BACKGROUND AND AIMS Controversy surrounds the risk of colorectal cancer (CRC) in ulcerative colitis (UC). Many studies have investigated this risk and reported widely varying rates. METHODS A literature search using Medline with the explosion of references identified 194 studies. Of these, 116 met our inclusion criteria from which the number of patients and cancers detected could be extracted. Overall pooled estimates, with 95% confidence intervals (CI), of cancer prevalence and incidence were obtained using a random effects model on either the log odds or log incidence scale, as appropriate. RESULTS The overall prevalence of CRC in any UC patient, based on 116 studies, was estimated to be 3.7% (95% CI 3.2–4.2%). Of the 116 studies, 41 reported colitis duration. From these the overall incidence rate was 3/1000 person years duration (pyd), (95% CI 2/1000 to 4/1000). The overall incidence rate for any child was 6/1000 pyd (95% CI 3/1000 to 13/1000). Of the 41 studies, 19 reported results stratified into 10 year intervals of disease duration. For the first 10 years the incidence rate was 2/1000 pyd (95% CI 1/1000 to 2/1000), for the second decade the incidence rate was estimated to be 7/1000 pyd (95% CI 4/1000 to 12/1000), and in the third decade the incidence rate was 12/1000 pyd (95% CI 7/1000 to 19/1000). These incidence rates corresponded to cumulative probabilities of 2% by 10 years, 8% by 20 years, and 18% by 30 years. The worldwide cancer incidence rates varied geographically, being 5/1000 pyd in the USA, 4/1000 pyd in the UK, and 2/1000 pyd in Scandinavia and other countries. Over time the cancer risk has increased since 1955 but this finding was not significant (p=0.8). CONCLUSIONS Using new meta-analysis techniques we determined the risk of CRC in UC by decade of disease and defined the risk in pancolitics and children. We found a non-significant increase in risk over time and estimated how risk varies with geography.

https://gut.bmj.com/content/gutjnl/48/4/526.full.pdf

The risk of colorectal cancer in ulcerative colitis: a meta-analysis

Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease occurring in 1 in 200 to 1 in 1,000 individuals. ADPKD is characterized by cystic lesions in the kidneys and often by structural abnormalities in the gastrointestinal tract and cardiovascular system. The pathogenesis of the disorder appears to involve both cellular proliferation and altered extracellular matrix synthesis. Diagnosis can be established most readily by the sonographic demonstration of renal cysts or by gene linkage analysis. Renal manifestations of ADPKD include hypertension, infection, nephrolithiasis and malignancy. The prominent extrarenal manifestations include hepatic cysts, mitral valve prolapse and intracranial aneurysms. Although only 2% of nephrons appear to be involved in cyst formation, the renal function often slowly deteriorates. Presently, there is a 52% probability of an ADPKD subject’s being alive without renal replacement therapy at age 73. ADPKD patients with endstage renal disease respond to renal replacement therapy as well as other patient groups.

Autosomal dominant polycystic kidney disease.

https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.1840160434

Congenital diseases of intrahepatic bile ducts: variations on the theme "ductal plate malformation".

The genus Entamoeba contains many species, six of which (Entamoeba histolytica, Entamoeba dispar, Entamoeba moshkovskii, Entamoeba polecki, Entamoeba coli, and Entamoeba hartmanni) reside in the human intestinal lumen. Entamoeba histolytica is the causative agent of amebiasis and is considered a leading parasitic cause of death worldwide in humans. Although recent studies highlight the recovery of E. dispar and E. moshkovskii from patients with gastrointestinal symptoms, there is still no convincing evidence of a causal link between the presence of these two species and the symptoms of the host. New approaches to the identification of E. histolytica are based on detection of E. histolytica-specific antigen and DNA in stool and other clinical samples. Several molecular diagnostic tests, including conventional and real-time PCR, have been developed for the detection and differentiation of E. histolytica, E. dispar, and E. moshkovskii in clinical samples. The purpose of this review is to discuss different methods that exist for the identification of E. histolytica, E. dispar, and E. moshkovskii which are available to the clinical diagnostic laboratory. To address the need for a specific diagnostic test for amebiasis, a substantial amount of work has been carried out over the last decade in different parts of the world. The molecular diagnostic tests are increasingly being used for both clinical and research purposes. In order to minimize undue treatment of individuals infected with other species of Entamoeba such as E. dispar and E. moshkovskii, efforts have been made for specific diagnosis of E. histolytica infection and not to treat based simply on the microscopic examination of Entamoeba species in the stool. The incorporation of many new technologies into the diagnostic laboratory will lead to a better understanding of the public health problem and measures to control the disease.

/pdf/laboratory-diagnostic-techniques-for-entamoeba-species-2wdhseuvsk.pdf

Laboratory Diagnostic Techniques for Entamoeba Species

The detection of Entamoeba histolytica, the causative agent of amebiasis, is an important goal of the clinical microbiology laboratory. To assess the scope of E. histolytica infection, it is necessary to utilize accurate diagnostic tools. As more is discovered about the molecular and cell biology of E. histolytica, there is great potential for further understanding the pathogenesis of amebiasis. Molecular biology-based diagnosis may become the technique of choice in the future because establishment of these protozoa in culture is still not a routine clinical laboratory process. In all cases, combination of serologic tests with detection of the parasite (by antigen detection or PCR) offers the best approach to diagnosis, while PCR techniques remain impractical in many developing country settings. The detection of amebic markers in serum in patients with amebic colitis and liver abscess appears promising but is still only a research tool. On the other hand, stool antigen detection tests offer a practical, sensitive, and specific way for the clinical laboratory to detect intestinal E. histolytica. All the current tests suffer from the fact that the antigens detected are denatured by fixation of the stool specimen, limiting testing to fresh or frozen samples.

Laboratory Diagnosis of Amebiasis

https://www.gastrojournal.org/article/0016-5085(80)90204-8/pdf

Serologic testing for amoebiasis

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.1840020414

Polycystic Liver Disease: A Study of Cyst Fluid Constituents

Weanling Sprague-Dawley rats were given increasing doses of lactose over a seven-week period. The mid-jejunum was selected for disaccharidase analysis at a pH of 6.0. Lactase and cellobiase activity were stimulated significantly by total mean-paired analysis. While sucrase and maltase tended to increase. there was no statistically significant change.

The Stimulation of Lactase by Feeding Lactose

Bezoars have not been readily recognized as a postgastrectomy complication. A review of the literature and this report of 2 cases stress the importance of this phenomenon. Roughage, delayed emptying, narrow stoma, and decreased gastric secretions, as well as improper mastication and inadequate teeth, play a role in producing bezoars. Prevention, with emphasis on the avoidance of foods with high fiber content and on good oral hygiene, is the preferred measure. However, a short trial of papain and surgery are indicated once the bezoar has formed.

Marcel Patterson

Papers

Serologic testing for amoebiasis

Polycystic Liver Disease: A Study of Cyst Fluid Constituents

The Stimulation of Lactase by Feeding Lactose

Bezoars—A complication of the postgastrectomy state

The presentation of amoebiasis.