Polypoid lesions of the gallbladder are cystic bulge-like lesions of the gallbladder mucosa, a general term for morphologic names. With the widespread use of imaging technology in clinical practice, the detection rate of gallbladder polypoid lesions is gradually increasing, with a detection rate of 4%-7% in adults undergoing abdominal ultrasonography. inflammatory polyps, adenomyosis of the gallbladder, etc. Most of the incidentally found polypoid lesions are benign, and very few are malignant or precancerous.
I. Epidemiology
The incidence of PLG varies widely in the healthy population as reported in the literature. 6.3% of 3510 adults have been reported in China, while the incidence in foreign countries is 5%-7%, mostly in middle-aged patients and more common in women. 3.9:1 male to female incidence ratio has also been reported. 3%-12% of PLG is detected in gallbladder resection specimens. In some bulk reports PLG’s are commonly cholesterol polyps, while the incidence of malignant lesions is about 3% to 8%.
II. Classification
The majority of gallbladder polyp-like lesions are benign, and 82%-87% of domestic reports are benign. Pathologically, they can be divided into tumor polyp, including adenoma and adenocarcinoma, less common lipoma, hemangioma, smooth muscle tumor, neurofibroma, etc.; non-tumor polyp, including cholesterol polyp, inflammatory polyp, adenomyosis and adenomatous hyperplasia, yellow granuloma, ectopic gastric mucosa or pancreatic spleen tissue, etc.
Third, the formation factors of gallbladder polyp-like lesions
1, the formation factors of common gallbladder polyp-like lesions
(1) cholesterol polyp: cholesterol polyp is a common type of PLG, mainly due to abnormal lipid metabolism in bile, especially cholesterol metabolism disorder. There are no digestive enzymes in bile, but it has its special role. The results of some scholars found that gallbladder removal is a high risk factor for colorectal cancer. Under the physiological condition, each component is dissolved in bile in a certain proportion and is in a state of equilibrium. When the equilibrium is broken, the process of active or passive transport of cholesterol in bile to the epithelial cells of gallbladder mucosa is enhanced, and it is deposited in the lamina propria of gallbladder mucosa, invades the mucosal space, and is engulfed by macrophages to form foam cells. The foam cells accumulate in large numbers in the interstitial layer, causing the hyperplastic mucosa to bulge and protrude into the gallbladder, which forms cholesterol polyps.
(2) Inflammatory polyps: inflammatory polyps rank 2nd among benign lesions of PLG. Long-term stimulation of gallbladder by biological and chemical factors can cause chronic inflammation of gallbladder, and the process of chronic inflammatory damage and repair promotes the formation of inflammatory polyps of gallbladder. Its bulge is composed of capillaries, fibroblasts and chronic inflammatory cells. The gallbladder around the polyp has obvious inflammation, is not a true tumor, and no malignant transformation is recorded.
(3) Adenomyomatous hyperplasia of gallbladder: also known as adenomyomatous hyperplasia, it is a benign lesion of gallbladder mainly with mucosal epithelium and muscle layer hyperplasia, characterized by hyperplasia of epithelium and smooth muscle, accounting for more than 8.7% of gallbladder resections. Most scholars believe that the disease is the result of hypertrophy of the gallbladder wall due to mucosal hyperplasia, increased area of the gallbladder and smooth muscle hyperplasia, together with abnormal proliferation of nerve fibers in the gallbladder wall and gradual evolution based on incomplete gallbladder germinal cystification. Some scholars also believe that the occurrence of this disease may be based on chronic inflammation and neurogenic dysfunction of the gallbladder, which leads to abnormal gallbladder dynamics, especially spastic contraction of the gallbladder neck sphincter, resulting in restricted bile drainage, abnormally high intracapsular pressure, mucous membrane into the muscle layer to form diverticula and induce hyperplasia of the muscle layer.
(4) Gallbladder adenoma: Some scholars believe that chronic inflammation and gallbladder stones are closely related to the occurrence of gallbladder adenoma. Long-term chronic inflammatory stimulation and mechanical damage by stones, the mucosal epithelium of gallbladder appears more obvious fibrous connective tissue, blood vessels and proliferation of epithelial cells, glands and parenchymal cells in the process of repeated wear, regeneration and repair, which eventually causes proliferation to protrude into the gallbladder lumen to form polyps.
2.Other factors in the development of PLG
(1) The relationship between smoking and alcohol consumption and PLG: Smoking may be a susceptibility factor for PLG, and the incidence of PLG is significantly higher in smokers than in nonsmokers. Some scholars have found that alcohol consumption in middle-aged women has a protective effect on gallbladder disease, and the greater the amount of alcohol consumed, the lower the risk of gallbladder disease. It has also been suggested that long-term alcohol consumption causes metabolic disorders in the body, and ethanol can inhibit higher brain functions, causing chronic inhibition of the nerve center and the nerves regulating gallbladder activities, limiting bile drainage and depositing bile stagnation in the gallbladder mucosa, which can easily form polyps.
(2) The relationship between age and gender and PLG: A study on 9,750 healthy people of different ages and genders showed that the difference between the incidence of PLG in men and women in each age group was statistically significant; the difference between the incidence of PLG in men and women in different age groups was statistically significant. There is a close relationship between PLG and age, and the incidence of tumor polyps is higher than that of non-tumor polyps in people aged >50 years, i.e., the risk of cancerous polyps increases with age, but the opposite is true for those aged <50 years.
(3) Relationship between diet and PLG: 157 patients diagnosed with gallbladder polyps were studied, and 11 factors such as their gender, age, occupation and nutritional status were collected. Multi-factor logistic regression analysis showed that patients’ serum cholesterol level and nutritional status had a significant effect on the occurrence of PLG. Not eating breakfast, insufficient calories, vitamin C deficiency, sucrose, refined starch, and less fibrous food make the bile in the gallbladder not empty in time and predispose to PLG formation.
(4) Relationship between chronic hepatitis virus and PLG: Some scholars believe that patients with chronic hepatitis are prone to gallbladder disease. The causes of its occurrence are.
①Cholesterol metabolism and bile secretion changes: the liver is the main site of cholesterol metabolism in the body. is maximum and abnormal deposits are formed in the gallbladder wall.
(ii) Inflammation: hepatitis B virus resides in human liver cells and activates the body’s immune system to produce autoimmune inflammation, causing increased activity of macrophages in the gallbladder to phagocytose cholesterol in the gallbladder.
(③) Gastrointestinal hormone secretion and metabolic disorders, causing impaired regulation of Oddi sphincter tone, bile viscosity, poor excretion, and cholesterol phagocytosis by macrophages on the gallbladder mucosa.
IV. Clinical manifestations
Patients with gallbladder polyp-like lesions are mostly asymptomatic, and a few patients have no conscious symptoms and are only found incidentally during ultrasonography. Common symptoms include: right upper abdominal discomfort, vague pain, abdominal distension, right shoulder radiating pain, which may be accompanied by nausea, anorexia, abdominal distension and discomfort. Fever and jaundice may be present in a few cases. Positive signs mainly include right upper abdominal pressure pain. Most of the patients in China have different degrees of the above symptoms and signs. Young patients may have no discomfort or mild symptoms, and many of them have clinical symptoms gradually and obviously as their age increases. It is mostly believed that polyp-like lesions do not cause clinical symptoms, but there is a lack of definite evidence. Whether the clinical symptoms are related to the location and size of the polyps has not been reported.
V. Diagnosis
The diagnosis of gallbladder polypoid lesions mainly relies on imaging examinations, including ultrasound, CT and cholecystography.
(1) Ultrasonography: The core issue of ultrasonographic assertion is the differentiation of adenoma from non-adenomatous polyps. The lesion is immobile, has no acoustic shadow, is hyperechoic compared to bile, and is attached to the wall of the gallbladder. Ultrasonography should describe the size of the lesion, its number, whether it is combined with gallbladder stones, and the diameter of the largest lesion in two or more polypoid lesions. Cholesterol-like polyps are characterized by multiple small polyps with one or more constant intensity and sparse light clusters of 0.2 to 12.5 px in diameter in the gallbladder wall on ultrasound, not moving and without acoustic shadow. The presence of a tip, solitary, diameter >10 mm, and surface lobulation suggests a high likelihood of adenomatous polyps.
(2) Ultrasonography: compared with color Doppler ultrasound ultrasonography can clearly show the blood flow signal and microvascular circulation within the lesion, i.e., whether the lesion is rich in blood supply or not, and also enhance the gray-scale signal of the tissue around the lesion to determine the nature of the lesion. Ultrasonography has two presentations.
(i) the lesion is not rich in blood supply, contrast filling is seen throughout the imaging, and the arterial phase shows simultaneous homogeneous enhancement with the surrounding gallbladder wall, but the enhancement is higher than that of the liver parenchyma at the same time, and it always shows homogeneous enhancement in the delayed phase.
The lesion is rich in blood supply and shows rapid and heterogeneous enhancement in the arterial phase, which is stronger than that of the surrounding gallbladder wall, and rapid and heterogeneous contouring in the portal and delayed phases, which is earlier than that of the surrounding normal liver parenchyma and gallbladder wall.
Generally speaking, non-surgical conservative treatment can be considered for gallbladder polyp-like lesions presenting the first manifestation mentioned above, regardless of whether the lesion is larger than 10 mm or not. For those who present the second manifestation above by ultrasonography, early surgery should be performed regardless of the size of the lesion.
(3) Endoscopic ultrasonography: endoscopic ultrasonography can clearly identify the internal structure of gallbladder polyp-like lesions, whether there is a tip and the relationship with the gallbladder wall. Cholesterol polyps are characterized by granular and uniform strong echogenicity in the majority of the tipped ones, and the structure of the gallbladder wall layers is clearer at the tipped part. The echogenicity of bulge-like lesions of gallbladder cancer is mostly heterogeneous, and the mucosa of the attached gallbladder wall is disorganized or appears locally indistinct. Adenomyoma-like lesions are often hypoechoic. Small adenomas are limited to the first layer of the bulge of the gallbladder wall, and EUS is more accurate than ultrasound.
(4) CT: The lesion is often difficult to detect on plain scan because of its small size and the small density difference between the lesion and the bile. Most CT plain scans only show papillary, mulberry-shaped high-density foci. In benign gallbladder polyp-like lesions, the venous phase is usually about 10 HU higher than the flat scan lesions, and the gallbladder wall is uniformly strengthened and egg-shell-like; while in malignant gallbladder polyp-like lesions, the arterial phase lesions are obviously strengthened, and the venous phase lesions are further strengthened, and the venous phase is usually about 30 HU higher than the flat scan lesions. CT examination can clarify the infiltration and lymph node metastasis, but it is not significant for small bulging lesions.
VI. Treatment
The treatment of gallbladder polyp-like lesions focuses on preoperative differentiation between benign and malignant. 1989 the 4th National Conference on External Biliary Tract proposed 4 indicators for identifying tumor risk factors in PLG: solitary lesion, lesion diameter greater than 10 mm, broad-based, and tendency to increase in size. It has also been suggested that any polyp larger than 8 mm, whether solitary or multiple, and regardless of the presence of symptoms, has a higher likelihood of malignancy and should be surgically removed. Combined gallbladder stones, isolated PLG and symptomatic polyps are additional predictors of malignant risk. It has also been suggested that PLG of ≤10 mm in diameter can be safely observed based on ultrasonographic findings, and PLG of <6 mm in diameter are rarely true neoplastic polyps, while lesions >10 mm in diameter are potentially malignant and should be cholecystectomized despite their rare occurrence.