[EXPERIENCE OF CONTROLLING INTESTINAL INFECTIOUS DISEASES IN THE IAGODNY I REGION OF THE MAGADAN TERRITORY].
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Intestinal parasitic diseases were diagnosed in 100 HIV-infected patients at different stages of disease (its asymptomatic form, persistent generalized lymphoadenopathy, pre-AIDS, and AIDS) (Group 1), 100 Tashkent residents (Group 2), and 349 patients with gastrointestinal diseases, allergic dermatoses, and skin depigmentation foci (Group 3). The HIV-infected patients were found to have virtually all parasites, such as Giardia lamblia, Cryptosporidium parvum, Chilomastix mesnili, Entamoeba coli, Iodamoeba butschlii, Entamoeba histolytica/dispar, Endolimax nana, Blastocystis hominis, Enlerobius vermicularis, Ascaris lumbricoides, Hymenolepis nana, detectable in the population of Tashkent. The highest infestation with intestinal protozoa, including nonpathogenic amoebas and helmninths, was found in Groups 1 and 3. However, in all the forms of HIV infection, the infestation with E. histolytical/dispar was 10 times greater than that in Groups 2 and 3 (1% and 0.8%, respectively). G. lamblia was detected in 16, 21, and 45.2% in Groups 1, 2, and 3, respectively. In all the HIV-infected patients, the content of CD8 lymphocytes was increased, but that of CD20 lymphocytes was normal. Parasites were detectable with different levels of CD4 lymphocytes, but C. parvum was found only if its count was > 200/ml. In the HIV-infected patients, the hyperproduction of IgE was caused mainly by helminths rather than protozoa. In these patients, the increased level of IgE was also noted in the absence of parasites.
OBJECTIVE: To identify the causes of intestinal infectious diseases in a military unit in the past 10 years. METHODS: The data of these diseases were acquired from a disease control and prevention center of a military command, including the epidemic cards, the first pages of medical record and investigation reports of the infectious diseases. Statistical analysis was performed after summarization of the data. RESULT: From 1992 to 2001, 3 612 cases of intestinal infectious diseases were reported in the military unit, most of which were bacillary dysentery (32.40%), hepatitis A (26.80%), typhoid (14.34%) and infectious diarrhea (7.34%), and 40.13% of them were intestinal infectious diseases. Fifteen epidemic outbreaks were documented from 1988 to 2002, including 9 arising from water and 6 from food contamination. CONCLUSION: Intestinal infectious diseases are seasonal and strict food and water hygiene should be maintained.
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Intestinal mucosal immunoglobulin secretion in vitro has been studied by culture of endoscopic biopsy tissues obtained from various sites along the gastrointestinal tract. IgA and IgM were the predominant immunoglobulins produced by intestinal tissues distal to the stomach and secretion of both reached a maximum in the small intestine of normal individuals. In patients with inflammatory bowel disease, characteristic alterations in immunoglobulin production were observed in cultures of large intestinal tissue. In ulcerative colitis (UC), significant reductions in IgA secretion (P less than 0.03) occurred in the rectum during remission and IgM in the colon in active disease (P less than 0.01). However, in active Crohn's disease (CD), rectal IgM secretion was enhanced (P less than 0.004) and IgA diminished (P less than 0.01). IgG secretion was increased throughout the colon in UC especially in distal sites, due largely to significant increases in pre-formed immunoglobulin (P less than 0.02). Similar total increases were observed in colonic tissues from patients with CD, although IgG synthesis in biopsies from rectal sites was normal. These findings suggest that specific abnormalities of intestinal mucosal immunoglobulin synthesis occur in patients with both UC and CD.
BACKGROUND: Diseases of the small intestine are rare and often difficult to diagnose because of a lack of sensitive methods. A new technique called wireless capsule endoscopy has recently been developed; it allows visualisation of the entire small intestinal surface. MATERIAL AND METHODS: The patient swallows a capsule containing a small digital camera, a battery and a radio transmitter. The capsule takes 2 pictures per second during its passage through the intestines; pictures are transferred by radio signals that are detected by sensors on the abdominal skin, stored on a data recorder and later analysed on a PC. RESULTS: By the end of November 2003 we had performed 80 capsule endoscopies in 69 patients. All patients were referred because of suspected small bowel disease and had been through an extensive diagnostic workup before capsule endoscopy was performed. Most of them were referred because of obscure gastrointestinal bleeding or iron deficiency anaemia. Small bowel pathology was found in one third of the patients. INTERPRETATION: Capsule endoscopy seems to be a major improvement in the diagnosis of small intestinal diseases. It is a non-invasive and painless procedure.
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Intestinal cancer is uncommon in Crohn's disease but the risk of developing such a tumor is increased. Linitis plastica of the small bowel or colon is very rare. We report a case of ileocolonic linitis plastica which occurred 21 years after an ileocecal resection for Crohn's disease. Partial small bowel obstruction in relation with stricture of the preanastomotic loop prompted us to suspect disease recurrence. The tumor was not diagnosed either on preoperative work-up, or during surgery but only on the histological examination of the resected specimen. Palliative chemotherapy with 5 FU and folinic acid was performed. The patient was asymptomatic after a 17-month follow-up. This observation focuses on the clinical signs and course of linitis plastica. It also illustrates the difficulty of tumor diagnosis in Crohn's disease. Malignant transformation must be suspected if signs of active disease re-occur after a lengthy quiescent period.
A computed tomographic (CT) analysis of 36 patients with differential diagnosis of intestinal tuberculosis (IT) or Crohn's disease (CD) in barium gastrointestinal studies was undertaken to identify distinguishing bowel wall or mesenteric features which could provide a radiological definitive diagnosis. Final diagnoses obtained in 32 cases were tuberculosis (N = 18), CD (N = 9), carcinoid (N = 2), chronic appendicitis (N = 2) and bowel infarction (N = 1). In IT, the bowel wall changes were varied: absence of wall thickening (N = 6), minimal asymmetric wall thickening with and without mucosal tethering (N = 8), minimal symmetric wall thickening often with mild peritonitis (N = 3), exophytic mass encircling bowel lumen (N = 4). Mural stratification (target sign) was not found. CD showed concentric or symmetrical wall thickening ranging from 0.6 to 1.5 mm and mural stratification occurred in about a half of the cases. Lymphadenopathy was the commonest associated feature in both but in IT, the nodes were larger and a third had necrotic centers. Displacement of bowel loops was more often due to enlarged lymphadenopathy in IT while in CD it was frequently due to fibrofatty change. CT was able to provide the correct diagnosis in 26 out of these 32 (81%) cases of indeterminate barium studies. CT is recommended when barium gastrointestinal studies are unable to differentiate between intestinal tuberculosis and Crohn's disease.
Intestinal permeability was assessed in patients with inflammatory bowel disease by measuring the urine excretion of 51chromium-labeled ethylenediaminetetraacetate over periods up to 24 h after oral administration. Twenty-eight control subjects and 10 patients with ulcerative colitis excreted less than 2.6% of the test dose in 24 h. Ten patients with small bowel Crohn's disease excreted 3.3%-14.0%, and 10 of 11 patients with ileocolonic involvement had increased excretion. At the same time, 5 of 11 patients with Crohn's colitis were clearly outside the normal range, suggesting small bowel involvement. The 24-h urine excretion of 51chromium-labeled ethyl-enediaminetetraacetate after oral administration appears to be a sensitive, noninvasive test for assessing small intestinal integrity, and may be a valuable adjuvant in the differential diagnosis of inflammatory bowel disease.
Domestic cats with small intestinal disease may develop cobalamin deficiency because of reduced small intestinal uptake of this vitamin. This study assessed the impact of cobalamin deficiency on biochemical and clinical findings in cats with intestinal disease. Nineteen pet cats, all with severe hypocobalaminemia (< or =100 ng/L) and histories of gastrointestinal signs, were studied. Cats received cobalamin, 250 microg SC once weekly, for 4 weeks. Biochemical indices of cobalamin availability (e.g., serum methylmalonic acid, homocysteine, and cysteine concentrations), serum feline trypsinlike immunoreactivity (fTLI) and serum folate concentrations, and clinical findings were recorded at the start of the study and after 4 weeks of cobalamin therapy. Serum methylmalonic acid (MMA) concentrations (median; range) decreased after cobalamin supplementation (5373.0; 708.5-29,329.0 versus 423.5; 214.0-7219.0 nmol/L, P < .0001). Serum homocysteine concentrations were not significantly altered (mean +/- SD 8.2 +/- 2.9 versus 10.3 +/- 4.5 micromol/L, P = .1198), whereas cysteine concentrations increased significantly (122.3 +/- 38.8 versus 191.5 +/- 29.4 micromol/L, P < .0001). Mean body weight increased significantly after cobalamin therapy (3.8 +/- 1.1 versus 4.1 +/- 1 kg, P < .01), and the average body weight gain was 8.2%. Significant linear relationships were observed between alterations in serum MMA and fTLI concentrations and the percentage body weight change (P < .05 for both, Pearson r2 = 0.26 and 0.245, respectively). Mean serum folate concentration decreased significantly (mean +/- SD 19 +/- 5 microg/L versus 15.4 +/- 6.2 microg/L, P < .001). Reduced vomiting and diarrhea were observed in 7 of 9 and 5 of 13 cats, respectively. These results suggest that cobalamin supplementation in cats with small intestinal disease and severe hypocobalaminemia is associated with normalization of biochemical test results and improvements in clinical findings in most affected cats.
Intestinal parasites are common among labourers from foreign countries and in immigrants. Some worm-infections like ascaridiasis or enterobiasis occur in children quite often even in the cold climates. In cases of ascaridiasis only a heavy infection causes clinical symptoms. The diagnosis is made through the detection of eggs in the stools, as all the other worm-infections are diagnosed from the stool-test. Piperazine-derivatives are highly effective against ascaris; another useful drug is Pyrantel-Pamoate. Toxocara canis, which affects normally only dogs, can occur occasionally in humans. Its larvae migrate in the body and cause granulomas. The main clinical symptom of threadworms (enterobiasis) is itching around the anus. This parasite can be eradicated through Pyrvinium-Pamoate. The first symptom a patient notices in cases of taeniasis are proglottides--parts of the worms--which are passed with the stools. The drug of choice against all kinds of tapeworms is Niclosamide. Hookworms are rampant in tropical countries. Heavy infections can cause severe anemias, especially in children. Bephenium-Naphthoate and Bitoscanate are effective drugs against this parasite. The whipworm (Trichuris trichura) is very common in the warm countries. It can be treated by Tiabendazole and nowadays also with Mebendazole, which is virtually atoxic. Infections with Strongyloides stercoralis are difficult to eradicate, as there are different ways of reinfection. In case an infection with strongyloides is accompanied by other serious diseases cachexia and even fatal outcome has been seen.
AIM: To investigate the genetic relationship between Hirschsprung's disease (HD) and intestinal neuronal dysplasia (IND) in Chinese population. METHODS: Peripheral blood samples were obtained from 30 HD patients, 20 IND patients, 18 HD/IND combined patients and 20 normal individuals as control. Genomic DNA was extracted according to standard procedure. Exons 11,13,15,17 of RET proto-oncogene were amplified by polymerase chain reaction (PCR). The mutations of RET proto-oncogene were analyzed by single strand conformational polymorphism (SSCP) and sequencing of the positive amplified products was performed. RESULTS: Eight germline sequence variants were detected. In HD patients, 2 missense mutations in exon 11 at nucleotide 15165 G-->A (G667S), 2 frameshift mutations in exon 13 at nucleotide 18974 (18974insG), 1 missense mutation in exon 13 at nucleotide 18919 A-->G (K756E) and 1 silent mutation in exon 15 at nucleotide 20692 G-->A(Q916Q) were detected. In HD/IND combined patients, 1 missense mutation in exon 11 at nucleotide 15165 G-->A and 1 silent mutation in exon 13 at nucleotide 18888 T-->G (L745L) were detected. No mutation was found in IND patients and controls. CONCLUSION: Mutation of RET proto-oncogene is involved in the etiopathogenesis of HD. The frequency of RET proto-oncogene mutation is quite different between IND and HD in Chinese population. IND is a distinct clinical entity genetically different from HD.
All the previous studies which have associated arteriovenous malformations of the colon with chronic inflammatory disease have always been performed on a diseased intestine. This study, which uses the intravascular injection of resin, shows morphological evidence that angiodysplasia of the colon and intestinal inflammatory disease can coexist independently. This fact suggests that in cases of severe hemorrhage in a patient with inflammatory disease of the small intestine, it cannot simply be assumed that it originates in the macroscopically abnormal intestine, and that angiographic examination is a wise measure to rule out the possibility of arteriovenous malformations in the "normal" intestine.