PMC9136437_01
Imaging data. The images from left to right are the plain, arterial, and venous phases of enhanced abdominal CT. (a-c) Before the recipient underwent comprehensive treatment, the liver V-segment space-occupying lesions showed fast forward and fast appearance; (d-f) Prior to the recipient's liver transplantation, the space-occupying lesions in segments IV, V, and VIII of the liver showed a scattered lipiodol deposition, uneven enhancement in the arterial phase, and reduced enhancement in the venous phase. (g-i) After liver transplantation, blood and fluid accumulation was observed under the liver capsule and around the spleen.
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The transplantation process was smooth, but afterward, the patient developed acute renal failure and a hematoma around the liver (Figure 1).
PMC9136437_02
Imaging data. The images from left to right are the plain, arterial, and venous phases of enhanced abdominal CT. (a-c) Before the recipient underwent comprehensive treatment, the liver V-segment space-occupying lesions showed fast forward and fast appearance; (d-f) Prior to the recipient's liver transplantation, the space-occupying lesions in segments IV, V, and VIII of the liver showed a scattered lipiodol deposition, uneven enhancement in the arterial phase, and reduced enhancement in the venous phase. (g-i) After liver transplantation, blood and fluid accumulation was observed under the liver capsule and around the spleen.
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The transplantation process was smooth, but afterward, the patient developed acute renal failure and a hematoma around the liver (Figure 1).
Postoperative pathology of the patient's diseased liver. Based on the morphology, it is considered to be a moderately differentiated hepatocellular carcinoma, with a large amount of necrosis (necrosis accounts for about 90%, and the surviving tumor components account for about 10%), an MVI grade of M0, and no tumor involvement at the surgical margin.
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Pathological analyses confirmed the diagnosis of HCC, and massive tumor necrosis was observed (necrosis accounted for ~90%, while the surviving tumor accounted for ~10%; Figure 2).
(a)-(d): Changes in laboratory indicators after LT.
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On POD-10, liver function began to improve, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (ALP) levels all returned to normal (Figure 3(d)). Procalcitonin (PCT) levels began to rise to 10.3 ng/mL (reference range (ref) 0-0.05) (Figure 3(b)).
Images of large erythematous plaques on the chest, abdomen, back, and palms with multiple ecchymoses over the left waist. The oral mucosa began to present with ulcers: (a)-(e) The 19th day after liver transplantation and (f)-(j) The 36th day after liver transplantation.
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An oral examination revealed white ulcers on both sides of the buccal mucosa and lips (Figure 4(a)-(e)), and severe bone marrow suppression was observed, as well as a white blood cell (WBC) count of 0.86 x 109/L (ref: 3.5-9.5), a platelet (PLT) count of 35 x 109/L (ref: 125-350), and a hemoglobin (HGB) level of 70 g/L (ref: 130-175) (Figure 3(a), The esophageal and oral ulcers also continued to worsen, which prevented the patient from eating (Figure 4(f)-(j)).
Skin biopsy showed epidermal dyskeratosis, basic vacuolization, and lymphocytic infiltration.
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Skin biopsy specimens exhibited epidermal dyskeratosis, basic vacuolization, and lymphocytic infiltrates, which were consistent with grade-1 acute lt-GVHD (Figure 5).
(a)-(b) Changes in immune function after LT.
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Analysis of serum T-lymphocyte subsets revealed that the ratio of CD4:CD8 was reversed (1:13.3 instead of 2:1) (Figure 6(b), Table 3) and the concentration of serum immunoglobin M was reduced to 0.3 g/L, as determined by immunoglobulin electrophoresis (Figure 6(a)).
Time course of the key-events and interventions.
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Despite these intensive treatments, the patient's serum immunoglobin M level was reduced to 0 g/L, and she succumbed to septic shock and multiple organ dysfunction syndrome (MODS) on the 55th day after LT (Figure 7).