7 research outputs found

    Clinical management of carbamazepine intoxication during anti-tubercular treatment: a case report

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    We describe a 67-year-old man with medical history of focal post-stroke seizure and type 2 diabetes mellitus treated with carbamazepine, clobazam, gliclazide, insulin glargine, and omeprazole we visited for the onset in the last 7 days of asthenia, cough with mucus, breathing difficulty, chest pain, and weight loss. After clinical and laboratory tests, pulmonary tuberculosis was diagnosed, and a treatment with isoniazid, ethambutol, pyrazinamide rifampicin, and pyridoxine was started. Therapeutic drug monitoring of tuberculosis treatment documented that all drugs were in normal therapeutic range. Four days after the beginning of the treatment, we documented the improvement of fever, and three days later the patient showed sleepiness, visual disorder and asthenia. Clinical and pharmacological evaluation suggested a carbamazepine toxicity probably related to a drug interaction (Drug Interaction Probability Scale score = 6). The impossibility to switch carbamazepine for another antiepileptic drug, due to a resistant form of seizure, induced the discontinuation of tuberculosis treatment, resulting in the normalization of serum carbamazepine levels in one day (10 µg/ml) and in the worsening of fever, requiring a new clinical and pharmacological evaluation. The titration dosage of carbamazepine and its therapeutic drug monitoring allowed to continue the treatment with both antitubercular drugs and carbamazepine, without the development of adverse drug reactions. To date, tuberculosis treatment was stopped and clinical evaluation, radiology and microbiology assays documented the absence of tubercular infection and no seizures appeared (carbamazepine dosage 800 mg/bid; serum levels 9.5 µg/ml)

    Clinical management of carbamazepine intoxication during anti-tubercular treatment: a case report

    Get PDF
    We describe a 67-year-old man with medical history of focal post-stroke seizure and type 2 diabetes mellitus treated with carbamazepine, clobazam, gliclazide, insulin glargine, and omeprazole we visited for the onset in the last 7 days of asthenia, cough with mucus, breathing difficulty, chest pain, and weight loss. After clinical and laboratory tests, pulmonary tuberculosis was diagnosed, and a treatment with isoniazid, ethambutol, pyrazinamide rifampicin, and pyridoxine was started. Therapeutic drug monitoring of tuberculosis treatment documented that all drugs were in normal therapeutic range. Four days after the beginning of the treatment, we documented the improvement of fever, and three days later the patient showed sleepiness, visual disorder and asthenia. Clinical and pharmacological evaluation suggested a carbamazepine toxicity probably related to a drug interaction (Drug Interaction Probability Scale score = 6). The impossibility to switch carbamazepine for another antiepileptic drug, due to a resistant form of seizure, induced the discontinuation of tuberculosis treatment, resulting in the normalization of serum carbamazepine levels in one day (10 µg/ml) and in the worsening of fever, requiring a new clinical and pharmacological evaluation. The titration dosage of carbamazepine and its therapeutic drug monitoring allowed to continue the treatment with both antitubercular drugs and carbamazepine, without the development of adverse drug reactions. To date, tuberculosis treatment was stopped and clinical evaluation, radiology and microbiology assays documented the absence of tubercular infection and no seizures appeared (carbamazepine dosage 800 mg/bid; serum levels 9.5 µg/ml)

    Carotid Body Paragangliomas and Matrix Metalloproteinases

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    Paragangliomas (PGLs) are slow-growing, typically, benign tumors that arise from the extra-adrenal paraganglion of the autonomic nervous system. PGLs arising from the carotid body are relatively rare tumors but constitute the majority of head and neck PGLs (60e70%).1 Carotid body tumors (CBTs) belong to the classification of PGLs, because they originate from paraganglia in chromaffin-negative glomus cells derived from the embryonic neural crest, functioning as part of the sympathetic nervous system. These cells normally act as special chemoreceptors located along blood vessels, particularly in the carotid bodies (at bifurcation of the common carotid artery in the neck).2 CBTs are usually classified using the criteria described by Shamblin et al.3 Matrix metalloproteinases (MMPs), enzymes that regulate cell matrix composition, play a role in several clinical conditions,4,5 including embryogenesis, wound healing,6,7 inflammation, arthritis, cardiovascular diseases,8 pulmonary diseases, and cancer.9 Several studies10e15 have shown that specific MMPs are involved in cancer processes that promote metastasis.The aim of this study is to examine the levels of MMPs in patients with benign and malignant neoplastic CBTs

    An uncommon case of arterial aneurysms association with high serum levels of plasma levels of Matrix Metalloproteinase-9 and Neutrophil Gelatinase-Associated Lipocalin

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    The association of an axillary artery aneurysm and an abdominal aortic aneurysm is extremely rare. In this study, we describe this association in a 69 year-old-man. We measured this patient's metalloproteinases (MMPs) and Neutrophil Gelatinase-Associated Lipocalin (NGAL) levels over a three years period before the abdominal aortic aneurysm rupture. We speculate that high serium levels of MMPs and NGAL may have a prognostic role and may predict aneurysm rupture in patients with an uncommon association of arterial aneurysms

    An uncommon case of arterial aneurysms association with high plasma levels of Matrix Metalloproteinase-9 and Neutrophil Gelatinase-Associated Lipocalin

    No full text
    The association of an axillary artery aneurysm and an abdominal aortic aneurysm is extremely rare. In this study, we describe this association in a 69 year-old-man. We measured this patient’s metalloproteinases (MMPs) and Neutrophil Gelatinase - Associated Lipocalin (NGAL) levels over a three years period before the abdominal aortic aneurysm rupture. We speculate that high serium levels of MMPs and NGAL may have a prognostic role and may predict aneurysm rupture in patients with an uncommon association of arterial aneurysms

    Prospective randomized double-blind trial of racecadotril compared with loperamide in elderly people with gastroenteritis living in nursing homes

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    Aim Our aim was to compare the efficacy and tolerability of loperamide and racecadotril in elderly patients with acute diarrhea. Research design and methods We performed a randomized, prospective, double-blind, and parallel group design implemented in geriatric nursing homes in Catanzaro, Italy, from February 2008 to March 2009. Patients of both sexes were randomly allocated to receive either one tablet of racecadotril 100 mg every 8 h or two tablets of loperamide 2.0 mg followed by one tablet after each unformed stool, up to four tablets in any 24- h period. Patients were treated until recovery, defined as the production of two consecutive normal stools or no stool production for a period of 12 h. Results Normal stools were collected 36 +/- 4 h after the beginning of racecadotril and in 63 +/- 6 h from the beginning of loperamide administration (P<0.01). The median time of abdominal pain in the intent-to-treat (ITT) population was 14 h for racecadotril and 28 h for loperamide. In the perprotocol (PP) population, the median time of abdominal pain was 14 h for racecadotril and 32 h for loperamide (P<0.01). About the 50% of patients experienced at least one adverse event during the study: 12% in the racecadotril group and 60% in the loperamide group. The most frequently occurring adverse events were nausea and constipation. Genetic analysis did not report the presence of rapid or poor metabolizers. Pharmacoeconomic analysis performed at the end of our study documented an increase in costs in the loperamide group with respect to the racecadotril group (P<0.01). Conclusions Racecadotril is more effective than loperamide-probably due to drug interaction with loperamide-and it is not related to pharmacogenetic susceptibility. Racecadotril is also more cost effective than loperamide
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