bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is protein‐deficient diabetes mellitus a pancreatitis?
Authors: Saraya Anoop , Acharya Subrat , Vashisht Sushma , Mittal Ambrish , Tandon Rakesh 
Published: March 2003

Background: Malnutrition‐related diabetes mellitus is a distinct clinical entity subdivided into protein‐deficient diabetes mellitus (PDDM) and fibrocalculus pancreatic diabetes (FCPD). Whereas FCPD has obvious pancreatitis manifested by pancreatic duct calculi, the evidence for involvement of the pancreas in PDDM is limited to the presence of ketosis‐resistant hyperglycaemia. Methods: We studied 10 patients with PDDM biochemically and radiologically. Endoscopic retro‐ grade cholangiopancreatography was performed to determine if they had any evidence of chronic pancreatitis. Results: Their mean faecal chymotrypsin level was low (13.2 ± 5.72 μg/g), as was their basal c‐peptide value (0.35 ± 0.15 mmol/L). Islet cell antibodies were not detected in any of these patients. Ultrasound examination revealed pancreatic atrophy. In two patients, however, the pancreas was bulky. The ERCP showed generalized thinning of the pancreatic duct, measuring 2.4 ± 0.06 mm in the head, 2.01 ± 0.08 mm in the body and 1.02 ± 0.03 mm in tail region; side branches were seen but they were too sparse and thin. Conclusions: The significance of these changes is not clear, but they may represent an ongoing pancreatic disease and may, indeed, be the earliest changes of chronic pancreatitis.
CORRELATION OF PRESENCE OF H. PYLORI WITH HISTOLOGICAL AND SYMPTOMATIC SCORE IN PATIENTS WITH NON ULCER DYSPEPSIA (NUD)
Authors: Joshi Anoop , Ahuja Vineet , Duttagupta S. , Sharma Mp 
Published: March 2003

BackgroundNon ulcer dyspepsia (NUD) is being postulated as one of the gastroduodenal manifestations of H. pylori infection. H. pylori infection may result in clinical symptoms as well as histological changes in (NUD).AimTo compare clinical symtoms score and histological changes in H. pylori (Hp) positive and negative untreated NUD patients.MethodsPatients with dyspeptic symptoms and abnormal UGI endoscopic examination were included in the study. During endoscopy 2 biopsies each were taken from antrum and corpus. These biopsies were used for rapid urease test (RUT) and histological evaluation. There were 2 group: Hp positive and Hp negative NUD patients. Patients were diagnosed to have H. pylori infection of either of the two test (RUT, histology) were positive. Clinical scoring using glasglow dyspepsia score (max 20) and histological analysis using Sydney system (max score 11) was done and compared for both the groups. Clinical scoring RUT & histological scoring were blinded to each other.Resultsto patients (29 Hp + and 17 Hp ‐ve) were enrolled in the study. The results in both groups were:

Hp +ve
Hp ‐ve
P value

Glasgow clinical score
10.9
11.4
ns

Chr. Gastritis

Antrum
89.6%
94.1%
ns

Corpus
93.1%
76.1%
ns

Activity

Antrum
41.3%
41.1%
ns

Corpus
41.1%
29.4%
ns

Lymphoid follicles

Antrum
34.4%
11.7%
ns

Corpus
37.9%
5.8%
P < 05

Atrophy

Antrum
24.1%
11.7%
ns

Corpus
20.6%
11.7%
ns

Int. Metaplasia

Antrum
13.7%
5.8% ns

Corpus
10.3%
0% ns

Total Histological

Antrum
3.37
1.76
0.0003

Corpus
3.68
1.29
0.0001

ConclusionClinical scoring does not correlate with presence of H. pylori or the histological severity. In NUD patients positive for H. pylori, there is a significant increase in the severity of gastritis both in the antrum and the corpus.
HEMATEMESIS AND MELENA IN BABY WITH HELICOBACTER PYLORI INFECTION
Authors: Purnomo Budi , Soeleman Eva J. , Digdowirogo Hadjat S. , Soehardjo Hartati N. 
Published: March 2003

H. pylori infection in a baby is very rare. Most Clinicians recommended treating this infection in such cases. Time of H. pylori begin to colonize human gastroduodenal is not known. We report a case: an 8‐month old baby girl who suffered from hematemesis and melena since 4‐month old.Case report:RK, an 8‐month baby girl was brought to children and maternity Hospital due to recurrent hematemesis and melena since 4 months ago. On physical examination, she looked pale without icterus or dyspnoe. Body weight was 6100 g. Vital signs were normal. Heart lungs, abdomen and extremities were within normal limit.Laboratory findings:hemoglobin 9.5 g/dl, hematrocrite 39%, leukocyte 13300 /ul, platelets 369000/ul, Prothrombin and thrombin time were normal. Radiology of the stomach with barium revealed third grade of gastroesophageal reflux. On gastroscopy, we found erosive gastritis and many nodules in duodenic bulb. Histopathological examination showed duodenitis grade I, H.pylori positive and chronic gastritis.We gave amoxycilin, omeprazole and metronidazole for a week and sucralfate, omeprazole for 2 months. After treatment, no symptoms was found. The baby have weight gain to normal percentile.ConclusionThe management of H.pylori infection in our case was late. We already found iron deficient anaemia due to hematemesis and melena, and malnutrition. After H. pylori eradication, all symptoms resolved.
HISTOPATHOLOGICAL PATTERN OF GASTRIC BIOPSIES OF HELICOBACTER PYLORI POSITIVE PATIENTS IN SARDJITO GENERAL HOSPITAL, YOGYAKARTA, INDONESIA
Authors: Nurdjanah Siti , Bayupurnama Putut 
Published: March 2003

Objective:To determine the gastric histopathological types distribution of H. pylori positive patients who were detected histopathologically.Material& Methods:Study design was prospective study. Consecutive patients who were suffering chronic dyspepsia underwent endoscopy examination between August 1998 and December 1999. The biopsy specimens were taken from gastric antrum and corpus and sent to the pathologist for histopathology type and H. pylori examinations. H. pylori were also confirmed with CLO and IgG‐Helicobacter pylori tests.Results:There were 92 patients (48 male (M) and 44 Female (F) who underwent gastric biopsies endoscopically between August 1998 and December 1999. Fifty‐six (60.87%) patients were chronic superficial gastritis, 11(11.96%) chronic antropic gastritis, 18 (19.56%) chronic gastritis 2 (2.17%) chronic gastritis with metaplasia, 3 (3.27%) gastric ulcer, and 2 (2.17%) gastric signet‐ring cell carcinoma. Twenty one (22.8%) patients with H. pylori positive by histopathology examination with CLO and IgG‐H.pylori tests. Those were 5 (8.90%) patients with chronic superficial gastritis, 7(63.63%) chronic atrophic gastritis, 3(100%) gastric ulcer, 2 (100%) chronic gastritis with metaplasia, 3(16.67%) chronic gastritis, 1(50%) signet‐ring cell carcinoma. The age range of the H. pylori positive patients were between 16 and 76 years old.Conclusion:Twenty one (22.8%) H. pylori positive patients out of 92 endoscopied patients and the high percentage tendency of H. pylori positively in chronic atrophic gastritis, gastric ulcer, and chronic gastritis with metaplasia, although most of the patients had chronic superficial gastritis. Further study is needed with larger with larger sample to get the clearer picture of H. pylori distribution based on gastric histopathological types.
ULTRASTRUCTURE OF HELICOBACTER PYLORI
Authors: Saito Nagahito , Oda Hisashi , Sato Fujio , Kato Mototsugu , Takeda Hiroshi , Sugiyama Toshiro , Asaka Masahiro 
Published: March 2003

The ultrastructure of cell gives suggestions to the elucidation of the function. The study about the ultrastructure of H. pylori is important to know the nature of the organism. It is beyond doubt that Helicobacter pylori (H. pylori) is related to the pathogenesis of gastric disorders and it has been sequenced the bacterial genome. Although many morphological studies have been performed about this organism by light microscopy, few reports about theprecise ultrastructure exist. In general, H. pylori are divided into two types: spiral forms and coccoid ones. It is considered that the former is changing into the latter in an undesirable environment. It remains obscure about the nature of the letter such as the detailed ultrastructure, the transformation process or the viability. There are antithetic concepts about the coccoid H. pylori. One is that this type of the organism remains in a degenerated state. The other is that such organism is viable and non‐culturable. In addition to these opinions. I exhibit the third view. That is, the coccoid form are divided into two types; type I whose ultrastructure is generally nonspecific and type II identically intact. Moreover, type II coccoid form is also suggested to process growth viability.In this symposium, the ultrastructure of the cultured H. pylori (ATCC43504) will suggest some hypotheses about the nature. Some other natures will be also hypothesized from our ultrastructural study.
Dilatation of benign oesophageal strictures: 10 years’ experience with Celestin dilators
Authors: Duseja Ajay , Chawla Yk , Singh Rp , Sharma Tr , Kaur U , Dilawari Jb 
Published: March 2003

Abstract
Background
: Endoscopic dilatation is the first line of treatment for benign oesophageal strictures. There are limited data available on the use of Celestin dilators.
Methods
: The efficacy and safety of Celestin dilators was evaluated retrospectively in 61 patients with benign oesophageal strictures. Three hundred and nintey‐three dilatations using Celestin dilators were performed over a period of 10 years on an outpatient basis in patients with corrosive, peptic and other causes of benign oesophageal strictures.
Results
: Initial success was achieved in all patients in the peptic and miscellaneous group and in 91% in the corrosive group of patients. Patients with corrosive strictures required significantly more dilatations for initial success compared with the peptic group (mean 5.82 vs 1.62 P < 0.1). At 6 months follow up after the initial success, 29% of the patients had an excellent response, 56% a good response and 15% a fair response. No patient had a poor response. During the long‐term follow up of 10 years, overall dilatation requirement decreased significantly. (72 vs 27 vs 14% of patients requiring dilatation at 1, 5 and 10 years P < 0.05). The dilatation requirement also decreased significantly within the groups (P < 0.05). Patients with corrosive stricture required more frequent dilatations on follow up compared with the other two groups. Complications in the form of oesophageal perforation occurred in only two patients. There was no mortality.
Conclusion
: Oesophageal dilatation with Celestin dilators is an effective and safe modality for managing patients with benign oesophageal strictures.
Expression of hepatic thrombopoietin mRNA in primary cultured hepatocytes and in rats with acute liver injury or bone marrow suppression with or without cirrhosis
Authors: Ishikawa Toru , Ichida Takafumi , Matsuda Yasunobu , Sugitani Soichi , Sugiyama Motoya , Kato Takashi , Miyazaki Hiroshi , Asakura Hitoshi 
Published: March 2003

Abstract
Background and Aims
: The main causes of thrombocytopenia in cirrhosis are thought to be platelet destruction and the reduction of thrombopoietin (TPO) expression in the liver. The mechanisms by which levels of TPO mRNA are regulated in cirrhosis have not been elucidated. In this study, we investigated some possible mechanisms.
Methods
: We used three experimental models: bone marrow suppression, acute liver injury and primary cultured hepatocytes. We used northern blots to assess the kinetics of TPO mRNA expression in the livers of irradiated rats (with and without cirrhosis) in acute liver injury and in primary cultured hepatocytes treated with hepatotoxin or cytokines.
Results
: Although the bone marrow was hypocellular, there was no apparent enhancement of TPO mRNA expression in the irradiated rats with cirrhotic livers compared with the unirradiated rats with cirrhotic livers. There were no conspicuous changes in hepatic TPO mRNA expression between the livers of the control rats and the three models of acute liver injury. There were no conspicuous changes in the levels of TPO mRNA between control hepatocytes and hepatocytes treated with hepatotoxin or cytokines.
Conclusions
: Our results suggest that bone marrow is not a regulator of hepatic TPO production in cirrhosis. The reduced TPO mRNA expression found in cirrhotic rats may not result merely from serious cellular damage; it may be associated with cirrhosis‐specific regulatory mechanisms for the expression of the TPO gene. Further studies are needed to search for other factors that may induce reduced TPO expression.
Treatment of chronic hepatitis B virus infection: who, when, what for and how
Authors: Liaw Yun‐Fan 
Published: March 2003

AbstractChronic hepatitis B virus (HBV) infection is a serious clinical problem because of its worldwide distribution and possible adverse sequelae. It is particularly important in the Asia–Pacific region where HBV infection is highly prevalent and usually acquired perinatally or in early childhood. It is now known that chronic HBV infection is a dynamic interaction between virus, hepatocyte and the host’s immune response. The natural history of chronic HBV infection can be divided into three phases: high replicative or viraemic ‘immune tolerance phase’ followed by ‘immune clearance phase’ and then the low replication ‘residual phase’. The clinical course of chronic HBV infection is characterized by a series of exacerbations and remissions during the ‘immune clearance phase’, which may lead to hepatic decompensation, progression of liver disease, development of cirrhosis and hepatocellular carcinoma (HCC). It is of paramount importance to arrest HBV replication as early as possible to reduce infectivity, improve hepatic injuries, prevent progression to cirrhosis or HCC and thereby prolong survival. There are many potentially effective agents with different mechanisms of action and there is substantial accumulated experience with these therapies, but there is also still a need for practical recommendations such as: (i) who should be treated; (ii) when to treat such patients; (iii) which drug(s) or strategy would be most cost‐effective for the patient under consideration; (iv) how the patient should be monitored; (v) what benefit the patient can expect from such treatments; (vi) what can be done for special groups of patients, such as decompensated cirrhosis immunocompromised patients or children; and (vii) what treatment of chronic HBV infection could be expected in the 21st century. The Asia–Pacific region not only has the greatest number of patients with chronic HBV infection, but also has conducted important clinical trials. It is relevant and mandatory to coordinate all current knowledge to reach a consensus and to make guidelines for the treatment of chronic HBV infection in this region.
Nucleoside analogues in the treatment of chronic hepatitis B
Authors: Leung Nancy 
Published: March 2003

AbstractMany nucleoside analogues have been investigated for the treatment of chronic hepatitis B. Some were withdrawn because of significant adverse effects and some are still in the early stage of clinical assessment. Lamivudine has been demonstrated to have consistent efficacy and safety in large‐scale, phase III clinical trials. It has achieved a milestone in the treatment of chronic hepatitis B and is now commercially available in many countries. Being a potent inhibitor of hepatitis B viral replication, it achieved around 18% HBeAg seroconversion in HBeAg‐positive patients after 1 year of therapy. HBeAg seroconversion is a good endpoint for therapy and has been shown to be 80% durable. The response was better among patients with raised pretreatment alanine aminotransferase levels. Liver necro‐inflammation and fibrosis improved significantly after 1 year. Further improvement on extended therapy was observed together with an incremental increase in HBeAg seroconversion. Similar efficacy was demonstrated in HBeAg‐negative viraemic patients. The main drawback is the emergence of drug‐resistant variants starting from the sixth to ninth month of treatment. This can be associated with varying degrees of relapse of disease activity and may offset the benefit of therapy. With extended therapy, drug‐resistant variants continue to emergence at a rate of around 20% per year. Adefovir dipivoxil and entacavir are nucleoside or nucleotide analogues shown to suppress both the wild‐type and lamivudine‐resistant virus. Combination of these nucleoside/nucleotide analogues with immune modulators may be the answer to eradicate the virus in short‐term therapy and avoid the issue of drug resistance.
Molecular mechanism of the reversibility of hepatic fibrosis: With special reference to the role of matrix metalloproteinases
Authors: Okazaki Isao , Watanabe Tetsu , Hozawa Sigenari , Arai Masao , Maruyama Katsuya 
Published: March 2003

AbstractThe participation of matrix metalloproteinases (MMP) and their specific inhibitors, the tissue inhibitors of matrix metalloproteinases (TIMP), in both the formation and degradative recovery processes of liver fibrosis were mainly reviewed from the molecular biological aspect. Since authors first reported increased activity of interstitial collagenase in the early stage of hepatic fibrosis in rats induced by chronic CCl4 intoxication, in baboons fed alcohol chronically and in patients with alcoholic fibrosis, other investigators have also demonstrated increased activity biologically and histochemically. However, species‐specific differences in response have been found and gene‐level research on the rat model has not demonstrated increased mRNA transcription of collagenase. It has also been clarified that activated stellate cells can also produce matrix components. Very recently, authors observed the participation of interstitial collagenase in the recovery from experimental hepatic fibrosis by using polymerase chain reaction northern blotting and in situ hybridization. The in situ hybridization findings not only demonstrated the cells responsible for interstitial collagenase, but also suggested a great deal about the mechanism of recovery from fibrosis. Hepatic stellate cells are activated via the expression of c‐myb and nuclear factor‐κB (NFκB) which is induced by oxidative stress, and inhibited by antioxidant (1‐α‐tocopherol) and butylated hydroxytoluene. The activation mechanism is now being revealed. The relationship between the activation mechanism of stellate cells and the production and secretion of MMP and TIMP in the formation and recovery process of hepatic fibrosis should be investigated from the promoter gene level. This approach might help develop a new strategy for the treatment of liver fibrosis.
Polyunsaturated fatty acids reduce non‐receptor‐mediated transcellular permeation of protein across a model of intestinal epithelium in vitro
Authors: Rosella Ourania , Sinclair Andrew , Gibson Peter R 
Published: March 2003

Abstract
Background
: Dietary polyunsaturated fatty acids influence the natural history of intestinal inflammatory diseases. Varying the types of long‐chain fatty acids that are exposed to cells alters the physicochemical properties of cell membranes. This study aimed to determine whether such variations alter transcellular and paracellular permeability in intestinal epithelium.
Methods
: Monolayers of Caco‐2 cells, allowed to differentiate by culturing for 7 days following confluence, were used as the model for intestinal epithelium. Paracellular permeability was assessed by measurement of transepithelial resistance, while transcellular permeability was assessed by the transepithelial flux of horseradish peroxidase.
Results
: Exposure of the cells to 100 μmol/L of palmitic acid, oleic acid, eicosapentaenoic acid, or linoleic acid, was not toxic to cells (measured by leakage of lactate dehydrogenase), and altered cell membrane fatty acid composition (as measured by gas chromatography). Flux of horseradish peroxidase was significantly affected by 24 h fatty acid exposure (P = 0.038,
ANOVA), being decreased by 23 ± 6% (mean ± SEM) by eicosapentaenoic acid and 25 ± 3% by linoleic acid. Oleic acid, palmitic acid and butyrate, had no effect. Transepithelial resistance also varied significantly across the treatment groups (P < 0.001) due to a 28 ± 5% increase induced by butyrate. The long‐chain fatty acids had no effect.
Conclusions
: Both ω‐3 and ω‐6 polyunsaturated fatty acids reduce transcellular, non‐receptor‐mediated permeation of proteins across differentiated Caco2 cell monolayers, without altering paracellular permeability. Alteration of intestinal barrier function should be considered as a possible mechanism of action of dietary polyunsaturated fatty acids.
Pooled analysis of Helicobacter pylori eradication regimes in Asia
Authors: Wang Wei Hong , Wong Benjamin Chun Yu , Lam Shiu Kum 
Published: March 2003

Abstract
Background and Aims
: Differences in Helicobacter pylori strains and their resistance to antimicrobials between Asian and Western countries may affect the success in eradicating this bacterium. Our objective was to systematically review the regimens that have been tested in Asia.
Methods
: Data on anti‐H. pylori therapies reported from Asia in a large number of publications identified up to December 1998 were pooled into a few groups based on the combination of drugs used. A comparison of different groups was made by calculating the pooled eradication rates.
Results
: Seventy‐three studies with 134 treatment arms were reviewed. Pooled eradication rates of dual, triple and quadruple therapies were 61.0, 86.5 and 93.4%, respectively. Proton pump inhibitor (PPI)‐based combinations were more widely used and effective, with overall eradication rates of 90.7% in triple therapy and 93.4% in quadruple therapy. Bismuth combined with tetracycline and metronidazole also showed a high eradication rate of 92.0%.
Conclusions
: Proton pump inhibitor‐based triple therapy with either clarithromycin, amoxycillin or metronidazole was one of the most commonly used and effective anti‐H. pylori triple therapy regimens in Asia. The classical triple therapy with a bismuth, tetracycline and metronidazole combination has a similar efficacy. The results of anti‐H. pylori treatment in Asia are not different from those in Western countries.
Mortality association of enhanced CD44v6 expression is not mediated through occult lymphatic spread in stage II colorectal cancer
Authors: Clarke Gerard , Ryan Eleanor , O'keane J Conor , Crowe John , Mathúna Padraic Mac 
Published: March 2003

Abstract
Background and Aims
: In the absence of other metastatic disease, the presence of lymph node metastasis remains the most important determinant of survival in colorectal cancer (CRC). Cluster designation 44 variant 6 (CD44v6) over‐expression is associated with worse outcome in all stages of CRC. The CD44v6 is believed to confer metastatic potential through its facilitation of migration, extravasation and proliferation, although the specific means by which it conveys an adverse prognosis in CRC is unknown. The aim of the present study was to determine if CD44v6 over‐expression in Stage II CRC subjects was associated with the presence of lymph node micrometastases.
Methods
: We assessed tumour CD44v6 expression in 43 randomly sampled subjects who had resections for Stage II CRC between 1984 and 1991 by using immunohistochemistry. Micrometastases were sought in corresponding lymph node (LN) sections using keratin immunohistochemistry.
Results
: There was a statistical trend between tumour CD44v6 over‐expression and mortality (P = 0.09) and a significant relationship between LN cytokeratins and mortality (P = 0.01). There was no association between the detection of LN cytokeratins and tumour CD44v6 over‐expression.
Conclusion
: We conclude that the adverse survival effect of CD44v6 over‐expression is not mediated though lymphatic spread and postulate that it may therefore facilitate haematogenous metastasis.