**5. Conclusion**

A pleural effusion (PE) is present when there is an excess fluid in the pleural space. It indicates an imbalance between pleural fluid formation and its removal. Pleural fluid is formed from the systemic vessels of the pleural membranes at an approximate rate of 0.6 ml/h and is absorbed at a similar rate by the parietal pleural lymphatic system [6]. Pleural fluid accumulates due to local factors, systemic factors or translocation of fluid. At normal circumstances, pleural fluid entering the pleural space from the capillaries in the parietal pleura is removed by the lymphatics which can absorb 20 times more fluid than is formed.

suspicion of cardiac failure. The cut-off value however, varied widely from 600 to 4000 pg/ml (with 1500 pg/ml being most commonly used), and most studies excluded patients with more

The findings in a study done by Mehdi Kashmiri showed taking a value of pleural cholesterol >55 mg/dl and pleural/serum cholesterol >0.3 to define exudative effusion resulted in less erroneous classification with a sensitivity of 93%, a specificity of 100%, a positive predictive value (PPV) of 100% and an accuracy of 95.2%. Using Light's criteria gave a sensitivity of 95%, a specificity of 95%, a PPV of 97.6% and an accuracy of 95.2%. Using cholesterol in differentiating exudate from transudate was especially useful in patients with congestive heart failure

There are other biochemical parameters other than pleural fluid cholesterol to identify the exudative pleural effusions. The difficulties in classifying pleural fluid effusion are wiped

It has been observed that increase in uric acid level was present in pleural fluid of transudative pleural effusion than exudative pleural effusion. The optimum cut-off level for pleural fluid uric acid was 5.35 mg/dl with sensitivity of 89.32% and specificity of 92.60% [42]. Increase in uric acid in pleural fluid can be regarded to be a manifestation of tissue hypoxia [43]. Most of the patients with reasons to produce transudative effusion had oxidative stress or hypoxemia to explain the increased uric acid synthesis. The respiratory tract, indeed, remains a major target of oxidative damage caused by both endogenous and exogenous processes [44, 45]. The major causes of tissue damage associated with chronic inflammatory lung disease are the

Metintas et al. [46] stated that the binding of uric acid is minimal to plasma protein and it is diffuse freely to different compartments. They suggested that the increase permeability, due to change in pleural-capillary pressure in formation of transudate, is the cause of the increase of uric acid levels in pleural fluid. So all these factors explains why uric acid level increases in

In cases where no cause for an exudative effusion can be identified or CHF suspected, the sequential application of the fluid LDH, followed by the serum to pleural fluid protein (SF-P) and then the serum to pleural fluid albumin (SF-A) gradients, may assist in reclassifying

Leers Mathie P.G. from Netherlands [48] found that combination of the parameters: pleural cholesterol and pleural LDH had accuracy of 98%, sensitivity of 98% and 95% specificity for diagnosing exudative pleural effusion compared that calculated by light's criteria being accu-

A pleural effusion (PE) is present when there is an excess fluid in the pleural space. It indicates an imbalance between pleural fluid formation and its removal. Pleural fluid is formed from the systemic vessels of the pleural membranes at an approximate rate of 0.6 ml/h and is

than one possible etiology for their effusion [40].

away with few parameters other than cholesterol.

reactive species produced by phagocytes.

transudative condition than exudative one.

racy of 93%, sensitivity 100% and specificity 73%.

pleural effusions as transudates [47].

**5. Conclusion**

who received diuretics [41].

86 Cholesterol - Good, Bad and the Heart

Pleural fluid accumulates in settings of increased hydrostatic pressure, increased vascular permeability, decreased oncotic pressure, increased intrapleural negative pressure and decreased lymphatic drainage. On the basis of pathophysiology, pleural effusion can be transudates or exudates. It is important to classify the pleural fluid for diagnosis and appropriate management. Transudates occur when the mechanical factors influencing the formation or reabsorption of pleural fluid are altered, like a decrease in plasma or elevated systemic or pulmonary hydrostatic pressure. Exudates results from inflammation or irritation or other disease processes involving pleura resulting in increased permeability.

Light et al. found criteria to have sensitivity and specificity of 99 and 98%, respectively, for differentiating transudative and exudative PEs (ratio of protein in pleural fluid and serum >0.5; ratio of LDH in pleural fluid and serum >0.6 and pleural fluid LDH >2/3rd of upper limit of serum LDH) [20]. It is found that 25% of patients with transudates pleural effusion are mistakenly identified as having exudative effusion by Light's criteria. In cases of heart failure on diuretic therapy, the transudative pleural effusions have high protein. Pleural cholesterol is thought to be derived from degenerating cells and vascular leakage from increased permeability. The cause of the increased cholesterol concentration is unknown, but two hypotheses are available: one states that cholesterol production by different cells has been recognized and it is possible that destruction of white and red blood cells in pleural effusion can cause an increase in the fluid cholesterol level and second relates with increased pleural permeability that causes cholesterol concentrations to increase.

Pleural fluid cholesterol as proposed by Heffner's meta-analysis can diagnose exudative pleural effusion without need of serum values. This can avoid the financial burden and double pricks (serum and pleural fluid) in anxious patients to go through the series of tests to confirm the exudative pleural effusion. With a classifying threshold of 1.16 mmol/l, pCHOL has a sensitivity of 97.7% and specificity of 100% for diagnosis of exudates with accuracy of 98.3% compared to Light's criteria (98% sensitivity and 82% specificity). pCHOL is highly correlated than protein ratio with clinical diagnosis for exudates [29]. Moreover in pleural effusion with etiologies as transudates, parapneumonic, tubercular and neoplastic pleural effusion, pCHOL levels were 0.53 ± 0.28, 1.81 ± 0.59, 2.08 ± 0.58 and 1.58 ± 0.65 mmol/L, respectively.

Study done by Leers Mathie PG, it was found that pleural cholesterol and pleural LDH had accuracy of 98%, sensitivity of 98% and 95% specificity for diagnosing exudative pleural effusion compared that calculated by light's criteria being accuracy of 93%, sensitivity 100% and specificity 73% [47].

It is concluded that pCHOL has a better sensitivity, specificity and accuracy in differentiating transudates and exudates than the parameters of Light's criteria. This also avoids the plasma protein and gradients, sLDH, pleural fluid protein and LDH. Therefore it is more efficient, easier and more cost effective method to differentiate exudates from transudates. This study also suggests that determination of pCHOL should be in routine practice in cases of pleural effusion.
