Whipple's disease is a chronic infectious systemic disease caused by the bacterium Tropheryma whipplei. Nondeforming arthritis is frequently an initial complaint. Gastrointestinal and general symptoms include marked diarrhoea (with serious malabsorption), abdominal pain, prominent weight loss, and low-grade fever. Possible neurologic symptoms (up to 20%) might be associated with worse prognosis. Diagnosis is based on the clinical picture and small intestinal histology revealing foamy macrophages containing periodic-acid-Schiff- (PAS-) positive material. Long-term (up to one year) antibiotic therapy provides a favourable outcome in the vast majority of cases. This paper provides review of the literature and an analysis of our 5 patients recorded within a 20-year period at a tertiary gastroenterology centre. Patients were treated using i.v. penicillin G or amoxicillin-clavulanic acid + i.v. gentamicin for two weeks, followed by p.o. doxycycline (100 mg per day) plus p.o. salazopyrine (3 g per day) for 1 year. Full remission was achieved in all our patients.

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Summary: Double balloon enteroscopy (DBE) was introduced 15 years ago. The complications of diagnostic DBE are rare, acute pancreatitis is most redoubtable one (incidence about 0.3%). Hyperamylasemia after DBE seems to be a rather common condition respectively. The most probable cause seems to be a mechanical straining of the pancreas. We tried to identify patients in a higher risk of acute pancreatitis after DBE. We investigated several laboratory markers before and after DBE (serum cathepsin B, lactoferrin, E-selectin, SPINK 1, procalcitonin, S100 proteins, alfa-1-antitrypsin, hs-CRP, malondialdehyde, serum and urine amylase and serum lipase). Serum amylase and lipase rose significantly with the maximum 4 hours after DBE. Serum cathepsin and procalcitonin decreased significantly 4 hours after DBE compared to healthy controls and patients values before DBE. Either serum amylase or lipase 4 hours after DBE did not correlate with any markers before DBE. There was a trend for an association between the number of push-and-pull cycles and procalcitonin and urine amylase 4 hours after DBE; between procalcitonin and alfa-1-antitrypsin, cathepsin and hs-CRP; and between E-selectin and malondialdehyde 4 hours after DBE. We found no laboratory markers determinative in advance those patients in a higher risk of acute pancreatitis after DBE.

Scleroderma renal crisis (SRC) is classical renal disease in systemic sclerosis (SSc). SRC is a relatively rare manifestation, approximately in 5% of patients. In terms of severity, manifestation in the form of SRC is the most common cause of acute organ failure. In SSc patients, SRC is defined as a new onset of accelerated arterial hypertension and rapidly progressive anuric or oliguric renal failure. SRC is primarily vascular injury with increased activity of the renin-angiotensin activity. These events lead to release or activation of cytokines and growth factors that result in the typical proliferative vascular lesions. Successful approach is routine use of angiotensin-converting enzyme inhibitors in the treatment of SRC (except prevention) and other advances in renal replacement therapy in SSc management. It is crucial to detect manifestations of SRC early and to manage appropriately in collaboration with intensive care medicine, cardiologists, and nephrologists. In contrast to SRC, clinical presentation of interstitial renal disease is poor, often without evidence of renal abnormality. Interestingly, other renal manifestations are glomerulonephritis and vasculitis. These manifestations are associated with overlapping mechanisms. The objective of this chapter is to focus on actual knowledge about the renal involvement in SSc and current treatment principles and possibilities.