The aim of the study was to validate the prediction rule of M.J. Fine and coworkers for clinical outcome variables and three prognostic rules for the individual outcome of community-acquired pneumonia in an elderly population (rule 1: respiratory frequency $30 breaths . min -1 , diastolic blood pressure #60 mmHg, blood urea nitrogen >7 mM; rule 2: respiratory frequency $30 breaths . min -1 , diastolic blood pressure #60 mmHg, mental confusion; and rule 3: systolic blood pressure #80 mmHg, cardiac frequency $90 beats . min -1 , lactate dehydrogenase activity $260 IU . L -1 ; death was predicted in the presence of at least two of three parameters). Overall 168 consecutive episodes of community-acquired pneumonia in patients aged $65 yrs and hospitalized in a primary care hospital were studied prospectively.Fine's rule was tested for its ability to predict length of hospital stay, requirement for intensive care unit (ICU) admission and death. For the three prognostic rules of individual outcome, performance regarding predicting death was determined.Mortality was 17/168 (10%). Fine's rule accurately predicted length of stay, the requirement for ICU admission and the risk of death from pneumonia as compared to the original derivation and validation cohorts. All three rules achieved moderate-tohigh specificity (73%, 88% and 80%, respectively) and high negative predictive values (95%, 94% and 93%, respectively) but had a low sensitivity (65%, 47% and 47%, respectively). Rule 2 most closely reflected the risk of death from pneumonia when Fine's classification was used as reference.Fine's rule proved to give valid estimations regarding clinical outcome variables of community-acquired pneumonia in the elderly. The prognostic rules may be useful in determining individual patients at lower risk of death caused by pneumonia.

Pulmonary alveolar proteinosis (PAP) is a rare disease of unknown aetiology characterized by accumulations of lipoproteinaceous material within the alveoli. The alveolar macrophages become increasingly foamy, and are thought to have a role in the pathogenesis of PAP. However, the mechanisms of macrophage recruitment are unclear.In the bronchoalveolar lavage fluid (BALF) of four patients with PAP and 20 normal control subjects, the following were examined: the monocyte chemotactic activity due to the chemokine monocyte chemoattractant protein (MCP)-1 with the use of a chemotactic chamber assay, the levels of MCP-1 by enzyme-linked immunosorbent assay, and the MCP-1 expression on lavage cells by immunocytochemistry and in situ hybridization.The monocyte chemotactic activity in the BALF of the PAP patients was markedly elevated, and the activity was completely absorbed by treatment with anti-MCP-1. The MCP-1 levels in the BALF were surprisingly high in the PAP group (25,100472 pg . mL -1 ), whereas low levels of MCP-1 were detected in the normal control subjects (mean: never smokers 4.8; smokers 10.4 pg . mL -1 ). MCP-1 protein and messenger ribonucleic acid were expressed by macrophages from the PAP patients, and the expression was reduced according to foaming of the cells; there were monocyte-like macrophages with strong expression, small foamy cells with moderate expression, large foamy cells with a faint expression of MCP-1, and ghost cells with no expression. However, the increase of macrophage number in the PAP BALF was relatively small.These data suggest that monocyte chemoattractant protein -1 expression by alveolar macrophages represents an amplification mechanism for the recruitment of additional macrophages to the alveoli in pulmonary alveolar proteinosis. It is possible that an ingestion of an excess of alveolar materials in pulmonary alveolar proteinosis may impair the macrophage function and the survival, resulting in the lack of a prominent increase in the macrophage number in bronchoalveolar lavage fluid.