Cardiac arrhythmia triggered by diuretic-induced hyponatremia.

Diuretics have a long and distinguished history in the treatment of hypertension and heart failure. Clinical practice guidelines recommend that diuretics should be considered to be as suitable as other antihypertensive agents for the initiation and maintenance of antihypertensive treatment. However, diuretics may potentially cause electrolyte disturbances and metabolic side effects. Diuretic-induced hyponatremia is probably more prevalent than generally acknowledged. We present an unusual case of indapamide-induced hyponatremia and hypokalemia complicated by cardiac arrhythmia. The adverse drug reaction was reversible and non-life-threatening, but this case serves as a reminder that careful evaluation and constant monitoring are necessary when prescribing diuretics.

Symptomatic and pathophysiological observations in a modified animal model of allergic rhinitis.

There are many animal models for studying allergic rhinitis. However, they either need a too long establishment period or fail to show significant late allergic responses. In the model described in this paper, guinea pigs were sensitized and challenged intranasally with ovalbumin according to a modified protocol. As controls, antihistamine-treatment and non-sensitized, non-treatment groups were studied in parallel. Early and late symptoms, passive cutaneous anaphylaxis (PCA) reaction, nitric oxide synthase (NOS) immunoreactivities, pathological changes in nasal mucosa and nasal lavage fluid (NLF), and histamine, TXB2 and p-LTs levels in NLF were evaluated. In contrast to the control groups, the model group exhibited typical symptoms, including late phase nasal blockage, and increased levels of IgG1 and IgE. Considerable eosinophil infiltration and eNOS immunoreactivities in nasal mucosa, and increased levels of histamine, TXB2 and p-LTs in NLF were also observed. This model was not only capable of showing satisfactory symptomatic and pathophysiological changes in allergic rhinitis but also showed good responses to antihistamine treatment. The model can be established in six weeks. For the first time, respiratory rate was employed as an index to reflect the nasal blockage of guinea pigs and it proved to be a reliable indicator.

Inhibitory effects of budesonide, desloratadine and dexamethasone on cytokine release from human mast cell line (HMC-1).

OBJECTIVE: To determine the inhibitory potency of budesonide on interleukin (IL)-4, 6 and 8, GM-CSF and TNF-alpha release from the human mast cell line (HMC-1) in comparison with the systemic glucocorticosteroid, dexamethasone, and H(1) antagonist, desloratadine. METHODS: HMC-1 was stimulated with 25 ng/ml phorbol 12- myristate 13-acetate (PMA) and 2.5 x 10(-7) M ionomycin (A23187) for 6, 12 and 24 h in both the presence and absence of 10(-6)-10(-10) M concentrations of the test drugs. Culture supernatants were collected and assayed by ELISAs. RESULTS: HMC-1 produced substantial amounts of GM-CSF and IL-8 and smaller amounts of TNF-alpha, IL-4 and IL-6 after being stimulated with PMA together with A23187. Budesonide and dexamethasone had potent inhibitory effects and desloratadine had modest inhibitory effects on the release of these cytokines. Budesonide was more potent than dexamethasone at most concentrations and time points. IL-4 was the cytokine which was most susceptible to inhibition by the three tested drugs. The inhibitory effects, in some cases, were time- and concentration-dependent. CONCLUSION: Budesonide had a potent inhibitory effect on cytokine release from HMC-1. Its potency was greater than that of both dexamethasone and desloratadine.