Transarterial thrombolysis of portal and mesenteric vein thrombosis: a promising alternative to common therapy.
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Publications and source records attributed to W Stock.
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We report 96 patients (107 legs) with recurrence after varicose vein surgery. We define a recurrent varicose vein as a new transfascial insufficiency after incomplete interruption of the saphenofemoral as well as popliteal junction with reflux in the epifascial venous system. 92 patients underwent external primary surgery. Morphologically an insufficient high ligation of the V. saphena magna (Moszkowicz's operation) led in 30 cases to a recurrent varicose vein. In 47 cases an incomplete isolated, in 29 cases an incomplete saphenofemoral ligation during a Babcock procedure and in one case an incomplete saphenopopliteal ligation for V. saphena parva insufficiency were the reasons for the recurrence. As recurrent surgery we performed 106 ligations of the saphenofemoral junction. In 38 of these cases an isolated saphenofemoral ligation and in 68 cases an additional stage-adjusted ligation of the V. saphena magna were carried out. In one case of recurrent saphenopopliteal insufficiency a repeated ligation of the V. saphena parva was performed. The recurrence is an avoidable complication of a not perfect primary surgery. The main cause is an inadequate access with incomplete saphenofemoral or -popliteal ligation.
The vast majority of adults with acute lymphoblastic leukemia (ALL) now achieve remission with current intensive chemotherapy regimens. Nevertheless, most adults with ALL will eventually relapse and die of their disease. Specific clinical and molecular-cytogenetic prognostic factors have been identified that are beginning to provide insights for the development of risk-adapted management strategies that appear to improve survival for several high-risk patient groups, including those with mature B-cell ALL and B-lineage ALL patients with a Philadelphia chromosome. We review standard and some recently described prognostic factors in adult ALL, describe current therapy based on a risk-adapted approach, and look toward the future with a brief discussion of novel, targeted treatments that could be incorporated into postremission strategies to improve survival for adults with ALL.
A major complication of portal and mesenteric vein thrombosis is acute bowel ischaemia resulting in infarction and requiring immediate resection of the involved segment. Sufficient collaterals can prevent acute haemorrhagic infarction, but bowel stenosis due to chronic ischaemia may develop. We report two cases of ischaemic jejunal stenosis occurring 4 weeks after successful treatment of portal and mesenteric vein thrombosis. Diagnosis of high-grade segmental stenosis of the jejunum was established by contrast medium radiography of the gastrointestinal tract. After laparotomy and resection of the stenosed jejunal segment, both patients recovered well from the operation and were released from hospital. Follow-up examinations revealed an unremarkable state of health. Ischaemic bowel stenosis should be considered in patients with recurring abdominal pain after mesenteric and portal vein thrombosis. A close follow-up of every patient after treatment for mesenteric and portal vein thrombosis should be carried out to ensure early diagnosis of this complication.
Systematic ligand-binding studies of the biospecific interaction between steroids and antisteroid antibodies can be performed in real time using biosensor techniques. In this study, quartz crystal microbalance (QCM) and surface plasmon resonance (SPR) biosensor systems were applied. Different biotinylated testosterone (T) and 17beta-estradiol (E2) derivatives were preincubated with streptavidin and immobilized on the sensor surfaces. We obtained low matrix densities of antigen enabling the investigation of the binding kinetics and position specificities of various anti-E2 and anti-T monoclonal antibodies (mAbs) to these steroidal compounds. The highest immunoreactivity of anti-E2 and anti-T mAbs is not necessarily for the specific modified steroid that was used as a protein-coupled hapten for immunization. The kinetic data confirm that both 3- and 19-specific anti-T mAbs do not discriminate between the 3- and 19-biotinylated T derivatives, whereas the 7alpha-biotinylated T probe showed no affinity to these two anti-T mAbs. In the case of the 3-specific anti-E2 mAb, comparable interaction data were found for 3- and 6alpha-biotinylated E2 compounds. The 6-specific anti-E2 mAb showed comparable ligand binding, but a significant higher dissociation rate to the position-specific antigen. The QCM and SPR results correspond well to the data from cross-reactivity studies in solution as well as to enzyme immunoassay equilibrium measurements.
Disorders of white cells are very common in clinical practice. White-cell development and numbers are controlled by a mixture of external stimuli including cytokines, matrix proteins, and accessory cells. Several different white-cell lineages are recognised; each has a role in host defence. Both white-cell deficiency and overproduction can lead to disease. Some forms of inherited white-cell deficiency are potentially treatable with gene therapy.
To test the hypothesis that cell cycle regulatory gene abnormalities are determinants of clinical outcome in adult acute lymphoblastic leukemia (ALL), we screened lymphoblasts from patients on a Southwest Oncology Group protocol for abnormalities of the genes, retinoblastoma (Rb), p53, p15(INK4B), and p16(INK4A). Aberrant expression occurred in 33 (85%) patients in the following frequencies: Rb, 51%; p16(INK4A), 41%; p53, 26%. Thirteen patients (33%) had abnormalities in 2 or more genes. Outcomes were compared in patients with 0 to 1 abnormality versus patients with multiple abnormalities. The 2 groups did not differ in a large number of clinical and laboratory characteristics. The CR rates for patients with 0 to 1 and multiple abnormalities were similar (69% and 54%, respectively). Patients with 0 to 1 abnormality had a median survival time of 25 months (n = 26; 95% CI, 13-46 months) versus 8 months (n = 13; 95% CI, 4-12 months) for those with multiple abnormalities (P <.01). Stem cells (CD34+lin-) were isolated from adult ALL bone marrows and tested for p16(INK4A) expression by immunocytochemistry. In 3 of 5 patients lymphoblasts and sorted stem cells lacked p16(INK4A) expression. In 2 other patients only 50% of sorted stem cells expressed p16(INK4A). By contrast, p16 expression was present in the CD34+ lin- compartment in 95% (median) of 9 patients whose lymphoblasts expressed p16(INK4A). Therefore, cell cycle regulatory gene abnormalities are frequently present in adult ALL lymphoblasts, and they may be important determinants of disease outcome. The presence of these abnormalities in the stem compartment suggests that they contribute to leukemogenesis. Eradication of the stem cell subset harboring these abnormalities may be important to achieve cure.
During the past 2 decades, there has been considerable progress made in the treatment of childhood and adult lymphocytic leukemia (ALL). Currently, 70% to 90% of adults achieve a complete remission, and 25% to 50% of these patients may experience prolonged disease-free survival and may be cured of their disease. Unfortunately, most adults with ALL will ultimately experience a recurrence and die of their leukemia. Although most children with ALL may now be cured with current therapeutic regimens, the ability to distinguish good-risk patients from those who are likely to relapse has important clinical implications. Relapse, in most pediatric and adult cases, is thought to result from residual leukemia cells that remain following achievement of "complete" remission but are below the limits of detection using conventional morphologic assessment of the bone marrow. Sensitive techniques are now available to detect subclinical levels of residual leukemia, termed minimal residual disease.
Although allogeneic transplantation can be curative for patients with sickle cell disease, the toxicity of conditioning regimens has precluded its use in adults with significant end-organ damage. Newer conditioning regimens have been developed that are less toxic and that may broaden the applicability of allogeneic transplantation in this disorder. We report two adults with end-stage sickle cell disease, who underwent allogeneic transplantation from an HLA-identical sibling donor after conditioning with fludarabine/melphalan and ATG. Both patients had been extensively transfused and one had multiple RBC antibodies. One of the patients also had end-stage renal disease, and was dialysis dependent. Engraftment occurred promptly in both patients. Both achieved 100% donor chimerism and both were free of pain crises after transplant. The first patient died of a respiratory failure related to chronic graft-versus-host disease (GVHD) on day 335 after transplantation. The second patient developed severe gastro-intestinal GVHD and TTP and died on day 147 after transplantation. Conditioning with fludarabine/melphalan and ATG followed by allogeneic stem cell transplantation resulted in prompt and reliable engraftment in adults with end-stage sickle cell disease. The incidence of severe GVHD was unacceptably high and may be related to the ethnicity of the patients or to the inflammatory state associated with pre-existing sickle cell disease.
The surgical management of large defects of the Achilles tendon and overlying skin is very demanding and necessitates, as a rule, a free vascularized graft. The ideal characteristics of a thin layer of skin and a strong tendon component, combined with a reliable blood supply and minimal morbidity at the donor site, have only been partially met by all previous grafts used in this situation. The authors performed reconstructions in five patients with large defects of the Achilles tendon and overlying skin by using a perforator flap derived from the tensor fasciae latae flap. A vascularized skin-subcutis-fascia lata flap could be raised by dissecting out two to three perforating arteries through the tensor fasciae latae muscle to the ascending branch of the lateral circumflex femoral artery; the muscle was left in situ in the process. All the flaps took well without complications. At final examination after an average of 20 months, the reconstructed Achilles tendon showed good functional results, although there was a 50 to 70 percent reduction in power during plantar flexion when compared with the normal side. A very good aesthetic result could be obtained after a debulking operation was performed on the skin flap.
We report the case of a patient with rare CD5+ hairy cell leukemia, which was unusual, as there was also a discrepancy between the bone marrow and peripheral blood immunophenotypes. We propose that some degree of maturation within the malignant clone and the predominance of more mature CD5- hairy cells in the peripheral blood can explain this observation. The patient was treated with a conventional course of cladribine (2'-chlorodeoxyadenosine) and achieved complete remission. We conclude that the unusual CD5+ immunophenotype of this patient did not affect prognosis or change the response to standard therapy.
The continuous, in vivo infusion of low-dose IL-2 selectively expands the absolute number of human natural killer (NK) cells after 4-6 weeks of therapy. The mechanism responsible for this expansion is unknown and was examined in this study. NK cells cultured at low concentrations of IL-2, comparable to those found during in vivo therapy, proliferate for 6 days and then exit the cell cycle. However, NK cells in vivo did not traverse the S/G(2)/M phase of the cell cycle during low-dose IL-2 therapy. Low concentrations of IL-2 delay programmed cell death of NK cells but have the same effect on resting T cells that do not expand in vivo. When CD34(+) bone marrow hematopoietic progenitor cells are cultured for 21 days with low concentrations of IL-2, they differentiate into CD56(+)CD3(-) NK cells, not T cells. Thus, the selective expansion of human NK cells during continuous in vivo infusion of low-dose IL-2 likely results from enhanced NK-cell differentiation from bone marrow progenitors, combined with an IL-2-dependent delay in NK-cell death, rather than proliferation of mature NK cells in the periphery.
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The SHP-1 phosphatase associates with the receptors for erythropoietin, stem cell factor, and interleukin-3, and negatively regulates the mitogenic signals generated during engagement by their respective ligands. The erythroid progenitors of patients with polycythemia vera are hypersensitive to the mitogenic effects of these growth factors despite the fact that the numbers and binding affinities for their receptors are not increased. To determine whether post-receptor signaling defects may account for growth factor-hypersensitivity in polycythemia vera, we determined the expression of SHP-1 in highly purified erythroid progenitors from polycythemia vera patients. Our data demonstrate that in approximately 60% of the patients, expression of SHP-1 in the colony forming unit-erythroid population is diminished. The decreased expression of the protein may result from a transcriptional defect, as suggested by the diminished SHP-1 mRNA expression in the erythroid progenitors of these patients. Studies to determine the level of maturation of polycythemia vera and normal cells indicated that there was no difference between the two at early colony forming unit-erythroid stage of differentiation although polycythemia vera cells showed retarded differentiation kinetics at late colony forming unit-erythroid stage of differentiation. Furthermore, SHP-1 expression in normal colony forming unit-erythroid demonstrated downregulation of mRNA and protein levels during terminal differentiation, suggesting that its function is required for growth control during the early stages of erythropoiesis. These results indicate an important role for SHP-1 in the regulation of normal human erythroid progenitors and suggest that defective expression of the protein may contribute to the pathogenesis of polycythemia vera.
In the course of an infection with human immunodeficiency virus, a large variety of complications affecting all organ systems can occur. However, complications affecting the vascular system demanding surgical intervention are rare. In the case presented we report a 67-year-old HIV-seropositive patient who underwent surgery for a huge abscess in the thigh. Intraoperatively unexpectedly we found a mycotic aneurysm of the femoral superficial artery and the causactive bacterium proved to be Salmonella enteritidis. Because of the rising number of HIV-infected patients we suspect that the amount of complications involving the vascular system and demanding surgical intervention will also increase. Therefore, when diagnosing and deciding on therapy for patients with AIDS, the physician must be aware that vascular complications due as a result of HIV infection might occur more frequently in the future.
Morbidity and mortality after emergency procedures in 105 patients with perforated colonic diverticulitis were evaluated in a retrospective study. In different stages of diverticulitis (Hinchey classification: I, 8.6%; II, 14.3%; III, 57.1%; IV, 20.0%) mortality was 12.4%. Preoperative sepsis syndrome with leucopenia and disturbed liver function, cardiac risk factors and obesity were independent prognostic factors in multiple logistic regression. Accompanied by immunosuppression the mortality rate remarkably increased to 33%. The stage of peritonitis showed no influence on the prognosis. In multivariate analysis, surgical procedure (primary resection 12.4%. Hartmann's procedure 61.9%, non-resection procedures 25.7%) showed influence only on increased general complications.
Patients with myelodysplastic syndromes (MDS) show a decrease in the number and function of natural killer (NK) cells, including lymphokine activated killer (LAK) cell activity. Interleukin-2 (IL-2) stimulates the proliferation and activity of these lymphocytes. Anecdotal clinical experience has shown haematological and cytogenetic improvement in myelodysplasia by low-dose IL-2 treatment. A total of 10 patients with MDS were treated with 1 million units of IL-2 subcutaneously daily for 12 weeks. Even though improvement in CD16+/CD56+ cell numbers was seen in a majority of the patients, the haematological status and transfusion requirements remained unchanged. There was minimal toxicity from this therapy.