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INTRODUCTION AND IMPORTANCE: Hydroxyurea is a cytotoxic drug commonly used to treat various myeloproliferative disorders. However, prolonged oral administration of this drug may trigger skin side effects and ulcers. There are few clinical reports on treating leg ulcers caused by hydroxyurea and even fewer clinical reports on managing recurrent ulcers after treatment. CASE PRESENTATION: An 87-year-old woman with essential thrombocythemia presented with a painful skin ulcer on her left calf. After failed outpatient treatment, she opted for hospitalisation for free skin grafting. Four months later, ulcers reappeared at the transplant site, leading to her readmission to the hospital. The diagnosis revealed that the leg ulcers were caused by hydroxyurea. Despite this, she persisted with hydroxyurea treatment and subsequently underwent posterior tibial artery perforator flap surgery. During the two-year follow-up, a new ulcer developed on the medial condyle of her other calf. However, no new ulcers or local pain were observed in the area where perforator flap grafting was performed. CLINICAL DISCUSSION: Leg ulcers caused by hydroxyurea are rare clinically and can easily be misdiagnosed. There is currently minimal research on ulcer recurrence after treatment. Posterior tibial perforator flaps may more effectively promote the healing of recurrent ulcers. CONCLUSION: Compared to conservative treatment and skin grafting surgery, the posterior tibial artery perforator flap offers a dependable blood supply and enhances the likelihood of wound healing. It can be considered an option, particularly for recurrent and refractory ulcers, even without discontinuing medication.
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INTRODUCTION AND IMPORTANCE: The median arcuate ligament syndrome (MALS) is a rare disorder that produces a spectrum of symptoms due to compression of the arcuate ligament, clinically manifested primarily by abdominal pain, nausea, vomiting, and weight loss. The mechanism of these symptoms has not yet been revealed, and the current treatment methods are still somewhat controversial. CASE PRESENTATION: We present a 54-year-old woman who presented with intermittent epigastric pain for nine months. During the onset, she lost 7.5 kg. After routine examinations in a nearby hospital, no abnormality was found. She was referred to us. CTA showed compression of the celiac artery. Further selective celiac angiography at the end of inspiration and expiration confirmed MALS. After consultation with the patient, the decision to have a laparotomy was made. The celiac artery was completely skeletonized, and external compression on the artery was released. Postoperative symptoms improved significantly. One-year follow-up after the operation, she had a weight gain of 4.8 kg and was satisfied with the surgical results. CLINICAL DISCUSSION: The manifestations of MALS are varied and challenging. Our patient presented with weight loss and intermittent abdominal pain. The mutual confirmation of multiple investigations can provide a more comprehensive overview of celiac artery compression. We confirmed using ultrasonography, CT angiography, and selective digital subtraction angiography in this case. The celiac artery compression was relieved after open surgery. Our patient's symptoms improved significantly after surgery. We hope our treatment method can provide a reference for MALS diagnosis and treatment. CONCLUSION: It is challenging to diagnose MALS. Cross-confirmation of multiple examinations can provide a more comprehensive view of celiac compression. Surgical decompression of the celiac artery (open or laparoscopic surgery) may be an effective therapy for MALS, especially in centers with experience.
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This study aims to discover the therapeutic effect of chemokine (CXC motif) receptor 4 (CXCR4) antagonist AMD3100 combined with transcatheter arterial chemoembolization (TACE) in a rat model with hepatocellular carcinoma (HCC). An orthotopic model of HCC was established and treated with TACE (doxorubicin-lipiodol emulsion) with or without AMD3100. The tumor volume was measured by magnetic resonance imaging (MRI). Histopathological changes were detected by hematoxylin-eosin (HE) staining. HCC cell apoptosis was assessed by terminal deoxyribonucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labeling (TUNEL) staining. Immunohistochemistry was used to detect the expression of CD34, hypoxia-inducible factor 1α (HIF-1α), vascular endothelial growth factor (VEGF), and Ki67. Gene and protein expressions were quantified by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and western blotting, respectively. Both TACE and AMD3100 reduced the tumor volume in orthotopic rat model of HCC with the decreased CXCR4 expression in tumor tissues, and the combination had better effect. However, TACE increased the microvessel density (MVD) in HCC tissues of rats, while AMD3100 treatment reduced MVD in HCC tissues. AMD3100 reduced the TACE induced MVD in HCC tissues with the reduction of HIF-1α and VEGF expression. Either AMD3100 or TACE could promote HCC cell apoptosis accompanying by decreased cell proliferation, and their combined use had better therapeutic effects. CXCR4 antagonist AMD3100 enhance therapeutic efficacy of TACE in rats with HCC via promoting the HCC cell apoptosis, reducing cell proliferation, and inhibiting MVD, thus reducing tumor volume.
