Unexpected platelets elevation in a patient with idiopathic thrombocytopenia treated with oseltamivir for influenza infection.

Oseltamivir is a neuraminidase inhibitor approved for the prevention and treatment of influenza. Few haematological side effects have been reported with oseltamivir. We report herein the case of an unexpected platelet increase in a 46-year-old woman with idiopathic thrombocytopenia (ITP) treated with oseltamivir for influenza. The mechanism may involve the neuraminidase inhibition which decrease platelet surface sialic acid content and reduce their removal by the reticuloendothelial system. Oseltamivir may be responsible for platelet increase especially in patients with ITP.

Bullous pemphigoid induced by vildagliptin: a report of three cases.

To report three cases of bullous pemphigoid in patients treated with vildagliptin. Case 1: An 86-year-old woman presented with bullous pemphigoid after 1 month of treatment with vildagliptin and metformin. After introduction of clobetasol, the symptoms resolved although vildagliptin was continued. However, the skin lesions reappeared 3 months later. Sustained remission was achieved only after definitive withdrawal of vildagliptin. Case 2: A 79-year-old man presented with bullous pemphigoid after 37-month treatment with gliclazide, vildagliptin and metformin. The disease at first responded to clobetasol but 3 months later the lesions reappeared. They finally regressed when the gliptin was discontinued. Case 3: A 77-year-old woman, treated with gliclazide and vildagliptin for 26 months, presented with bullous pemphigoid, which responded well to discontinuation of the gliptin and topical clobetasol. Gliptins are new molecules for treatment of type 2 diabetes mellitus, which have been suspected of implication in bullous pemphigoid. Such cases have been described in the literature (seven with vildagliptin and three with sitagliptin). In nine of these cases, the gliptin was associated with metformin, but the latter had never been considered responsible. The mechanism implicated in the development of bullous pemphigoid has not yet been clearly identified, but may involve a modified immune response or alteration of the antigenic properties of the epidermal basement membrane. These reports support the risk of bullous pemphigoid in patients exposed to gliptins.

[Ecchymosis during montelukast therapy: about one case]. / Ecchymoses associées à la prise de montélukast: à propos d'un cas.

A young girl aged 13-years-old treated with montelukast, fluticasone/salmeterol, desloratadine, fluticasone furoate and salbutamol has presented numerous spontaneous bruises after that treatment with montelukast was substituted by the generic form. Stopping montelukast allow a significant improvement in bruises.

Effect of automated drug distribution systems on medication error rates in a short-stay geriatric unit.

RATIONALE, AIMS AND OBJECTIVES: To assess the impact of an automated drug distribution system on medication errors (MEs). METHODS: Before-after observational study in a 40-bed short stay geriatric unit within a 1800 bed general hospital in Valenciennes, France. Researchers attended nurse medication administration rounds and compared administered to prescribed drugs, before and after the drug distribution system changed from a ward stock system (WSS) to a unit dose dispensing system (UDDS), integrating a unit dose dispensing robot and automated medication dispensing cabinet (AMDC). RESULTS: A total of 615 opportunities of errors (OEs) were observed among 148 patients treated during the WSS period, and 783 OEs were observed among 166 patients treated during the UDDS period. ME [medication administration error (MAE)] rates were calculated and compared between the two periods. Secondary measures included type of errors, seriousness of errors and risk reduction for the patients. The implementation of an automated drug dispensing system resulted in a 53% reduction in MAEs. All error types were reduced in the UDDS period compared with the WSS period (P<0.001). Wrong dose and wrong drug errors were reduced by 79.1% (2.4% versus 0.5%, P=0.005) and 93.7% (1.9% versus 0.01%, P=0.009), respectively. CONCLUSION: An automated UDDS combining a unit dose dispensing robot and AMDCs could reduce discrepancies between ordered and administered drugs, thus improving medication safety among the elderly.

Alopecia induced by tumour necrosis factor-alpha antagonists: description of 52 cases and disproportionality analysis in a nationwide pharmacovigilance database.

OBJECTIVES: The aim of this research was to describe the cases of TNF-α antagonist-related alopecia reported in the French Pharmacovigilance Database (FPVD) and to investigate the association between exposure to TNF-α antagonists and occurrence of alopecia. METHODS: All spontaneous reports of TNF-α antagonist-related alopecia recorded in the FPVD between January 2000 and April 2012 were colligated and described. We conducted disproportionality analyses (case/non-case method) to assess the link between the occurrence of alopecia and exposure to TNF-α antagonists. Cases were all reports of alopecia and non-cases were all other reports recorded during the study period. Exposure to TNF-α antagonists was sought in cases and in non-cases. Reporting odds ratios (RORs) were calculated to assess the association. Docetaxel was used as positive control and acetaminophen as negative control. We performed sensitivity analyses excluding cases of androgenic alopecia and those occurring in psoriatic patients. RESULTS: Among 282 590 spontaneous reports of adverse drug reactions (ADRs) collated in the FPVD, 1068 cases (alopecia reports) were identified. Of these cases, 52 (4.9%) occurred during exposure to TNF-α antagonists (18 involved infliximab, 17 adalimumab, 15 etanercept and 2 certolizumab). Exposure to TNF-α antagonists was more frequent among alopecia reports than among other ADR reports for all TNF-α antagonists pooled (ROR 3.0, 95% CI 2.3, 4.0) as well as for each antagonist separately, with similar values. Sensitivity analyses yielded similar results. The RORs were 29.9 (95% CI 25.3, 35.5) with docetaxel and 0.3 (95% CI 0.2, 0.4) with acetaminophen. CONCLUSION: The present study confirms a strong link between TNF-α antagonist exposure (class effect) and the occurrence of alopecia.

Rectal bleeding and hemostatic disorders induced by dabigatran etexilate in 2 elderly patients.

OBJECTIVE: To report rectal bleeding associated with hemostatic disorders in 2 elderly patients treated with dabigatran etexilate. CASE SUMMARY: A 79-year-old woman (weight, 69 kg) was hospitalized in a gastroenterology unit for severe rectal bleeding. She had been treated for 2 months with dabigatran etexilate 110 mg twice daily for chronic atrial fibrillation. On admission, her creatinine clearance (CrCl) was 20.7 mL/min/1.73 m(2), prothrombin time (PT) less than 10% (reference range 70-130%), and international normalized ratio (INR) 14.5 (venous blood). Eleven days after admission, hematologic and renal function were normalized and rectal bleeding stopped. An 84-year-old man (weight, 71 kg) was admitted for rectal bleeding with acute renal failure and dehydration that began while he was treated with dabigatran etexilate 110 mg twice daily for atrial fibrillation. On admission, CrCl was 33.5 mL/min/1.73 m(2), PT 13%, and INR 7.53 (venous blood). Dabigatran etexilate was stopped on admission. At the end of the hospitalization, CrCl was 66.5 mL/min/1.73 m(2), PT 54%, and INR 1.53. In both cases, an objective causality assessment revealed that those adverse reactions were probably related to dabigatran etexilate. DISCUSSION: In these 2 cases of rectal bleeding during dabigatran etexilate therapy, coagulation monitoring showed elevated PT and INR; neither patient had been exposed to vitamin K antagonists. These cases indicate the importance of PT and INR monitoring when using dabigatran etexilate, mainly in patients with a high risk of overdose, such as elderly patients or those with renal function impairment. CONCLUSIONS: It is critical to identify and subsequently manage dabigatran etexilate toxicity because there is no specific antidote to reverse the drug's anticoagulant effects.