Pulmonary co-infection with nocardia species and nontuberculous mycobacteria mimicking miliary tuberculosis in a patient with Crohn's disease under combined immunosuppressive therapy.

Nocardiosis is a rare infection caused by ubiquitous soil-born, acid-resistant, Gram-positive bacteria that can be life-threatening in immunocompromised patients. Originally usually diagnosed in HIV-positive patients, only few cases have been reported in patients on immunosuppressive therapy for inflammatory bowel disease or rheumatologic disorders. We present a case of a 32-year-old man who was treated with infliximab, prednisolone, and azathioprine for severe terminal ileitis. Although the clinical status improved under triple immunosuppressive therapy, weight loss, weakness, and fatigue persisted. Laboratory studies revealed iron deficiency anemia, hypalbuminemia and raised inflammatory markers. Chest computed tomography scan showed multiple pulmonary nodules and a large cavity in the left upper lobe (segment 3a). Empiric tuberculostatic therapy was introduced for suspected miliary tuberculosis but stopped for lack of clinical improvement and negative tuberculosis tests (interferon-gamma release assay, microscopy, polymerase chain reaction). Finally, the diagnosis of pulmonary nocardiosis with concomitant pulmonary Mycobacterium avium infection was confirmed microbiologically, and the patient was treated with high-dose co-trimoxazole, clarithromycin, ethambutol, and rifampicin for 12 months.This case report underlines the increased risk of severe and rare infections like nocardiosis with combination immunosuppressive therapy and the necessity for thorough diagnostic screening for opportunistic infection. Although long-term antibiotic treatment for nocardiosis is mandatory, the optimal timing to restart immunosuppressive therapy remains ambiguous.

[Gastroparesis in Noonan syndrome]. / Gastroparese bei Noonan-Syndrom.

We present a case of a 26-year-old female patient with bloating, postprandial nausea and recurrent vomiting after solid food intake. A gastric emptying scintigraphy showed a delayed gastric emptying, defining gastroparesis. Because of her past medical history of short stature and pulmonary stenosis, we initiated genetic counseling where the diagnosis of Noonan syndrome was made. Dietary therapy and medication with domperidone quickly led to relief of the discomfort due to gastroparesis. However, prokinetics are not indicated for long-term therapy, as cardiac arrhythmia may occur. A risk-benefit assessment should be done. There are several novel approaches which need to be further investigated.

EGF-dependent induction of BCL-xL and p21CIP1/WAF1 is highly variable in HNSCC cells--implications for EGFR-targeted therapies.

The anti-apoptotic protein BCL-x(L) and the cell cycle inhibitor p21(CIP1/WAF1) were previously implicated in head and neck cancer. Several reports point to a role of the epidermal growth factor receptor (EGFR, ErbB-1, HER1) in regulating their expression. In the present study, we investigated the influence of EGFR on these tumor-associated factors. HNSCC cell lines were incubated with EGF or with the EGFR-specific kinase inhibitor AG1478. Western blot analysis and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) were deployed to measure BCL-x(L) and p21(CIP1/WAF1) protein and mRNA levels. A dose-dependent rise of BCL-x(L) as well as p21(CIP1/WAF1) protein was noted after incubation with EGF, whereas inhibition with AG1478 reduced basal expression levels. No influence on BCL-2 was seen. Interestingly, qRT-PCR revealed that p21(CIP1/WAF1) but not BCL-x(L) transcript levels were induced after EGF treatment. Taken together, it can be stated that p21(CIP1/WAF1) and BCL-x(L) but not BCL-2 levels are tightly regulated by EGFR in HNSCC cell lines. BCL-x(L) induction appears to be due to protein stabilization rather than transcriptional activation, which is the likely cause of p21(CIP1/WAF1) induction. The noted variability in EGF response of HNSCC cells could reflect frequently observed variations in clinical response rates after implementation of anti-EGFR therapies.

Optimal timing of oral refeeding in mild acute pancreatitis: results of an open randomized multicenter trial.

OBJECTIVES: The aim of this study was to compare 2 protocols regarding the initiation of oral nutrition in patients with mild acute pancreatitis. METHODS: We randomized 143 patients to the Lipase directed (LIP) (n = 74) and the self selected PAT (n = 69) group. In the (PAT) group, the patients restarted eating through self-selection. In the LIP group, serum lipase had to normalize before eating. RESULTS: The mean time between admission and oral nutrition was 2 days (interquartile range [IQR], 1-3) in the PAT group and 3 days (IQR, 2-4) in the LIP group (P < 0.005). Before and after the first meal, the mean Δ visual analogue scale (VAS) was +3.14 mm (±11.5 mm) in the PAT group and +2.85 mm (±16.4) in the LIP group (P = 0.597). The length of hospital stay was 7 days (median; IQR, 5-10.5) in the PAT group and 8 days (median; IQR, 5.75-12) in the LIP group (P = 0.315). CONCLUSIONS: We were not able to demonstrate a difference in postprandial abdominal pain or in the length of hospital stay. Patients with self-selected eating, however, were able to restart eating 1 day earlier, and this difference was found to be significant. Our data suggest that normalization of serum lipase is not obligatory for enteral nutrition in mild acute pancreatitis.