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Review

Protein losing enteropathy: comprehensive review of the mechanistic association with clinical and subclinical disease states

&
Pages 147-168 | Published online: 17 Jul 2017

Figures & data

Figure 1 Schematic diagram of normal intestinal mucosa.

Notes: The epithelial cells present a diffusion barrier between the interstitial space and the lumen. The albumin that slowly leaks from the plasma (concentration=CP) to the interstitial space (CTis) is removed by the lymphatics. The luminal albumin concentration (CLumen) is zero.
Figure 1 Schematic diagram of normal intestinal mucosa.

Figure 2 The predicted relationship between the increase in GI albumin clearance and the resulting steady-state serum albumin (serum albumin/normal albumin) in a PLE subject with normal renal and hepatic functions.

Abbreviations: GI, gastrointestinal; PLE, protein losing enteropathy.
Figure 2 The predicted relationship between the increase in GI albumin clearance and the resulting steady-state serum albumin (serum albumin/normal albumin) in a PLE subject with normal renal and hepatic functions.

Figure 3 Schematic diagram illustrating the pathophysiology for the PLE produced by increased lymphatic pressure resulting from increased venous pressure (PVein).

Note: The lymphatic ruptures into the intestinal lumen, allowing decompression and retrograde drainage of the systemic lymph.
Abbreviation: PLE, protein losing enteropathy.
Figure 3 Schematic diagram illustrating the pathophysiology for the PLE produced by increased lymphatic pressure resulting from increased venous pressure (PVein).

Figure 4 Fecal α-antitrypsin clearance in various disease states.

Notes: The “normal” clearance corresponds to the control data for the Crohn’s disease study (mean=8.3 mL/day, range of 1.5–19.2 mL/day). In patients with heart failure, the clearance is normal except for one patient. In contrast, most subjects with Crohn’s or celiac disease have a statistically significant increase in clearance.
Figure 4 Fecal α-antitrypsin clearance in various disease states.

Figure 5 Schematic diagram of the PLE occurring in diseases with mucosal erosions.

Note: Because of the large breaks in the epithelial permeability barrier, the capillaries become the rate-limiting step in the leak of serum albumin and the interstitial albumin (CTis) locally equilibrates with the lumen (CTiss=CLumen=0).
Abbreviation: PLE, protein losing enteropathy.
Figure 5 Schematic diagram of the PLE occurring in diseases with mucosal erosions.

Figure 6 The lactulose/mannitol permeability ratio in Crohn’s and celiac diseases.

Figure 6 The lactulose/mannitol permeability ratio in Crohn’s and celiac diseases.

Figure 7 Schematic diagram of the PLE occurring in diseases without mucosal erosions.

Notes: It is assumed that the increased permeability results from a defect in the epithelial tight junctions. The epithelium is the rate-limiting step in the albumin leak and the interstitial albumin (CTis) is greater than that in the lumen (CLumen=0).
Abbreviation: PLE, protein losing enteropathy.
Figure 7 Schematic diagram of the PLE occurring in diseases without mucosal erosions.