Atypical Melanocytic Matricoma: A Case Report with Molecular Studies.

ABSTRACT: Melanocytic matricoma is a rare benign pilar tumor characterized by matrical differentiation and interspersed dendritic melanocytes. It may show cellular atypia and brisk mitotic activity. Histological characterization of some lesions may be difficult. In addition, because the reported cases are few and have limited follow-up, there is insufficient experience to define outcome-based criteria for malignancy. Some cases of melanocytic matricoma with more prominent atypia have been reported as malignant, but their clinical behavior is uncertain. We present a melanocytic matricoma with interspersed benign dendritic melanocytes, but moderate basaloid atypia, focally brisk mitotic activity, and atypical mitoses. Despite the apparently good delimitation of this tumor, higher magnification revealed a slightly irregular border. However, overt malignant features such as necrosis, frank asymmetry, deep infiltration, and ulceration were not present. This tumor showed a complex aberrant genomic profile with multiple whole chromosomes or chromosomal arms, losses, and duplications. The tumor mutational burden was high. A loss-of-function alteration in CDKN2A and a loss-of-function mutation in TP53 were also present. This unexpected molecular profile contrasts with the relatively bland histology of the tumor and is in line with the difficulties in microscopic differential diagnosis between melanocytic matricoma and an indolent malignant pilomatrical tumor. We suggest that molecular studies and longer follow-up periods may help to further understand and more precisely categorize borderline pilomatrical tumors with melanocytic hyperplasia.

Functional results and quality of life after bilateral scaphoid reconstruction: a case series.

Unilateral scaphoid non-union remains a major problem, which can lead to major functional limitations. Until now there is no evidence of outcome of the rare case of bilateral scaphoid non-unions and in how far two-stage bilateral reconstruction affects functional results and the quality of life. Between 1997 and 2010, altogether four bilateral scaphoid non-unions were treated in the centre and retrospectively analyzed. The mean follow-up was performed 36.8 months after reconstruction. The measures included analysis of patient data, analysis of functional measures and quality of life after follow-up. The reconstructions were performed with implantation of a free, non-vascularized iliac crest bone graft (4), osteosynthesis with implantation of a pedicled vascularized bone graft (3) and osteosynthesis with cancellous bone graft (1). The mean range of motion of the wrist was extension/flexion 111.3°. The average grip strength by JAMAR dynamometer showed right versus left sight 32.7 kg (±3.5) versus 33.7 (±2.9). The evaluation of the DASH score resulted in 11.6 (±12.5), the SF36 scale in 87.1 (±9.2) points. The present case series for the first time demonstrated functional mid-term results of the rare event of bilateral scaphoid reconstruction after non-union. With respect to the impact on one affected hand, functional results, DASH score and quality of life are excellent and thus justify good prognosis in patient education after injury.

Darbepoetin-alpha enhances hepatectomy-associated stimulation of colorectal liver metastatic growth.

BACKGROUND: Liver insufficiency after major hepatectomy still represents a serious challenge in liver surgery. Although some previous studies indicate that erythropoietin (EPO) and its analogue darbepoetin-alpha (DPO) may improve liver function and liver regeneration, little is known on their effect on tumor growth after hepatectomy. Because EPO may promote tumor progression, we herein studied the effect of DPO on tumor growth after major hepatectomy. METHODS: CT26.WT colorectal cancer cells were implanted into the left liver lobe of BALB/c mice. Animals underwent 50% hepatectomy (Phx) and received 10 microg/kg DPO-treatment. Additional Phx animals received only saline treatment. Nonhepatectomized animals with DPO-treatment or saline treatment served as controls. One week after hepatectomy angiogenic blood vessel formation, leukocyte-endothelial cell interaction, tumor cell proliferation, apoptotic cell death, and tumor growth were studied using intravital fluorescence microscopy, histology, Immunohistochemistry, and Western blot analysis. RESULTS: Phx significantly enhanced the growth of liver metastases. This was associated with an increase of tumor capillary density and tumor cell proliferation. In nonhepatectomized animals, DPO only slightly affected metastatic growth. In hepatectomized animals, however, DPO significantly enhanced the Phx-induced stimulation of tumor growth. This was associated with an increased tumor capillary density, a decreased leukocyte-endothelial cell interaction, and a reduced cleaved caspase-3 expression of the CT26.WT cells. CONCLUSIONS: : Our data indicate that DPO significantly enhances the hepatectomy-induced stimulation of colorectal liver metastatic growth by increasing neovascularization, suppressing intratumoral leukocyte recruitment, and reducing tumor cell apoptosis. Thus, EPOs may not be used in patients undergoing hepatectomy for malignant tumor resection.

Nasal Reconstruction: Extending the Limits.

Reconstructing the 3-dimensional structure of the nose requires the maintenance of its aesthetic form and function. Restoration of the correct dimension, projection, skin quality, symmetrical contour, and function remains problematic. Consequently, modern approaches of nasal reconstruction aim at rebuilding the units rather than just covering the defect. However, revising or redoing a failed or insufficient reconstruction remains very challenging and requires experience and creativity. Here, we present a very particular case with a male patient, who underwent 37 operations elsewhere and presented with a failed nasal reconstruction. We describe and illustrate the complex steps of the nasal rereconstruction, including the reconstruction of the forehead donor site, surgical delay procedures for lining, and the coverage with a third paramedian forehead flap.

Portal branch ligation induces a hepatic arterial buffer response, microvascular remodeling, normoxygenation, and cell proliferation in portal blood-deprived liver tissue.

Portal branch ligation (PBL) may prevent liver failure after extended hepatic resection. However, clinical studies indicate that tumors within the ligated lobe develop accelerated growth. Although it is well known that tumor growth depends on the host's microvascularization, there is no information about how PBL affects the hepatic microcirculation. Our aims were to determine hepatic artery response, liver microcirculation, tissue oxygenation, and cell proliferation after PBL. Therefore, we used intravital multifluorescence microscopy, laser-Doppler flowmetry, immunohistochemistry, and biochemical techniques to examine microcirculatory responses, microvascular remodeling, and cellular consequences after left lateral PBL in BALB/c mice. During the first 7 days, PBL induced a reduction of left hilar blood flow by approximately 50%. This resulted in 80% sinusoidal perfusion failure, significant parenchymal hypoxia, and liver atrophy. After 14 days, however, left hilar blood flow was found to be restored. However, remodeling of the microvasculature included a rarefaction of the sinusoidal network, however, without substantial perfusion failure, compensated by a hepatic arterial buffer response and significant sinusoidal dilatation. This resulted in normalization of tissue oxygenation, indicating arterialization of the ligated lobe. Interestingly, late microvascular remodeling was associated with increased endothelial nitric oxide synthase expression, significant hepatocellular proliferation, and weight gain of the ligated lobe. Thus PBL induces only an initial microcirculatory failure with liver atrophy, followed by a hepatic arterial buffer response, microvascular remodeling, normoxygenation, and hepatocellular proliferation. This may explain the accelerated tumor progression occasionally observed in patients after PBL.