Enteroliths Causing Intermittent Obstruction in a Patient with Crohn''s Disease

Calcified enteroliths as a cause of intermittent small bowel obstruction is an uncommon clinical entity. The pathophysiological mechanism involves stasis of intestinal contents and has been associated with Meckel's diverticulum, tuberculosis, and regional enteritis. This case describes prophylactic operative intervention in a symptomatic patient with enteroliths as a result of Crohn's disease.     

Complement C3 deposition onto bacteria by neonatal serum is not enhanced after the infusion of intravenous immunoglobulin

To determine the effect of intravenous immunoglobulin (IVIG) on the capacity of serum from septic neonates to deposit complement C3 and IgG onto the bacteria isolated from their blood, 500 mg/kg of IVIG was administered to 18 neonates suspected of being septic. Blood was obtained just before the infusion, and again 15 minutes after its completion. Group B streptococcus type II, group B streptococcus type III, Staphylococcus aureus, and Staphylococcus epidermidis were isolated from the pre-infusion blood of four neonates. Bacteria were incubated with the appropriate serum, washed, and the amount of C3 and IgG subsequently bound to the organisms was quantified by radioimmunobinding assay. Sera from the four septic neonates and sera from four neonates of similar gestational age but whose blood cultures were negative were compared with pooled sera from healthy adults. Before the administration of IVIG, C3 deposition onto the bacteria by sera from five of the seven neonates tested was significantly less than that observed for adult sera. Following the infusion, no increase in C3 deposition was observed for any of the seven sera assayed, and in two cases C3 deposition fell significantly. In contrast, in seven of eight cases, IVIG enhanced the IgG deposition to levels greater than or equal to those observed for adult sera. Therefore, following the infusion of IVIG into neonates with proven or suspected sepsis, the deposition of C3 onto invasive bacteria by their serum was not enhanced even though IgG deposition was increased.     

Evidence for small intracellular vesicles in human blood phagocytes containing cytochrome b558 and the adhesion molecule CD11b/CD18

Human neutrophils contain a rapidly mobilizable pool of so-called secretory vesicles distinct from the azurophil granules and specific granules. Using human albumin as a marker for these intracellular vesicles in immuno-electron microscopy, we found that part of the cytochrome b558 in non-purified whole blood neutrophils colocalized in these vesicles. This was detected with monoclonal antibody (MoAb) CLB- 48, binding to the high molecular weight subunit of cytochrome b558. Approximately 65% of the albumin-containing vesicles showed MoAb CLB-48 labeling. This was also found in eosinophilic granulocytes and in monocytes. Cytofluorimetric determination of cytochrome b558 expression on the plasma membrane of intact, nonpurified granulocytes (and monocytes) with MoAb 7D5, which is directed against an extracellular epitope of cytochrome b558, did not show any binding. However, granulocytes (and monocytes) significantly bound 7D5 after density centrifugation. The positive binding of 7D5 to purified neutrophilic granulocytes correlated with a strongly reduced labeling of cytochrome b558 in the albumin-positive vesicles. Binding of CD11b MoAb CLB-B2.12 to the alpha subunit of the complement receptor type 3 (CR3) on the surface of intact, nonpurified neutrophils was detected to a limited extent in whole blood samples, but was strongly increased upon density gradient centrifugation of the cells, as we have described before. Investigation at the ultrastructural level showed that the CD11b antigen codistributed with albumin in vesicular structures in nonpurified phagocytes, especially in neutrophils and eosinophils. Together, these data substantiate the idea of an intracellular store that can be easily mobilized (even under the simple stress condition of density gradient centrifugation). Such mobilization may result in the expression of cytochrome b558 on the plasma membrane, as was indicated in this study. Apart from cytochrome b558, several other surface membrane molecules, as we show here for the integrin CD11b/CD18 (CR3), are probably also located in these rapidly mobilizable intracellular vesicles.     

Hormone replacement therapy and cardiovascular disease.

Oestrogen alone probably confers a degree of protection against ischaemic heart disease and stroke and is appropriate for women requiring hormone replacement therapy (HRT) who have undergone hysterectomy. However, the cardiovascular effects of the progestogens used with oestrogen in the much larger number of women who have not undergone hysterectomy are unknown. Some widely used progestogens have adverse effects on lipoprotein levels and may raise blood pressure. The antithrombin III level may be involved in determining the response to oestrogen in different settings. The indications for HRT and the effects of different formulations on cardiovascular disease constitute one of the most pressing but complex issues in present-day medical practice. These questions can only be satisfactorily answered by the randomised controlled trials that should have been initiated several years ago and the feasibility of which is only now being investigated.     

Patients with a deficiency of natural killer cell activity lack the VEP13-positive lymphocyte subpopulation

Many patients with B-type chronic lymphocytic leukemia (CLL) exhibit a profound defect in their natural killer (NK) cell activity, the basis of which is still obscure. Hence, we analyzed the NK cells from peripheral blood samples from 11 patients with CLL for phenotype and function, after removal of the leukemic cells with a monoclonal antibody (BA-1) plus complement. Phenotypic analysis of these nonleukemic cells with monoclonal antibodies (MoAbs) against NK cells revealed that the CLL patients had higher percentages of HNK-1-positive cells (23.5% compared to controls with 14.7%). In contrast, VEP13- positive cells were absent or low in seven patients (0.8% compared to controls with 11.2%) and normal in four patients (10.5%). When testing NK cell activities against K562 or MOLT 4 target cells, patients with no or minimal numbers of VEP13-positive cells were found to be deficient, while patients with normal percentages of VEP13-positive cells had NK cell activity comparable to controls. Isolation by fluorescence-activated cell sorter of HNK-1-positive cells from patients lacking VEP13-positive cells and NK cell activity indicated that the majority of the HNK-1-positive cells in these patients had the large granular lymphocyte morphology that is characteristic of NK cells. Thus, the deficiency of NK cell activity in CLL patients appears to result from the absence of cells carrying the VEP13 marker.