Usually, these polyps are asymptomatic but gastric polyps may be the cause of dyspepsia, heartburn, bleeding from the upper gastrointestinal tract, and, rarely, gastric outlet obstruction while colorectal polyps may be the cause of rectal bleeding, anemia, constipation, diarrhea, weight loss, and abdominal pain.Individuals with chronic H. pylori infection have an increased risk of acquiring a cancer that is directly related to this infection. These cancers are stomach adenocarcinoma, less commonly diffuse large B-cell lymphoma of the stomach, or extranodal marginal zone B-cell lymphomas of the stomach, or, more rarely, of the colon, rectum, esophagus, or ocular adenexa (i.e. orbit, conjunctiva, and/or eyelids). The signs, symptoms, pathophysiology, and diagnoses of these cancers are given in the cited linkages. Microbiology
Morphology
Helicobacter pylori is a helix-shaped (classified as a curved rod, not spirochaete) Gram-negative bacterium about 3 μm long with a diameter of about 0.5 μm . H. pylori can be demonstrated in tissue by Gram stain, Giemsa stain, haematoxylin–eosin stain, Warthin–Starry silver stain, acridine orange stain, and phase-contrast microscopy. It is capable of forming biofilms and can convert from spiral to a possibly viable but nonculturable coccoid form.Helicobacter pylori has four to six flagella at the same location; all gastric and enterohepatic Helicobacter species are highly motile owing to flagella. The characteristic sheathed flagellar filaments of Helicobacter are composed of two copolymerized flagellins, FlaA and FlaB. Physiology
Helicobacter pylori is microaerophilic – that is, it requires oxygen, but at lower concentration than in the atmosphere.
It has been found that mothers of patients with this disease have a higher incidence of ICP, suggesting that heterozygote carriers of these mutations are also predisposed to ICP.In addition to genetic changes to bile salt transport molecules, high levels of estrogen glucuronides have been shown to inhibit the bile salt export pump (BSEP) ABCB11, and high levels of progesterone to inhibit the ABCB4 (MDR3) phospholipid transporter.Consequently, both genetic mutations in hepatocyte proteins involved in bile secretion together with inhibition of those proteins by high levels of hormone metabolites in pregnancy may have roles in the pathogenesis of ICP. Environmental factors
A number of features of ICP suggest that environmental factors also have a role in the disease:

It has been reported that the incidence of ICP is higher in winter than summer. The incidence of ICP in Chile has dropped from 14% of pregnancies before 1975 to 4% in 2016. ICP recurs in between 60% and 90% of subsequent pregnancies. Low serum selenium levels have been linked to ICP, although the role of selenium in bile secretion is not known. Diagnosis
ICP is diagnosed by blood tests including a serum bile acid test and liver function test. While most pregnant women experience some itch from time to time, itching without a visible rash, or persistent or extensive itch symptoms should be reported to the midwife or obstetrician.