Pitfalls in diagnosis and treatment of alveolar echinococcosis: a sentinel case series.

BACKGROUND: Alveolar echinococcosis (AE) is a neglected zoonosis presenting with focal liver lesions (FLL) with a wide range of imaging patterns resembling benign as well as malignant FLLs. Complementary serology and histopathology may be misleading. OBJECTIVE: The objective of our study is to highlight pitfalls leading to wrong diagnoses and harmful interventions in patients with AE. DESIGN: This retrospective sentinel case series analyses diagnostic and treatment data of patients with confirmed AE. RESULTS: 80 patients treated between 1999 and 2014 were included in the study. In 26/80 patients treatment decisions were based on a wrong diagnosis. AE was mistaken for cystic echinococcosis (CE) in 12/26 patients followed by cholangiocellular carcinoma (CCA) in 5/26 patients; 61/80 patients had predominantly infiltrative liver lesions and 19/80 patients had a predominantly pseudocystic radiological presentation. Serology correctly differentiated between Echinococcus multilocularis and Echinococcus granulosus in 53/80 patients. Histopathology reports attributed the right Echinococcus species in 25/58 patients but failed to differentiate E. multilocularis from E. granulosus in 25/58 patients. Although contraindicated in AE 8/25 patients treated surgically had instillation of a protoscolicidal agent intraoperatively. One of the eight patients developed toxic cholangitis and liver failure and died 1 year after liver transplantation. CONCLUSIONS: Misclassification of AE leads to a critical delay in growth inhibiting benzimidazole treatment, surgical overtreatment and bares the risk of liver failure if protoscolicidal agents are instilled in AE pseudocysts.

[Effect of fructose and sorbitol on insulin-induced hypoglycemia]. / Beeinflussbarkeit einer insulin-induzierten Hypoglykämie durch Fructose und Sorbit.

Twelve metabolically normal subjects were given 0.325 g/kg fructose or glucose dissolved in water 30 minutes after intravenous infusion of insulin, 0.05 U/kg. Blood glucose concentration was then measured for up to 60 minutes or until the onset of hypoglycaemia (study I). In study II two bread units (BU) were given to six subjects in the form of dark bread, as well as 12 g of butter and water. In two other groups, of six subjects each, 1 BU was substituted either by fructose or sorbitol. Seven subjects who had been given insulin but only water to drink afterwards served as the control group. In study I, both glucose and fructose achieved a clear slowing in the blood-sugar drop compared with the control group. But with glucose there was initially a slight rerise and the final hypoglycaemic level was somewhat delayed. This minor difference between glucose and fructose was not demonstrable in study II with the addition of fat and carbohydrate substitution. Each carbohydrate combination similarly influenced the course of blood sugar concentration. The results indicate that diabetics should continue to be given glucose rather than fructose or sorbitol if hypoglycaemia occurs. On the other hand, both fructose and sorbitol, although acutely less effective in raising blood glucose concentration, do counteract as carbohydrates the development of insulin-induced hypoglycaemia.