Introduction In acute stroke or transient ischemic attack (TIA), rapid information about the plasma concentration of direct oral anticoagulants (DOAC) is important for treatment decisions such as systemic thrombolysis, endovascular therapy, or antidote administration in case of hemorrhagic stroke. As standard coagulation assays are either not sufficiently reliable or have long turn-around times, point-of-care-testing with DOAC dipstick may be of additional value in this setting.

A 46-year-old male patient reported difficulties in speech and swallowing following gastroenteritis. Marked open nasality (open rhinophonia) and swallowing difficulties with occasional passing of food into the nasopharynx was observed during speaking with the head held in an upright position. The patient was able to articulate clearly with the head reclined or in a lying position. Endoscopy identified complete bilateral soft palate paresis consistent with bilateral glossopharyngeal nerve palsy. Additional symptoms of cranial nerve palsy appeared in the course of the disease. Intravenous corticosteroids were ineffective. A marked improvement of symptoms was achieved after i.v. immunoglobulin therapy that was initiated following identification of serum IgM anti-GM 1 ganglioside antibodies under suspicion of cranial polyneuritis. Nasality was largely resolved under additional speech exercise therapy.

Ein 46-jähriger männlicher Patient berichtete nach einem Magen-Darm-Infekt über eine Störung der Artikulation und des Schluckens. Beim Sprechen in normaler Kopfhaltung waren ein deutliches offenes Näseln (Rhinophonia aperta) zu beobachten sowie Schluckbeschwerden mit gelegentlichem Übertritt von Nahrungsbestandteilen in den Nasenrachen. Bei Kopfreklination oder im Liegen konnte der Patient klar und deutlich artikulieren. Endoskopisch zeigte sich eine komplette Gaumensegelparese beidseits im Sinne einer bilateralen Lähmung des N. glossopharyngeus. Im Verlauf traten weitere Hirnnervenlähmungen auf. Eine i.v.-Therapie mit Kortikosteroiden half nicht. Erst unter i.v.-Immunglobulingabe bei Nachweis von IgM-Antikörpern gegen das Gangliosid GM 1 im Serum unter dem Verdacht auf eine Polyneuritis cranialis ergab sich eine deutliche Besserung der Symptomatik. Unter zusätzlicher logopädischer Übungsbehandlung kam es zur weitgehenden Behebung des Näselns.

Energy expenditure, whole body substrate oxidation rates and arterial substrate concentrations were measured in 14 patients with liver cirrhosis and 13 control subjects before and during sequential infusions of a long chain (LCT) or a medium chain triglyceride emulsion (MCT) without and with concomitant insulin plus glucose infusions.Resting energy expenditure, basal substrate oxidation rates and the arterial concentrations of glucose, lactate, triglycerides and ketones were normal, whereas plasma free fatty acids and glycerol were both increased in patients with liver cirrhosis.The arterial plasma triglyceride and free fatty acid concentrations as well as whole body lipid oxidation rate rose in response to LCT in both groups and the maximum lipid oxidation rate was 1.1 or 1.3 mg/kg fat free mass x min in controls and in cirrhotics, respectively (n.s.). Concomitantly, glucose oxidation rate fell to 65% of basal values in controls (p < 0.01), but remained nearly unchanged in the cirrhotic group (89% of the basal value; n.s.). The increase in plasma ketones was reduced to 67% of control values in liver cirrhosis (p < 0.01). Only a slight effect on energy expenditure was observed in both groups.When compared to controls, liver cirrhosis impaired insulin-induced increases in glucose disposal (-30%, p < 0.01) and in non oxidative glucose metabolism (-93%, p < 0.01). Concomitantly, normal increases in energy expenditure, glucose oxidation rate and the arterial plasma lactate concentrations and normal decreases in lipolysis, lipid oxidation and ketogenesis were observed in patients with liver cirrhosis.When lipids were given together with glucose, energy expenditure and lipid oxidation increased in controls, but glucose was the preferred fuel oxidised and lipid-induced thermogenesis was reduced in the cirrhotic group.Using a 50% MCT-emulsion, plasma free fatty acid concentrations further increased, but energy expenditure and lipid oxidation remained unchanged in both groups and further increases in plasma ketones were only observed in controls.Infusing glycerol in a subgroup of patients showed no thermogenic effect and a reduced glycerol clearance in liver cirrhosis.

Insulin-induced glucose metabolism was investigated in 26 patients with biopsy-proven liver cirrhosis and 10 control subjects. Two glucose clamp protocols together with continuous indirect calorimetry were performed to examine whether reduced rates of glucose oxidation and/or nonoxidative glucose metabolism explain insulin resistance in liver cirrhosis. Using a 4-hour, two-step protocol (0-2 hours, plasma glucose 5.2 mmol/L, plasma insulin 92 mU/L to test the half-maximum response; 2-4 hours, hyperglycemia 10.0 mmol/L, plasma insulin 442 mU/L to test the maximum cellular glucose disposal) liver cirrhosis reduced glucose disposal to 45% and 60% of control values, respectively. Simultaneously, insulin-induced increases in glucose oxidation, plasma lactate levels, and lipogenesis were normal, whereas nonoxidative glucose metabolism was reduced (-82% and -47% of controls, respectively). To determine whether reduced nonoxidative glucose metabolism was caused by reduced glucose disposal, glucose disposal was "matched" to normal values in a subgroup of cirrhotic patients. Nonoxidative glucose metabolism values were normal, but plasma lactate concentrations disproportionally increased (+96%) after "matching" glucose disposal. Insulin resistance was independent of the etiology of the cirrhosis, the biochemical parameters of parenchymal cell damage and liver function, and the clinical and nutritional state of the patients. It is concluded that liver cirrhosis impairs insulin sensitivity and maximum cellular glucose disposal. Reduced glucose disposal is caused by defective glucose storage. Insulin resistance is independent of the etiology of liver cirrhosis and of the clinical and nutritional state of the patient.

1. Resting energy expenditure and the metabolic responses to adrenaline (infusion rate: 0.03 micrograms min-1 kg-1 fat-free mass for 1 h) were investigated in 25 patients with liver cirrhosis. The patient group was heterogeneous and varied with respect to the aetiology of cirrhosis, the clinical condition (i.e. Child A or B), the nutritional status and the degree of hyperinsulinaemia. 2. When compared with 10 healthy control subjects the basal plasma adrenaline and noradrenaline concentrations were both increased in cirrhosis and remained elevated during adrenaline infusion (+39% and +31%, respectively; P < 0.05). Concomitantly, the peripheral plasma insulin concentration and the molar C-peptide/insulin ratio were increased in liver cirrhosis (+96% and +30%, respectively; P < 0.05). Hyperinsulinaemia was more pronounced in patients with ethanol-induced liver cirrhosis. 3. When expressed per kg fat-free mass, resting energy expenditure was enhanced in liver cirrhosis (+21%; P < 0.05) and was more pronounced (i.e. resting energy expenditures of +35% to +49% above estimated values) in patients with ethanol-induced cirrhosis, at advanced stages of the disease and in association with decreased body cell mass. 4. Infusion of adrenaline increased heart rate, O2 consumption and the plasma concentrations of glucose, lactate, free fatty acids, glycerol and 3-hydroxybutyrate, and similar transient increases and subsequent decreases in the respiratory quotient were observed in both groups. However, the lipolytic, ketogenic and thermic responses were reduced in cirrhotic patients. Reduced metabolic responses were more pronounced in hyperinsulinaemic patients.(ABSTRACT TRUNCATED AT 250 WORDS)