Abstract. Pilomatrix carcinoma is a very rare malignancy, with ~130 cases reported in the literature. In the past, pilomatrix carcinoma was considered to be a low-grade malignant tumor. Currently, however, its significant recurrence and metastatic potential has been well documented. Lymph node and systemic metastases are frequently observed. Wide surgical excision of the primary lesion is the principal modality of treatment, whereas adjuvant radiotherapy may be beneficial in local tumor control. Lymph node metastases may be treated surgically or with radiotherapy. Systemic disease is not responsive to chemotherapy, and is hence associated with a poor prognosis. Since the majority of nodal and systemic metastases present after the initial diagnosis and treatment, follow-up examinations of these patients may be warranted, despite the currently inadequate treatment options. In the present study, a case of pilomatrix carcinoma of the parotid region with early local recurrence only 2 months after complete excision with negative surgical margins is reported. The local recurrence was treated by excision and radiotherapy. The associated literature is also discussed.

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Acute ischemia of an extremity occurs in several stages, a lack of oxygen being the primary contributor of the event. Although underlying patho-mechanisms are similar, it is important to determine whether it is an acute or chronic event. Healthy tissue does not contain enlarged collaterals, which are formed in chronically malperfused tissue and can maintain a minimum supply despite occlusion. The underlying processes for enhanced collateral blood flow are sprouting vessels from pre-existing vessels (via angiogenesis) and a lumen extension of arterioles (via arteriogenesis). While disturbed flow patterns with associated local low shear stress upregulate angiogenesis promoting genes, elevated shear stress may trigger arteriogenesis due to increased blood volume. In case of an acute ischemia, especially during the reperfusion phase, fluid transfer occurs into the tissue while the vascular bed is simultaneously reduced and no longer reacts to vaso-relaxing factors such as nitric oxide. This process results in an exacerbative cycle, in which increased peripheral resistance leads to an additional lack of oxygen. This whole process is accompanied by an inundation of inflammatory cells, which amplify the inflammatory response by cytokine release. However, an extremity is an individual-specific composition of different tissues, so these processes may vary dramatically between patients. The image is more uniform when broken down to the single cell stage. Because each cell is dependent on energy produced from aerobic respiration, an event of acute hypoxia can be a life-threatening situation. Aerobic processes responsible for yielding adenosine triphosphate (ATP), such as the electron transport chain and oxidative phosphorylation in the mitochondria, suffer first, thus disrupting the integrity of cellular respiration. One consequence of this is irreparable damage of the cell membrane due to an imbalance of electrolytes. The eventual increase in net fluid influx associated with a decrease in intracellular pH is considered an end-stage event. Due to the lack of ATP, individual cell organelles can no longer sustain their activity, thus initiating the cascade pathways of apoptosis via the release of cytokines such as the BCL2 associated X protein (BAX). As ischemia may lead to direct necrosis, inflammatory processes are further aggravated. In the case of reperfusion, the flow of nascent oxygen will cause additional damage to the cell, further initiating apoptosis in additional surrounding cells. In particular, free oxygen radicals are formed, causing severe damage to cell membranes and desoxyribonucleic acid (DNA). However, the increased tissue stress caused by this process may be transient, as radical scavengers may attenuate the damage. Taking the above into final consideration, it is clearly elucidated that acute ischemia and subsequent reperfusion is a process that leads to acute tissue damage combined with end-organ loss of function, a condition that is difficult to counteract.

BackgroundMedian arcuate ligament syndrome is a rare condition with abdominal symptoms. Accepted treatment options are open release of median arcuate ligament, laparoscopic release of edian arcuate ligament, robot-assisted release of median arcuate ligament and open vascular treatment. Here we aimed to evaluate the central priority of open vascular therapy in the treatment of median arcuate ligament syndrome.MethodsWe conducted a monocentric retrospective study between January 1996 and June 2016. Thirty-one patients with median arcuate ligament syndrome underwent open vascular surgery, including division of median arcuate ligament in 17 cases, and vascular reconstruction of the celiac artery in 14 cases.ResultsIn a 20-year period, 31 patients (n = 26 women, n = 5 men) were treated with division of median arcuate ligament (n = 17) or vascular reconstruction in combination with division of median arcuate ligament (n = 14). The mean age of patients was 44.8 ± 15.13 years. The complication rate was 16.1% (n = 5). Revisions were performed in 4 cases. The 30-day mortality rate was 0%. The mean in-hospital stay was 10.7 days. Follow-up data were obtained for 30 patients. The mean follow-up period was 52.2 months (range 2–149 months). Patients were grouped into a decompression group (n = 17) and revascularisation group (n = 13). The estimated Freedom From Symptoms rates were 93.3, 77.8, and 69.1% for the decompression group and 100, 83.3, and 83.3% for the revascularisation group after 12, 24 and 60 months respectively. We found no significant difference in the Freedom From Re-Intervention CA rates of the decompression (100% at 12, 24 and 60 months post-surgery) and revascularisation (100% at 12 months, and 91.7% at 24 and 60 months post-surgery) groups during follow-up (p = 0.26).ConclusionsOpen vascular treatment of median arcuate ligament syndrome is a safe, low mortality-risk procedure, with low morbidity rate. Treatment choice depends on the clinical and morphological situation of each patient.