THE DIFFICULTIES IN THE DIAGNOSIS OF PULMONARY HYPERTENSION ASSOCIATED WITH CHRONIC LUNG DISEASE.

OBJECTIVE: Introduction: Chronic lung disease (WHO group 3) is the second leading cause of pulmonary hypertension (PH). In turn, the development of PH influences the course of lung disease, worsening the clinical symptoms and prognosis. The aim: To analyse the difficulties in the diagnosis of pulmonary hypertension due to chronic lung disease. PATIENTS AND METHODS: Review and Discussion: According to recent literature, PH in the course of lung diseases develops as a result of both "parenchymal" and vascular pathology in patients with a genetic predisposition. Prolonged infection (especially viral) may be an additional promoting factor. Elevation of pulmonary arterial pressure (PAP) is usually moderate and correlates with severity of lung disease. In a small minority, PAP may reach that seen in WHO group 1 pulmonary arterial hypertension (PAH). CONCLUSION: Conclusions: Echocardiography and right heart catheterization are the principal tools for the diagnosis of PH in chronic lung diseases. Unfortunately, current medications for treating PAH have not shown benefit in controlled trials of group 3 PH, hence their routine use is not recommended. Patients with severe group 3 PH should be considered for referral to expert centres or entry into clinical trials.

Acute and chronic treatment with mianserin differentially affects the anticonvulsant activity of conventional antiepileptic drugs in the mouse maximal electroshock model.

RATIONALE: Epilepsy often coexists with depression. Therefore, the probability of simultaneous treatment with antiepileptics and antidepressants and the possibility of interactions between them are relatively high. OBJECTIVE: The effects of acute and chronic administration of mianserin on the protective activity of valproate (VPA), carbamazepine, phenytoin, and phenobarbital were evaluated in the maximal electroshock in mice. MATERIALS AND METHODS: Animals were subjected to electroconvulsions. Undesired effects were evaluated in the chimney test (motor impairment) and passive-avoidance task (memory deficit). Brain concentrations of antiepileptic drugs were assessed by immunofluorescence. RESULTS: When given acutely, mianserin (at doses greater than or equal to 20 mg/kg) significantly raised the electroconvulsive threshold. The antidepressant, at the subanticonvulsant doses, enhanced the anticonvulsant action of carbamazepine, phenytoin, and VPA. Mianserin administered chronically at 30 mg/kg significantly decreased the electroconvulsive threshold. In contrast to acute treatment, the antidepressant at subeffective doses diminished the anticonvulsant activity of VPA and phenytoin. Mianserin given either acutely or chronically did not affect the brain concentrations of antiepileptic drugs, so a pharmacokinetic contribution to the observed interactions is not probable. Acute and chronic treatment with mianserin and its combinations with antiepileptic drugs did not impair either motor coordination or long-term memory. CONCLUSION: Although acute application of mianserin may potentiate the anticonvulsant action of some antiepileptics, its chronic administration can lead to the opposite effect. Therefore, as far as the presented results can be transferred to clinical conditions, the antidepressant therapy with mianserin should be limited or even avoided in epileptic patients.

Immunological aspects of epilepsy.

In recent years, the concept of an immunological background of some types of epilepsy has been gaining an increasing number of supporters. The following article is an attempt to review the most significant studies that explore irregularities in patients with intractable epilepsy, search for and identify the immunological causal factors of seizures and, finally, associate these factors with particular syndromes that manifest in refractory epilepsy. We also discuss the efficacy of immunomodulatory treatment in the recognized syndromes. Last, we focus on the immunological abnormalities found in patients undergoing antiepileptic therapy with classical antiepileptic drugs as well as changes in the immune system that could be provoked by an epileptic seizure itself.