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Fatty change in donor livers is a risk factor for poor function after orthotopic liver transplantation. Various prevalences of steatosis have been reported in time 0 biopsies. The aim of this research was to determine, in a longitudinal study, the degree (percent of hepatocytes involved) and type (size of vacuoles) of fatty change shown by various histologic techniques. Four staining methods were used on sections from three liver wedge biopsies—at liver procurement, at the back‐table, and after reperfusion—from 83 consecutive donor livers. Results in Sudan III‐stained (SS) sections showed the greatest sensitivity (87.1%), negative predictive value (91.8%), and agreement rate (κ= 0.77) when compared with results in thin (1 μm) plastic‐embedded toluidine blue‐stained (TBS) sections. High‐grade steatosis (>30% steatotic hepatocytes) was identified in 49.4% of SS sections, 46.9% of TBS sections, 38.5% of frozen hematoxylin‐eosin (H&E)‐stained sections, and 20.7% of deparaffinated H&E‐stained sections. Microscopic observations disclosed two types of steatotic pattern: (1) A predominantly small‐droplet lipid vacuolzation (high‐grade microsteatosis), similar to the steatosis associated with Reye syndrome, was seen in 29% of SS sections and 25% of TBS sections—approximately one‐fourth of grafts; and (2) a combined pattern of large and small fat drops (high‐grade macromicrosteatosis) was seen in 20% of SS sections and 22% of TBS sections. We concluded that moderate to severe steatosis is a frequent finding in donor livers. The difficulty in detecting lipidic microvacuoles in H&E‐stained sections may be the reason for underestimating the grade of fatty change or even for diagnosing as normal some biopsies with high‐grade microsteatosis.

A rare case of pancreatic neuroendocrine neoplasm in a patient with tuberous sclerosis complex is described. The patient was a 31-year-old man who had multiple congenital subependymal nodules, bilateral cortical tubers, and seizures of difficult control. A 2.3 cm × 2 cm well-delimitated solid tumor in the tail of the pancreas was discovered during a monitoring abdominal computed tomography. A distal pancreatectomy was performed. Histologically, the tumor was formed by uniform cells with moderated cytoplasm arranged in a combined trabecular and nested pattern. The nuclear features were bland, and mitosis was infrequent. There was no vascular invasion. Immunoreactivity for cytokeratine AE1/AE3, chromogranin A, and synaptophysin confirmed the neuroendocrine nature of this neoplasia. Pancreatic hormones were negatives. One of the 5 lymph nodes isolated from the peripancreatic adipose tissue was positive for metastases. Small series and case reports have documented that in tuberous sclerosis many endocrine system alterations might occur, affecting the function of the pituitary, parathyroid, and other neuroendocrine tissue, including islet cells of the pancreas. However, the true association of these pathological conditions remains uncertain. As far as we know, there are 10 cases reported of pancreatic neuroendocrine tumors in a setting of tuberous sclerosis complex, in which 2 cases resulted in malignant, nonfunctioning pancreatic neuroendocrine tumors.

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