The literature review revealed that most patients with skin

The literature review revealed that most patients with skin invasion often have worsening intracranial GBM. In our review, the mean survival time was 4.4 months in nine of the 11 patients following initial recognition of skin invasion. Compared with other metastatic cases, the median survival time from the detection of metastases to death was 1.5 months, with patients usually dying due to rapid progression of intracranial lesions. Early recognition of cutaneous lesions, resection, and pathologic confirmation, followed by radiotherapy and chemotherapy with temozolomide, are recommended and may be beneficial.
Introduction Acute intestinal ischemic disorder (AIID), an uncommon but potentially lethal disorder, can be categorized into arterial occlusive mesenteric ischemia (AOMI), mesenteric venous thrombosis (MVT), and nonocclusive mesenteric ischemia (NOMI). AOMI is caused by mesenteric arterial thromboembolism and is associated with cardiovascular diseases, atherosclerosis, atrial fibrillation, and cardiogenic emboli. Although the hypercoagulable state commonly contributes to MVT, hypercoagulability-induced AOMI is rare, and the association between AOMI and the hypercoagulable state remains controversial. Here, we present a case of sequential arterial ischemic events involving the kidney, brain, and gastrointestinal tract over several years. Hypercoagulability is associated with a high plasma level of factor VIII and may have caused recurrent and multiple arterial thromboses in this patient.
Case Report Noncontrast computed tomography of the brain revealed recent infarction of the left basal ganglia (Figure 1A). Laboratory data showed prominent leukocytosis with a left shift (white blood cell count 21.0 × 103/mm3, normal 3.2–9.2 × 103/mm3; bands neutrophils 7%, normal 0%; segmented neutrophils 82.5%, normal 43–64%) and an elevated level of plasma C-reactive protein (CRP; 88.6 mg/L, normal < 8 mg/L). Furthermore, contrast-enhanced abdominal computed tomography revealed partial defects within the superior mesenteric artery (Figure 1B), focal dilatation of the jejunum with wall thickening, poor enhancement and pneumatosis intestinalis (Figure 1C), adjacent fat stranding, and focal ascites (Figure 1D). Pathological examination showed multiple thrombi within the mesenteric ikk pathway of the infarcted bowel but no apparent atherosclerosis of the vessels. Heparin was administered in the immediate postoperative period with a gradual transition to warfarin. A coagulation screen revealed a thrombophilia with an increased activity of plasma factor VIII and borderline deficiency of protein C (Figure 2). Plasma activities of factor V and antithrombin III were within the normal ranges (factor V 75%, normal 50–150%; antithrombin III 92%, normal 58–118%; Table 1). Tests conducted for antiphospholipid antibodies (anti-cardiolipin antibody, immunoglobulins M and G), autoimmune diseases—including systemic lupus erythematosus and rheumatoid arthritis (rheumatoid factor < 20 IU, normal < 20 IU)—occult malignancy, and copper deficiency were negative. The patient was discharged 2 weeks postoperatively and could independently perform daily activities with only mild neurological sequelae thereafter. He exhibited recurrent and multiple arterial thromboses without evidence of cardiogenic thromboembolism or systemic atherosclerosis; therefore, hypercoagulability was suspected. The plasma factor VIII level was consistently high with a borderline low activity of protein C at 64 months postoperatively (Figure 2). A lifelong anticoagulant therapy instead of antiplatelet therapy alone was suggested to this patient for hypercoagulability-induced recurrent and multiple arterial thromboses. The patient is presently healthy and regularly receives warfarin prophylaxis.
Discussion Despite advances in diagnostic and therapeutic modalities, the morbidity and mortality rates of AIID have remained high and without considerable improvement for several years. Prompt detection and adequate management of AIID remain challenging for physicians. AIID is categorized into AOMI, MVT, and NOMI according to their underlying etiologies and prognostic outcomes. AOMI can be caused by either mesenteric arterial embolism or thrombosis, although arterial embolism is more common. Similar to other embolic events, mesenteric arterial embolism mostly arises from a cardiac source, such as cardiac arrhythmia, valvular disease, congestive heart failure, and recent myocardial infarction. Multiple synchronous emboli affecting other visceral arteries are often observed in patients with cardiac arrhythmia. Furthermore, mesenteric arterial thrombosis generally results from atherosclerosis of the mesenteric vessels and the associated risk factors include smoking, hypertension, diabetes mellitus, dyslipidemia, and other atherosclerotic diseases. Patients with AOMI always have some predisposing factors.