Date:   11/30/2002 12:02:23 PM ( 22 y ago)
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URL:   https://www.curezone.org/forums/fm.asp?i=127724

I believe Porcelain Gallbladder is caused by the special way of thinking-special lifestyle, including un healthy Diet - consumption of too much heated food.

Many illnees in human body are often caused by the way people think. Our emotions, and stress often shape our organs, and it can often bring an inflamation to a specific organ, especially when diet is poor, and when person is not burning all the food he/she eats.


http://www.emedicine.com/radio/topic569.htm
Porcelain Gallbladder

Background: Extensive calcium encrustation of the gallbladder wall variably has been termed calcified gallbladder, calcifying cholecystitis, or cholecystopathia chronica calcarea. The term Porcelain Gallbladder has been used to emphasize the blue discoloration and brittle consistency of the gallbladder wall at surgery. Some authorities amalgamate the terms and call all calcified gallbladders porcelain gallbladders. The true incidence of porcelain gallbladder is unknown, but it is reported to be 0.6-0.8%, with a male-to-female ratio of 1:5. Most porcelain gallbladders (90%) are associated with gallstones.

Patients are usually asymptomatic, and porcelain gallbladder is found incidentally on plain abdominal radiographs, sonograms, or CT images. Surgical treatment of porcelain gallbladder is based on results from studies performed in 1931 and 1962, which revealed an association between porcelain gallbladder and gallbladder carcinoma. Porcelain gallbladder is uncommon, and recognizing the clinical and imaging characteristics of the disease is important because of the high frequency (22%) of adenocarcinoma in porcelain gallbladder. Surgery should not be delayed, even if the patient is asymptomatic, because the occurrence of carcinoma in porcelain gallbladder is remarkably high.


Pathophysiology: Histologically, flakes of dystrophic calcium exist within the chronically inflamed gallbladder wall. The muscular wall of the gallbladder undergoes fibrotic changes. Microliths are diffusely scattered throughout the mucosa, submucosa, and glandular spaces and in the Rokitansky-Aschoff sinuses. Calcification occurs in 2 forms: (1) a broad continuous band of calcification in the muscularis and (2) multiple punctate calcifications in the mucosa and glandular spaces of the mucosa. Gallstones are present in 90% of patients, hydrops obstructs the cystic duct. Most authorities consider gallbladder wall calcification to be secondary to a low-grade inflammation, but intramural hemorrhage and an imbalance in calcium metabolism also are implicated.

Calcification in the right upper quadrant of the abdomen has several causes. Calcification can be categorized by the organ system in which it appears; for example, calcification can affect the liver, gallbladder, right kidney, digestive tract, peritoneal cavity, right adrenal gland, and retroperitoneum. Diseases associated with these organs include large gallbladder opaque calculi, milk-of-calcium bile (see Image 9), echinococcal cysts (see Images 10-11), schistosomiasis and other granulomatous diseases, old healed liver infarcts (see Image 12), calcified renal cysts, renal calculi, calcified nonparasitic liver cysts, primary and metastatic liver tumors, benign liver tumors, and calcification in old adrenal hemorrhage and adrenal masses.


Frequency:


In the US: The overall incidence in the United States appears to be identical to the international incidence.
Internationally: Because most cases of gallbladder calcifications are not reported, determining the exact incidence is difficult. However, studies of cholecystectomy specimens reveal a 0.6-0.8% occurrence rate for extensive mural calcification.
Mortality/Morbidity: The clinical importance of porcelain gallbladder lies in its significant association with gallbladder carcinoma. Because the prognosis usually is poor in patients with gallbladder carcinoma, most authors agree that carcinoma occurs in the porcelain gallbladder with sufficient frequency to warrant prophylactic cholecystectomy.

Race: No racial predilection is reported. In regions in which gallstone disease has a high incidence, a high incidence of porcelain gallbladder might be expected; however, this relationship has not been demonstrated to date.

Calcified hydatid cysts in the liver are fairly common in endemic areas such as the Middle East, Eastern and Mediterranean Europe and North Africa. These cysts can mimic porcelain gallbladder on plain abdominal radiographs; however, the patient's country of origin or a history of travel to an endemic region suggests the diagnosis, and ultrasonographic examination reveals a separate gallbladder.

Sex: The male-to-female ratio is 1:5.

Age: The mean age of patients is 54 years, with an age range of 38-70 years. Porcelain gallbladder in the pediatric age group is exceptionally rare. Only 1 case is described in a 10-year-old girl; this patient underwent prophylactic cholecystectomy.

Clinical Details: Characteristically, the condition is clinically covert, although occasionally, a palpable mass may be found. Frequently, the diagnosis is made because of incidental findings on plain abdominal radiographs, sonograms, or CT images or, occasionally, by finding a palpable right upper quadrant abdominal mass.

An association between gallbladder malignancy and porcelain gallbladder has been established on the basis of results from studies performed in 1931 and 1962. Since then, sporadic case reports and collections of cases have appeared in literature, and their findings have reinforced the association.

However, observations from a recent study contradict this time-honored view. Towfigh et al reviewed the medical records of 10,741 patients who underwent cholecystectomy in 1955-1998. Pathology slides were evaluated for evidence of calcification and gallbladder carcinoma. The incidence of porcelain gallbladder was 0.14% (15 patients) in the series; 10 patients had symptoms suggestive of biliary colic or cholecystitis, and the diagnosis was incidental in 5.

All specimens showed histologic evidence of chronic cholecystitis and partial calcification of the gallbladder wall. Gallstones were found in 60% of the patients. None had gallbladder carcinoma. During the same period, 0.82% of the patients had gallbladder carcinoma, none of whom had gallbladder wall calcification. The study did not reveal carcinoma in patients with porcelain gallbladder. In addition, in patients with gallbladder carcinoma, none had porcelain gallbladder. The authors concluded that, with a better understanding of the natural history of porcelain gallbladder, patient treatment may change. However, until further studies confirm these findings, the importance of surgical treatment cannot be overemphasized when the frequency of carcinoma in porcelain gallbladder, as reported in previous studies, is considered.

Most authors agree that carcinoma occurs in the porcelain gallbladder with sufficient frequency to warrant prophylactic cholecystectomy. Most carcinomas associated with porcelain gallbladder are diffusely infiltrating adenocarcinomas, although squamous cell carcinoma is described as well. In rare cases, calcification that precipitated in mucous within neoplastic glandular tissue also may be visible on plain radiographs; this calcification can mimic a carcinoma that is developing in porcelain gallbladder. The mechanism by which a malignant transformation occurs in porcelain gallbladder is not known, although degeneration and regeneration within the gallbladder epithelium is suggested to produce a carcinogenic stimulus, or a chemical carcinogen may be formed or present within stagnant bile. Using animal models, Petrov and Krotkina were able to induce gallbladder carcinoma by implanting hard foreign bodies in the gallbladder wall.


 

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