Background Osteonecrosis (ON) is one of the major therapy‐related complications in childhood acute lymphoblastic leukemia (ALL). The purpose of the current study is to assess the frequency of ON in children with ALL and to detect whether polymorphisms in vitamin D receptor gene (VDR) and plasminogen activator inhibitor‐1 (PAI‐1) gene can affect the risk of ON. Patients and Methods Nighty‐six ALL children were enrolled. Serum 25‐hydroxyvitamin D 25(OH)D levels were performed in addition to the detection of polymorphisms in PAI‐1and VDR genes by polymerase chain reaction. Results Ten out of 96 patients had ON (four males and six females aged above 10 years) and had an insufficient level of 25(OH)D. Fifty‐two percent of patients had PAI‐1 GG genotype while 48% had PAI‐1 GA genotype. PAI‐1 polymorphism was detected in 60% of all ON cases. The frequencies of VDR genotypes were CT (56.3%), CC (39.6%), and TT (4.2%). Osteonecrosis was found in eight patients with CC genotype and in two patients with CT genotype. Conclusion Osteonecrosis can develop early during the therapy of ALL. Older age and insufficient level of 25(OH)D were considered important risk factor for the development of osteonecrosis. PAT‐1 and VDR gene polymorphism may be a genetic risk factor in its pathogenesis.

Background: An increased risk of cardiovascular complications is reported in survivors of childhood acute lymphoblastic leukemia (ALL). Early identification of impaired vascular health may allow for early interventions to improve outcomes. Aim: The study was conducted to assess the endothelial dysfunction in ALL survivors using a new marker, serum endocan, and measurement of the mean common carotid arteries intima media thickness (cIMT). Methods: A case-control study was conducted on 100 childhood ALL survivors (aged 6–18 years), with 80 healthy age and sex-matched children as a control group. Lipid profile, hepatitis markers, and serum ferritin where measured, in addition to the measurement of serum endocan. and cIMT by B-mode high-resolution ultrasonography for all study participants. Results: Triglycerides, total cholesterol, post prandial glucose, and serum ferritin were significantly higher in ALL survivors than controls ( p < 0.05). Dyslipidemia was detected in 6% of ALL survivors. ALL survivors showed statistically higher serum endocan levels (470.41 ± 556.1 ng/l, versus, 225.94 ± 185.2 ng/l, respectively) and increased cIMT levels compared with the control group (0.650 ± 0.129 mm versus 0.320 ± 0.095 mm, respectively) p < 0.05. Serum endocan was positively correlated with cIMT and blood cholesterol. Conclusions: The survivors of childhood ALL demonstrated an elevated level of serum endocan and increased cIMT. These can be used as predictors of endothelial dysfunction, and, as a consequence, the risk of developing premature atherosclerosis.

Acute Lymphoblastic Leukemia (ALL) is the most common malignancy in children. Venous thromboembolism (VTE) is relatively common in children with acute ALL that usually appears after the diagnosis or during therapy secondary to many associated risk factors. Here in we report for the first time a child who developed cerebral venous sinus thrombosis (CVST) prior to the diagnosis of ALL.

Acute lymphoblastic leukemia is the most common malignancy in children. In children, venous thromboembolism is relatively common. In most cases, venous thromboembolism manifests in patients who are diagnosed with acute lymphoblastic leukemia. Several risk factors associated with acute lymphoblastic leukemia predispose patients to the development of venous thromboembolism. Unlike most reported cases of venous thromboembolism, herein we report a child who developed cerebral venous sinus thrombosis prior to the diagnosis of acute lymphoblastic leukemia. The patient recovered from an attack of acute gastroenteritis with sepsis, pancytopenia, and disseminated intravascular coagulation 2 weeks before the development of thrombosis. Her laboratory workup for coagulopathy and disseminated intravascular coagulation was normal at the time of diagnosis of cerebral sinus thrombosis. The genetic workup for thrombophilia risk identified several genetic thrombophilia mutations: the homozygous factor XIII V34L and MTHFR A1298C mutations and heterozygous factor V Leiden mutation. Three weeks later, the patient was diagnosed with acute lymphoblastic leukemia. However, it remains questionable whether the thrombotic event was caused by the previous infection of gastroenteritis, sepsis, and disseminated intravascular coagulation picture (which was augmented by her genetic thrombophilia risk), or was it caused by acute lymphoblastic leukemia (that was not detected at early stages with its associated hypercoagulable state), or was it caused by a type of paraneoplastic syndrome. A multifactorial etiology is proposed.