Erythroderma secondary to gliclazide: a case report

Erythroderma is generalized exfoliative dermatitis, which involves more than 90% of the patient's skin. The most common cause of erythroderma is exacerbation of an underlying skin disease, malignancies or drug reaction. There is a long list of drugs responsible for erythroderma such as antiepileptics, sulfonamides, antibiotics, and angiotensin converting enzyme (ACE) inhibitors. We herein report a case of erythroderma due to gliclazide usage which is also proved by histopathologic examination and patch test. We could not find any case report of gliclazide, an oral antidiabetic, as a cause erythroderma in the literature.     

A case of septal panniculitis secondary to interferon treatment

The most common side effects of interferon-beta therapy following subcutaneous administration include pain, inflammation and induration at the injection site, which occur in approximately 20–60% of patients. Besides, transient injection-site erythema is frequently seen in beta-interferon therapy. Less frequent reactions at injection sites include vascular thrombosis, mucinosis, dermal and systemic sclerosis, necrosis, and ulceration. Here, we report a 44-year-old case diagnosed with multiple sclerosis, who developed pain and swelling following interferon-beta 1a treatment after an improperly administered intramuscular injection; and with this case report, we would like to draw attention to septal panniculitis, a serious drug complication, that develops following interferon-beta 1a treatment after an improperly administered intramuscular injection.     

Acute aortic dissection mimicking acute abdomen in a 14‐year‐old boy

Aortic dissection is extremely rare in children. Although it usually presents with severe chest pain, atypical clinical presentations mimicking various illnesses may cause misdiagnosis. In this report, the case of a 14‐year‐old boy with symptoms suggestive of acute abdomen, which was finally diagnosed as aortic dissection, is discussed.     

Use of custom-made stockings to control postoperative leg and foot edema following free tissue transfer and external fixation of fractures

Patients with lower extremity trauma treated with free tissue transfer and external fixation of fractures almost always have postoperative edema of the foot and leg. Although compressive elastic stockings have been advised to be worn by patients with venous or lymphatic insufficiency, no such stocking has been described for postoperative use by patients with external fixators. The aim of the present report was to describe a custom-made elastic compression stocking for patients who have undergone soft tissue reconstruction and fracture fixation with external fixators. These custom-made stockings can help to decrease postoperative edema during the nonambulatory and nonweight-bearing ambulatory period. They are easy to apply, affordable, and can be tailored from regular compression stockings according to the needs of the patients.     

Evaluation of ETV6/RUNX1 Fusion and Additional Abnormalities Involving ETV6 and/or RUNX1 Genes Using FISH Technique in Patients with Childhood Acute Lymphoblastic Leukemia

Childhood acute lymphoblastic leukemia (ALL) is the most common type of childhood leukemia. Specifically, ALL is a malignant disorder of the lymphoid progenitor cells, with a peak incidence among children aged 2–5 years. The t(12;21)(p13;q22) translocation occurs in 25 % of childhood B cell precursor ALL. In this study, bone marrow samples were obtained from 165 patients with childhood ALL. We analyzed the t(12;21) translocation and other related abnormalities using the fluorescent in situ hybridization (FISH) technique with the ETV6(TEL)/RUNX1(AML1) ES dual color translocation probe. Conventional cytogenetic analyses were also performed. ETV6 and RUNX1 related chromosomal abnormalities were found in 42 (25.5 %) of the 165 patients with childhood ALL. Among these 42 patients, structural changes were detected in 33 (78.6 %) and numerical abnormalities in 9 (21.4 %). The frequency of FISH abnormalities in pediatric ALL cases were as follows: 8.5 % for t(12;21)(p13;q22) ETV6/RUNX1 fusion, 6.0 % for RUNX1 amplification, 3.0 % for tetrasomy/trisomy 21, 1.8 % for ETV6 deletion, 1.21 % for ETV6 deletion with RUNX1 amplification, 1.21 % for ETV6 amplification with RUNX1 amplification, 0.6 % for polyploidy, 0.6 % for RUNX1 deletion, and 0.6 % for diminished ETV6 signal. The most common structural abnormality was the t(12;21) translocation, followed by RUNX1 amplification and ETV6 deletion, while the most commonly observed numerical abnormality was trisomy 21.     

Decorin suppresses tumor cell-mediated angiogenesis

The progressive growth of most neoplasms is dependent upon the establishment of new blood vessels, a process regulated by tumor-secreted factors and matrix proteins. We examined the in vitro and in vivo angiogenic ability of conditioned media obtained from fibrosarcoma, carcinoma, and osteosarcoma cells and their decorin-transfected counterparts. Human endothelial cells were investigated in vitro by evaluating three essential steps of angiogenesis: migration, attachment, and differentiation. On the whole, wild-type tumor cell-secretions enhanced endothelial cell attachment, migration, and differentiation, whereas their decorin-expressing forms inhibited these processes. Similarly, decorin-containing media suppressed endothelial cell sprouting in an ex vivo aortic ring assay. Since angiogenesis is an important component of tumor expansion, the growth rate of these cells as tumor xenografts was examined by implantation in nude mice. In vivo, the decorin-expressing tumor xenografts grew at markedly lower rates and showed a significant suppression of neovascularization. Immunohistochemical, Northern and Western blot analyses indicated that the decorin-expressing cells produced vascular endothelial growth factor (VEGF) at markedly reduced rates vis-á-vis their wild-type counterparts. Specificity of this process was confirmed by experiments where addition of recombinant decorin to the wild-type tumor cells caused 80-95% suppression of VEGF mRNA and protein. These results provide a novel mechanism of action for decorin, and indicate that decorin could adversely affect in vivo tumor growth by suppressing the endogenous tumor cell production of a powerful angiogenic stimulus.