The colitis of Behcet's disease: A separate entity?

Summary An additional case of Behcet's disease with colonic involvement has been presented. This association is rare, as only 13 prior cases with adequate data were available for comparison. Controversy exists as to whether these cases represented true involvement of the colon by Behcet's disease, coincidental inflammatory bowel disease and Behcet's disease, or merely autoimmune phenomena associated with inflammatory bowel disease. Unusual colonoscopic lesions noted in our patient and other features enumerated in the text suggested to us that at least some of these cases represented primary Behcet's disease involving the colon.     

Gastric blood flow

Summary In summary, the vascular bed of the stomach is an area of great potential importance to both gastric and vascular physiologists. There are available many technics for its investigation. Simultaneous study of both hemodynamic and secretory phenomena can be conducted on the stomach. In the next few years information concerning the circulation of the stomach may help elucidate problems in the physiology and pathology of gastric secretion. Hightower observed recently: The topic of visceral circulation, particularly as it pertains to the digestive tract, has not been commented upon in recent...Reviews of Physiology. This subject has become increasingly important in the past few years and is an area with which physiologists interested in the digestive system will become more and more concerned.³³     

Cardiac pathology after valve replacement by disc prosthesis: A study of 61 necropsy patients

Clinical and necropsy observations are described in 61 patients who had one or more cardiac valves replaced with a discoid prosthesis of the Hufnagel type. The most common (31 percent) cause of death among the 45 patients who died early (less than 65 days after operation) appeared to be prosthetic disproportion; that is, the prosthesis was too big for the aorta or ventricular cavity into which it was inserted so that inadequate space was present between the margins of the disc and the endocardium of ventricle or intima of aorta. Prosthetic thrombosis occurred in only 3 of the 45 patients who died early, but poppet movement appeared considerably altered in each. In contrast, thrombi were observed on a prosthesis in 14 of the 16 patients who died late (4 to 47 months [average 21] postoperatively), but in none did the thrombi appear of sufficient size to alter poppet function. Excessive bleeding occurred in 11 (24 percent) of the 45 early deaths and was primarily related to the insertion of a patch in the root of the aorta. Uncorrected valvular disease either by itself or by its ability to alter function of the prosthesis appeared responsible for death in 6 (13 percent) of the 45 patients who died early and in 2 (6 percent) of the 16 who died late. Insertion of a mitral poppet disc in a patient with uncorrected aortic regurgitation, even of mild degree, may be hazardous because the aortic regurgitant jet stream may interfere with proper function of the mitral disc. Likewise, insertion of a poppet disc only in the aortic valve position in a patient with combined aortic and mitral regurgitation may considerably increase the degree of mitral incompetence because the aortic prosthesis is intrinsically obstructive.Disc wear or variance was observed in all but one prosthesis in place for more than 1 year. Although hemolytic anemia of significant degree was not observed in any of the 16 patients who died late, the occurrence of renal hemosiderosis in 13 of the 16 patients indicates that the poppet disc prosthesis is considerably traumatic to erythrocytes. Thus, this type of prosthesis is not an ideal substitute cardiac valve. It clots, despite anticoagulant therapy, it is intrinsically stenotic, portions of it, that is, the disc, degenerate, and it causes hemolysis to erythrocytes.     

Utility of impedance cardiography for the identification of short-term risk of clinical decompensation in stable patients with chronic heart failure.

OBJECTIVES: This study sought to assess the potential utility of impedance cardiography (ICG) in predicting clinical deterioration in ambulatory patients with heart failure (HF). BACKGROUND: Impedance cardiography uses changes in thoracic electrical impedance to estimate hemodynamic variables, but its ability to predict clinical events has not been evaluated. METHODS: We prospectively evaluated 212 stable patients with HF and a recent episode of clinical decompensation who underwent serial clinical evaluation and blinded ICG testing every 2 weeks for 26 weeks and were followed up for the occurrence of death or worsening HF requiring hospitalization or emergent care. RESULTS: During the study, 59 patients experienced 104 episodes of decompensated HF (16 deaths, 78 hospitalizations, and 10 emergency visits). Multivariate analysis identified 6 clinical and ICG variables that independently predicted an event within 14 days of assessment. These included three clinical variables (visual analog score, New York Heart Association functional class, and systolic blood pressure) and three ICG parameters (velocity index, thoracic fluid content index, and left ventricular ejection time). The three ICG parameters combined into a composite score was a powerful predictor of an event during the next 14 days (p = 0.0002). Visits with a high-risk composite score had 2.5 times greater likelihood and those with a low-risk score had a 70% lower likelihood of a near-term event compared with visits at intermediate risk. CONCLUSIONS: These results suggest that when performed at regular intervals in stable patients with HF with a recent episode of clinical decompensation, ICG can identify patients at increased near-term risk of recurrent decompensation.     

Myocardial salvage by intracoronary thrombolysis in evolving acute myocardial infarction: evaluation using intracoronary injection of thallium-201

Immediate objective assessment of viabillty of reperfused myocardium following intracoronary (IC) thrombolysis by evaluation of ventricular function may be limited due to delay in restoration of function. Thus we assessed myocardial uptake of thallium-201 (TI-201) following IC injection postreperfusion as an index of myocardial salvage in 12 experimental dogs and in five patients with evolving acute myocardial infarction (AMI). In seven dogs with mean of 313 minutes of experimental coronary occlusion, immediate postreperfusion IC TI-201 images revealed absence of myocardial uptake in prevlously occluded zones. These TI-201 defects correlated with presence of necrosis as demonstrated by histochemical staining with triphenyl-tetrazolium chloride (TTC). In contrast, in five dogs with mean of 37 minutes of coronary occlusion, reperfused myocardium showed normal TI-201 uptake following its IC injection; this normal TI-201 uptake pattern correlated with absence of necrosis by TTC technique in all five dogs. In five patients with evolving AMI, control TI-201 images obtained following IV injection prior to IC thrombolysis showed myocardial perfusion defects corresponding to distribution of the occluded vessel. Following reperfusion, 30 to 50 mCi of TI-201 was injected into the reopened coronary artery. In two patients with mean symptom onset of reperfusion time of $\text{2}\text{1}\text{2}\text{hours}$, immediate postreperfusion IC TI-201 images demonstrated normal or improved TI-201 uptake in reperfused myocardium. By radionuclide ventriculography, segmental wall motion remained abnormal in the reperfused regions 6 hours postreperfusion and showed improvement by the time of 10-day study. In the remaining three patients with symptom onset to reperfusion time of 5 hours, immediate postreperfusion IC TI-201 images did not show improvement, correlating with persistent wall motion abnormalities 10 days postreperfusion. In all five patients, repeat 10-day IV TI-201 images were unchanged from the immediate postreperfusion IC TI-201 images. We conclude that (1) prereperfusion TI-201 imaging with repeat TI-201 injection into the reopened coronary artery appears to delineate the extent of myocardial salvage in both experimental and clinical studies and (2) this method of IC TI-201 imaging allows immediate assessment of myocardial viabillty which may facilltate decisions regarding the need for additional myocardial revascularization modalities.     

Administration of pegylated recombinant human megakaryocyte growth and development factor to humans stimulates the production of functional platelets that show no evidence of in vivo activation

This report describes the effect of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on platelet production and platelet function in humans. Subjects with advanced solid tumors received PEG-rHuMGDF daily for up to 10 days. There was no increase in circulating platelet count at doses of 0.03 or 0.1 microgram/kg/d by day 12 of study. At doses of 0.3 and 1.0 microgram/kg/d there was a threefold median increase (maximum 10-fold) in platelet count by day 16. The platelets produced in vivo in response to PEG-rHuMGDF showed unchanged aggregation and adenosine triphosphate (ATP)-release responses in in vitro assays. Tests included aggregation and release of ATP in response to adenosine diphosphate (ADP) (10, 5, 2.5, and 1.25 mumol/L), collagen (2 micrograms/mL), thrombin-receptor agonist peptide (TRAP, 10 mumol/L) and ristocetin (1.5 mg/mL). Administration of aspirin to an individual with platelet count of 1,771 x 10(3)/L resulted in the typical aspirin-induced ablation of the normal aggregation and ATP-release response to stimulation with arachidonic acid (0.5 mg/mL), collagen, and ADP (2.5 and 1.25 mumol/L). There was no change in the expression of the platelet-surface activation marker CD62P (P-selectin) nor induction of the fibrinogen binding site on glycoprotein IIb/IIIa as reported by the monoclonal antibody, D3GP3. An elevation of reticulated platelets was evident after 3 days of treatment with PEG-rHuMGDF and preceded the increase in circulating platelet count by 5 to 8 days; this reflected the production of new platelets in response to PEG-rHuMGDF. At later time points, the mean platelet volume (MPV) decreased in a manner inversely proportional to the platelet count. Levels of plasma glycocalicin, a measure of platelet turnover, rose 3 days after the initial increase in the peripheral platelet count. The level of plasma glycocalicin was proportional to the total platelet mass, suggesting that platelets generated in response to PEG-rHuMGDF were not more actively destroyed. Thus, the administration of PEG-rHuMGDF, to humans, increased the circulating platelet count and resulted in fully functional platelets, which showed no detectable increase in reactivity nor alteration in activation status.