[Palliative therapy of gastrointestinal obstruction]. / Palliativtherapie bei gastrointestinaler Obstruktion.

Gastrointestinal obstruction is a frequently observed emergency with tumor patients. In addition to tumor relapse, the development of a second tumor or intraperitoneal tumor spreading, and benign alterations in advanced tumor stages (radiogenic stenosis, adhesions) may also be the cause for the obstruction. The main objective of therapy is an attempt to eliminate the intestinal obstruction through surgery. If this is not possible because of advanced intra-abdominal tumor expansion, several endoscopic or interventional radiology methods, and drugs are available, that are used on an individual basis and based on prevailing experience to relieve the patient's condition.

Abnormal crosstalk between pancreatic acini and macrophages during the clearance of apoptotic cells in chronic pancreatitis.

In chronic pancreatitis (CP), both the progressive loss of acinar parenchyma and aggressive fibro-inflammatory reactions ultimately lead to irreversible organ destruction. Dying cells are normally removed by macrophages and elimination is associated with anti-inflammatory cytokine switch. We investigated whether defective clearance of damaged acini by macrophages such as compromised phagocytosis or altered cytokine reaction occurs in CP and thus represents a causative link between acinar loss and fibro-inflammation. In a checkerboard-like co-culture system, we assessed normal and CP macrophages for their phagocytic and cytokine responses to dying pancreatic acinar cells of normal or CP origin by FACS, confocal microscopy, QRT-PCR, and ELISA. In CP, phagocytosis of apoptotic acini by macrophages was not impaired; however, the associated cytokine responses were gradually perturbed. Most interestingly, only normal acini suppressed TGFbeta1 expression and accumulation specifically in normal macrophage cultures, while CP acini lost this ability. Both types of apoptotic acini induced pro-inflammatory cytokine bursts of varying strength in both types of macrophages; however, the most significant difference (more than 50-fold higher expression of IL-1beta, IL-6, and IL-8) was evident between CP/CP and normal/normal combinations, indicating that acinar and macrophage alterations synergistically lead to the ultimate CP-specific bias. In combination with in situ data comparing circulating inflammatory cells to pancreatic resident ones, our results indicate that cytokine expression in inflammatory cells undergoes spatiotemporal modulation, most likely through a successive interplay of acinar, stromal, and circulating factors. Thus, clearance of injured pancreatic acini by macrophages is associated with a unique cytokine reaction which may constitute a basis for progression of SAPE (sentinel acute pancreatitis event) to the irreversible fibro-inflammation in CP.

[Pancreatic carcinoma: conclusive clinical consequences based on molecular biology knowledge for therapy]. / Pankreaskarzinom: Schlüssige klinische Konsequenzen aus molekularbiologischen Kenntnissen für die Therapie.

Molecular research techniques developed in recent years have increased our knowledge of the pathophysiology of pancreatic cancer tremendously. We now know that the malignant phenotype of pancreatic cancer is defined by the expression of growth stimulatory factors, their receptors and gene alterations. To translate molecular knowledge into new clinical therapy will be the challenge of the future. Although we have not yet developed direct clinical applications for our molecular findings, new diagnostic and therapeutic approaches are in development. Gene therapies such as antisense technology, pro-drug activation and the transfer of non-functioning growth factor receptors are potential new therapeutic options for the future. Wider clinical use can be expected in upcoming years.

[Report of experiences with fibrinolytic therapy of deep venous thrombosis of the legs]. / Erfahrungsbericht über die fibrinolytische Therapie bei tiefen Beinvenenthrombosen.

It is reported on the fibrinolytic therapy of thrombosis of the deep veins of the legs, the pelvis and the arms. This treatment was analysed in 18 patients who were treated between 1983 and 1986. The possible causes of the development of thrombosis, such as ovulation inhibiting drugs and the postoperative state, are mentioned. Fibrinolysis was performed with streptokinase (awelysin) and urokinase (ukidan). In 11 patients streptokinase infusions therapy in ultra-high doses was carried out. Within 6 hours and 30 minutes the patients got 9.500,000 units of streptokinase. The complications of the streptokinase treatment are discussed. According to the age of the phlebothrombosis and the control phlebography 2 groups of patients were formed. In the first group including thromboses lasting for 1-6 days, 7 patients showed a complete recanalisation. In the second group including thromboses lasting for 1-3 weeks, only 4 patients developed complete recanalisation. The remaining patients had only a partial recanalisation. The post-lysis effect is stressed. Streptokinase therapy with ultra-high doses has become the standard procedure of fibrinolysis treatment in our hospital.