<b><i>Background:</i></b> Severe acute pancreatitis (AP) continues to be a serious gastrointestinal disease with relevant morbidity and mortality. <b><i>Summary:</i></b> Successful clinical management requires close interdisciplinary cooperation and coordination from experienced gastroenterologists, intensive care physicians, surgeons, and radiologists. While the early phase of the disease is characterized by intensive care aspects that focus primarily on treatment of organ failure, later complications are characterized especially by (infected) necrotic collections. Here, we discuss current clinical standards and developments for conservative and interventional management of patients with severe AP. <b><i>Key messages:</i></b> Early targeted fluid therapy within the first 48 h is critical to improve the outcome of severe AP. Thoracic epidural analgesia may have prognostically beneficial effects due to suspected anti-inflammatory effects and increased perfusion of splanchnic vessels. Enteral feeding should be started early during severe AP. Persistent organ failure (&#x3e;48 h) is the strongest predictor of poor prognosis, and local complications such as infected walled-off necrosis should be primarily treated by minimally invasive endoscopic step-up approaches that are usually superior to surgical therapy options.

Angiotensin II (Ang II) as a vasoactive hormone may be involved in progressive renal interstitial fibrosis. We investigated the influence of Ang II on cell proliferation and synthesis of extracellular matrix (collagen I, III and fibronectin) in human renal fibroblasts derived from normal (TK 173 cell line) and fibrotic (TK 188 cell line) kidneys which possess both Ang II type l and type 2 (AT1 and AT2) receptors. Incubation of the cells with Ang II increased the cell proliferation and the synthesis of extracellular matrix significantly in both cell lines. However, proliferation and extracellular matrix synthesis showed a greater increase in the cells derived from the fibrotic kidney. The Ang II mediated effect on cell proliferation and extracellular matrix synthesis was diminished in the presence of the AT1 receptor blocker losartan in both cell lines. No inhibition was observed using the AT2 receptor blocker PD123319. Ang II induced cell proliferation could be completely inhibited by incubation with human TGF-beta1 antibody. Incubation with Ang II did not affect TGF beta 1 production but in untreated cells TGF-beta 1 content was higher in the cells derived from the fibrotic kidney. This might be the reason for the more sensitive reaction on exposure to Ang II.

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Proton pump inhibitors are among the most commonly used drugs worldwide. They are considered to be largely safe and cause little side-effects. We report a 69-year-old woman who suffered from erythematous plaques 2 months after initiating therapy with esomeprazole. The diagnosis of subacute cutaneous lupus erythematosus was based on the clinical picture together with characteristic histological features of a skin biopsy specimen and the detection of anti-Ro/SSA antibodies. In particular, the temporal relationship with the onset of proton pump inhibitor therapy led to the high-level suspicion of a drug-induced pathogenesis. Strengthening the initially suspected diagnosis, the characteristic skin lesions resolved almost completely without specific therapy after discontinuation of the medication. If typical skin lesions occur in light-exposed areas in connection with the administration of PPI, the possibility of a drug-induced cutaneous lupus erythematosus should always be considered. Due to the frequent recurrence rate after renewed exposure, a new therapy with PPI should be avoided.