked to blow into a sealed bag. If the person is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria. The possibility of other causes of ulcers, notably malignancy (gastric cancer), needs to be kept in mind. This is especially true in ulcers of the greater (large) curvature of the stomach; most are also a consequence of chronic H. pylori infection.
The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (COX-1), which is essential for the production of these prostaglandins. Besides this, NSAIDs also inhibit stomach mucosa cells proliferation and mucosal blood flow, reducing bicarbonate and mucus secretion, which reduces the integrity of the mucosa. Another type of NSAIDs, called COX-2 selective anti-inflammatory drugs (such as celecoxib), preferentially inhibit COX-2, which is less essential in the gastric mucosa. This reduces the probability of getting peptic ulcers; however, it can still delay ulcer healing for those who already have a peptic ulcer. Peptic ulcers caused by NSAIDs differ from those caused by H. pylori as the latters appear as a consequence of inflammation of the mucosa (presence of neutrophil and submucosal edema), the former instead as a consequence of a direct damage of the NSAID molecule against COX enzymes, altering the hydrophobic state of the mucus, the permeability of the lining epithelium and mitochondrial machinery of the cell itself. In this way NSAIDs ulcers tend to complicate faster and dig deeper in the tissue causing more complications, often asymptomatically until a great portion of the tissue is involved.