ABSTRACT
An important cause of the high prescription levels of psychotropic medication for psychological symptoms is that these symptoms are assessed according to the same model as applied for physical symptoms, the disease model. This has led to a one-sided medical approach to psychological symptoms. A person-centred approach offers an alternative; the positive aspects of the disease-centred approach are retained and attention for the patient and his/her context become the central focal point for the general practitioner. Important elements of the person-centred approach are empathy, a good doctor-patient relationship, a shared approach to problem definition and understanding of the patient's problem, development of a therapeutic alliance, and a focus on the patient's hopes and expectations. If additional primary care-based treatment by mental health practice nurses is indicated, this model could be suitable since it is based on patients' strengths and focuses on personal growth rather than reduction of symptoms.
Subject(s)
Empathy , General Practitioners/psychology , Physician-Patient Relations , Psychotropic Drugs/administration & dosage , Female , Humans , Male , Mental Disorders/drug therapy , Mental Disorders/psychology , Primary Health CareABSTRACT
In the first part of this review the important role played by the bronchial hyperreactivity caused by chronic bronchopulmonary inflammation in asthma is described. Deliberately, more emphasis is placed on the role of pro-inflammatory eosinophils, alveolar macrophages, lymphocytes and platelets rather than on mast cells and neutrophils or the numerous mediators. The reason for this is that, on account of the large number of mediators and their multitude of functions and interactions in asthma, antagonism of a specific mediator will probably not be clinically relevant for optimally effective curative treatment of asthma. Inhibition of the infiltration and activation of pro-inflammatory cells is likely to be a more successful approach. In the second part, various animal models of bronchial hyperreactivity, which could be suitable for testing anti-asthmatic drugs, are discussed. Most animal models pay too little attention to chronic bronchopulmonary inflammation as the cause of bronchial hyperreactivity in asthma. In various models the bronchial hyperreactivity is provoked by a single mediator and this leads to selection of specific antagonists which are unlikely to be of clinical benefit. Rats appear to have certain advantages over guinea-pigs as experimental animals for bronchial hyperreactivity.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Asthma/drug therapy , Bronchial Hyperreactivity/drug therapy , Animals , Asthma/physiopathology , Bronchial Hyperreactivity/physiopathology , Disease Models, Animal , HumansABSTRACT
This study confirms the strong inhibition of therapeutic concentrations of the antiinflammatory agent nimesulide (NI) on the chemiluminescence (CL) of human leucocytes (HL) after stimulation with opsonized zymosan (C3Z), and extends the findings to peritoneal (RPL) and bronchoalveolar leucocytes (RBAL) collected from actively immunized rats 24 h after i.v. injection of Sephadex. Additionally we demonstrate that NI is a strong inhibitor of proteinase release (PR) from HL. The reference drugs tested for comparison were indomethacin (I), BW 755 C (BW), phenidon (PH), mepacrin (M) and nedrocromil (NE). The rank order of potency for suppression of PR and CL was nearly independent of the cell type and stimulus: PH greater than or equal to BW greater than M greater than NI = 4-OH-NI much greater than I greater than NE. NI was the superior inhibitor of HL activation compared with I as measured either by PR or CL (factor 7), and also of CL of RPL and RBAL (factor 2-3). NI inhibited the PR from HL and CL of RPL or RBAL almost equipotently (IC30: 10-20 micrograms/ml), whereas PH, BW, M and I were 6-10 times more effective as CL inhibitors compared with their PR inhibition. In contrast NE showed a preferential inhibition of PR. This unique inhibition profile on leucocyte activation in vitro may be related to the differences of NI and I which are also existing in their antiinflammatory activities in vivo.