The influence of supportive nutritional therapy via percutaneous endoscopically guided gastrostomy on the quality of life of cancer patients

Between April 1987 and May 1990 a total of 212 consecutive patients with tumours in the head and neck region were admitted to a prospective study comparing planned prospective enteral nutrition via percutaneous endoscopically guided gastrostomy (PEG; n=47) and oral nutrition (n=134). The nutritional status (anthropometric and laboratory chemical parameters) and the quality-of-life index according to Padilla et al. [Res Nurs Health 6: 117–126 (1983)] were determined prior to radiotherapy, 2, 4, 6 weeks later during radiotherapy and 6, 12 and 18 weeks after completion of radiotherapy. The quality-of-life score of the orally nourished patients decreased quickly during radiotherapy and improved only slowly afterwards. Although PEG patients had a worse starting score, their quality-of-life index did not deteriorate during therapy (statistically significant difference between the two groups). The same applies to the nutritional status. These results show that an early and constant enteral nutrition by PEG can stabilize the nutritional state and the quality of life of patients with tumours of the head and neck area during radiotherapy.Presented among best proffered papers at the 4th International Symposium: Supportive Care in Cancer, St. Gallen, Switzerland, 24–27 February 1993     

Genetically attenuated Plasmodium berghei liver stages induce sterile protracted protection that is mediated by major histocompatibility complex Class I-dependent interferon-gamma-producing CD8+ T cells

At present, radiation-attenuated plasmodia sporozoites ( gamma -spz) is the only vaccine that induces sterile and lasting protection in malaria-naive humans and laboratory rodents. However, gamma -spz are not without risks. For example, the heterogeneity of the gamma -spz could explain occasional breakthrough infections. To avoid this possibility, we constructed a double-knockout P. berghei parasite by removing 2 genes, UIS3 and UIS4, that are up-regulated in infective spz. We evaluated the double-knockout Pbuis3(-)/4(-) parasites for protective efficacy and the contribution of CD8(+) T cells to protection. Pbuis3(-)/4(-) spz induced sterile and protracted protection in C57BL/6 mice. Protection was linked to CD8(+) T cells, given that mice deficient in beta (2)m were not protected. Pbuis3(-)/4(-) spz-immune CD8(+) T cells consisted of effector/memory phenotypes and produced interferon- gamma . On the basis of these observations, we propose that the development of genetically attenuated P. falciparum parasites is warranted for tests in clinical trials as a pre-erythrocytic stage vaccine candidate.     

A possible mechanism for endogenous activation of the type I interferon system in myositis patients with anti-Jo-1 or anti-Ro 52/anti-Ro 60 autoantibodies

OBJECTIVE: To investigate type I interferon (IFN) system activation and its correlation with autoantibodies and organ manifestations in polymyositis (PM), dermatomyositis (DM), and inclusion body myositis. METHODS: Sera from 30 patients and 16 healthy controls, or purified IgG, were combined with material released from necrotized cells to stimulate IFNalpha production by peripheral blood mononuclear cells (PBMCs) from healthy blood donors. Muscle biopsy specimens from 25 patients and 7 healthy controls were investigated for blood dendritic cell antigen 2 (BDCA-2)-positive plasmacytoid dendritic cells (PDCs) and IFNalpha/beta-inducible myxovirus resistance 1 (MX-1) protein. RESULTS: Sera from 13 patients who were positive for anti-Jo-1 or anti-Ro 52/anti-Ro 60 autoantibodies induced IFNalpha production in PBMCs when combined with necrotic cell material. In addition, IgG prepared from anti-Jo-1-positive PM sera induced IFNalpha with necrotic material, but not when the latter was treated with RNase. BDCA-2 expression in PDCs in muscle tissue was increased in PM patients with anti-Jo-1 autoantibodies, while MX-1 staining in capillaries was increased in DM patients, compared with healthy individuals. IFNalpha-inducing capacity correlated with interstitial lung disease, while MX-1 expression in the capillaries correlated with DM. CONCLUSION: Immune complexes containing anti-Jo-1 or anti-Ro 52/anti-Ro 60 autoantibodies and RNA may act as endogenous IFNalpha inducers that activate IFNalpha production in PDCs. These PDCs could be of importance for inducing myositis, whereas in DM patients without autoantibodies the presence of MX-1 protein in capillaries suggests another cellular IFNalpha source and induction mechanism. Consequently, the type I IFN system may be of importance in both PM and DM, but via different pathways.     

Diagnostik und Therapie von Pseudotumoren der Orbita

Der Pseudotumor der Orbita ist ein unspezifischer entzündlicher Prozess dessen Genese unbekannt ist und der histologisch in 3 Gruppen unterteilt wird: der granulomat?se, lymphoide und sklerosierende Typ. Zwischen 1995 und 1998 haben wir 12 Patienten mit einem Pseudotumor der Orbita behandelt. Es handelte sich dabei um F?lle vom granulomat?sen (n=6), lymphoiden (n=3) und sklerosierenden (n=3) Typ. Bei 7 Patienten war der Pseudotumor im medialen Bereich der Orbita und in 4 F?llen im lateralen Bereich lokalisiert. Bei einer Patientin lag eine diffuse Infiltration ann?hernd aller orbitalen Strukturen vor. Die Probebiopsie wurde in 6 F?llen endonasal, in 2 F?llen über eine mediale Orbitotomie und bei 4 Patienten über eine laterale Orbitotomie durchgeführt. Die gut abgrenzbaren lymphoiden (n=3) und sklerosierenden (n=3) Pseudotumoren konnten im Rahmen der Probebiopsie komplett entfernt werden, so dass die Patienten nach wenigen Wochen beschwerdefrei waren. Bei den 6 Patienten mit einem granulomat?sen Pseudotumor wurde nach der definitiven Histologie eine prim?re Kortikosteroidtherapie durchgeführt. In 3 der 6 F?lle kam es dadurch zu einem Rückgang der Beschwerden mit kompletter Ausheilung. Bei den restlichen 3 Patienten war eine erneute Kortisontherapie erforderlich wobei diese nur in 2 F?llen erfolgreich war. Der Nachbeobachtungszeitraum betrug 6–28 (Mittel 16) Monate. Postoperative Komplikationen traten nicht auf.     

Untersuchungen zum Eicosanoidstoffwechsel in peripheren Blutzellen bei Patienten mit zystischer Fibrose

Hintergrund. Die autosomal-rezessiv vererbte zystische Fibrose ist die h?ufigste genetische Erkrankung der wei?en Bev?lkerung. St?rungen im Eicosanoidstoffwechsel scheinen in der Pathogenese der Erkrankung eine wichtige Rolle zu spielen. Im Rahmen der vorliegenden Studie werden Messungen zur Freisetzung von Prostaglandin E₂ (PGE₂) und Peptidleukotrienen (pLT) aus peripheren Blutzellen vorgestellt.     

Untersuchungen zum Eicosanoidstoffwechsel in peripheren Blutzellen bei Patienten mit zystischer Fibrose

BACKGROUND: The autosomal recessive inherited cystic fibrosis is the most common genetic disorder in white patients. Disturbances in the eicosanoid metabolism seem to play an important role in the pathogenesis of the disease. The present study shows examinations on the release of prostaglandin E2 (PGE2) and peptide leukotrienes (pLT) in peripheral blood cells. PATIENTS AND METHODS: In this respect heparinised blood samples of 10 cc were obtained from 25 patients with cystic fibrosis. The peripheral blood cells were separated from the remaining blood components. PGE2 and pLT were measured by a particularly developed sensitive enzyme immunoassay with specific monoclonal antibodies. Both the basal release of the metabolites and the concentrations after stimulation with arachidonic acid (AA) were explored. The control group consisted of 25 healthy individuals. RESULTS: A distinct elevation in the basal release of pLT compared to the control group was noticed. Further stimulation with AA could only be achieved to a remarkably smaller extent. In contrast to these findings no elevation of the basal release of PGE2 and no stimulative effect of AA could be detected. In general we observed a distinct shift in the eicosanoid metabolism in favour of pLT and their proinflammatory effects. CONCLUSIONS: The increased synthesis of pLT in patients with cystic fibrosis seems to play an important role in the pathogenesis of the disease. Future studies will have to proof, if we can achieve any improvement in the clinical courses in patients with cystic fibrosis using leukotriene receptor antagonists or 5-lipoxygenase inhibitors.