Platelets in idiopathic thrombocytopenic purpura are increased in size but are of normal density

To determine whether platelet size and volume are related to one another or to platelet age, subpopulations of platelets from patients with idiopathic thrombocytopenic purpura (ITP) have been produced on the basis of density using Percoll gradients. The density distribution of platelets from patients with ITP and from patients with other forms of thrombocytopenia (thought to be nonimmune in nature) was the same as in normal controls. However, the platelets in each density subpopulation from ITP patients were increased in size. beta-thromboglobulin (beta TG) content of platelets from each patient group and the normals increased with density and tended to be higher in ITP than in normal controls. beta TG concentration per unit platelet volume and its level in plasma were similar in ITP patients and in normal controls. This suggests that the apparently normal density of ITP platelets was not a result of degranulation of large, dense platelets. Thus platelet size and density are independently determined and the increased size of platelets in immune thrombocytopenia may be the result of abnormalities in their production.     

Large Bloody Ascites in Association with Pelvic Endometriosis: Case Report and Literature Review

Endometriosis is only rarely the cause of massive bloody ascites. This entity simulates gynecological malignancy and is seldom recognized before surgical exploration of the abdomen. It is more commonly seen in black nulliparous females. Hormonal modulation has obviated the need for surgical resection, in some cases. We report a case of such an entity and review the medical literature.     

Inflammatory bowel disease in rats： Bacterial and chemical interaction

AIM：To develop a novel model of colitis in rats, using a combination of iodoacetamide and enteropathogenic E. coli（EPEC）, and to elucidate the pathophysiologic processes implicated in the development of ulcerative colitis （UC）.
METHODS： Hale Sprague-Dawley rats （/7 = 158） were inoculated intrarectally on a weekly basis with 4 different combinations： （a） 1% methylcellulose （HC）, （b） 100 μL of 6% iodoacetamide （IA） in 1% HC, （c） 200 p.L containing 4×10^8 colony factor units （CFU） of EPEC, and （d） combined treatment of （IA） followed by bacteria （13） after 2 d. Thirty days post treatment, each of the four groups was divided into two subgroups; the inoculation was stopped for one subgroup and the other subgroup continued with biweekly inoculation until the end of the experiment. Colitis was evaluated by the clinical course of the disease, the macroscopic and microscopic alterations, activity of myeloperoxidase （HPO）, and by TNF-α gene expression. RESULTS： Findings indicative of UC were seen in the combined treatment （IA ＋ B） as well as the IA continued treatment groups： the animals showed slow rate of increase in body weight, diarrhea, bloody stools, high colonic ulcer score, as well as histological alterations characteristic of UC, with an extensive inflammatory reaction. During the course of the experiment, the MPO activity was consistently elevated and the TNF-α gene expression was upregulated compared to the control animals.
CONCLUSION： The experimental ulcerative colitis model used in the present study resembles, to a great extent, the human disease. It is reproducible with characteristics indicative of chronicity.     

Helicobacter pylori-Associated Upper Gastrointestinal Disease in Saudi Arabia: A Pathologic Evaluation of 298 Endoscopic Biopsies from 201 Consecutive Patients

In a prospective study, histopathological examination 298 upper gastrointestinal (UGI) biopsies, obtained from 201 consecutive patients, was made. Patients were referred with mild to severe dyspeptic symptoms. The aim of the study was to compare the rate of identification of Helicobacter pylori (H. pylori) in the histologically normal gastric mucosa with that in histologically confirmed gastritis or peptic ulcer disease. The gastroduodenal mucosa was histologically normal in 35 patients (17.4%); among those patients, H. pylori was identified in only three (9%). Chronic gastritis was histologically confirmed in 162 patients (80.6%). H. pylori was identified in 123 (76%) of those patients. The difference was statistically significant (p less than 0.00001). Furthermore, when cases with a histological diagnosis of superficial chronic active gastritis (SCAG) are considered separately, the identification rate of H. pylori increases to 88% (121 of 137). When this rate is compared with that of 8% (two of 25), found in superficial chronic quiescent gastritis (SCQG), the difference is highly significant (p less than 0.00001). Of 38 endoscopically diagnosed peptic ulcers, H. pylori was identified in the gastric mucosa of 34 (89%). The organisms were always seen in the antral gastric mucosa, but never in duodenal mucosa. Identification of H. pylori correlates significantly with the histologic activity of chronic gastritis, in both peptic ulcer disease and non-ulcer dyspepsia.