First report of successful treatment of chronic pediatric tibial osteomyelitis and fracture using autologous platelet-rich plasma.

Osteomyelitis is a refractory disease caused by microbial invasion of the bone, leading to destruction of the bone tissue. It is more common in children. Osteomyelitis requires long treatment at high cost and is associated with high rates of recurrence and disability. It can also be complicated by sepsis that, if not treated in time, can result in death. Here, we report the first case of a 10-year-old patient who presented with chronic tibial osteomyelitis complicated with fracture. The patient had received traditional treatment for osteomyelitis for over 14 months without success. However, after 4 months of treatment with autologous platelet-rich plasma, the fracture, infection, and osteomyelitis resolved completely. These clinical observations demonstrate the potential for using autologous platelet-rich plasma as a novel treatment for chronic pediatric osteomyelitis.

Hepatic adenoma in a 7-year-old girl: a case report and literature review.

BACKGROUND: Hepatocellular adenomas (HCAs) are rare benign tumors of the liver that occur predominantly in women taking oral contraceptives. In children, HCAs comprise < 5% of hepatic tumors. We report a case of HCAs in a 7-year-old girl with estrogen and glucose imbalance. CASE PRESENTATION: A 7-year-old girl was presented to our hospital with bilateral breast enlargement for 2 months, polydipsia, polyuria, polyphagia, hyperglycemia, and significant weight gain. Computed tomography (CT) showed a 7.2 cm×6.9 cm×5.3 cm round-shaped mass in the left inner lobe of the liver, ovarian ultrasound showed multiple follicles in the ovaries bilaterally, and cranial magnetic resonance imaging (MRI) showed an enlarged superior pituitary. Hematological and biochemical results were as follows: fasting glucose was 19.7 mmol/L, estradiol was 122.9 pmol/L, follicle-stimulating hormone 10.81 IU/L, luteinizing hormone 10.99 IU/L, insulin-like growth factor 1,513 ng/mL, glutamine aminotransferase 86 U/L, and alkaline phosphatase 362 U/L. Thyroid functions, methemoglobin, fetal protein, carcinoembryonic antigen, and chorionic gonadotropin were normal. The patient had a complete surgical resection of the liver tumor, and the postoperative histopathological diagnosis was HCAs. After the surgery, insulin was injected and the glucose levels were stable. During the 36-month follow-up period, neither tumor recurrence nor significant abnormalities were detected using color Doppler ultrasound of the liver. The child's precocious puberty is currently under control. CONCLUSIONS: HCAs are particularly rare in children with liver tumors, and risk factors for the development of HCAs in children include sex hormone imbalance, obesity, Fanconi anemia (FA), glycogen storage diseases (GSDs) type I, III, and IV, galactosemia, immunodeficiency, congenital portosystemic shunts (CPSS), cardiac hepatopathy status-post Fontan procedure, Hurler syndrome, familial adenomatous polyposis, germline HNF1A mutations, and maturity-onset diabetes of the young type 3. Most HCAs are detected during a physical examination without clinical symptoms, and some patients may present with symptoms such as abdominal pain, abdominal distension, and abdominal masse. Serum liver function tests can show increased alkaline phosphatase (ALP) and γ- glutamyl transferase (GT), whereas α-Fetoprofein (AFP) levels are normal. The definitive diagnosis relies mainly on histopathological examination. Because HCAs can rupture and bleed and become malignant. Early surgical treatment is recommended after detection.

Giant congenital nodular melanoma in a newborn: a case report and literature review.

BACKGROUND: Malignant melanoma (MM) arises predominantly after adolescence and is uncommon in children. Congenital MM in newborns is even rarer with a dearth of published literature; as a consequence, there is no uniform standard for the pathogenesis and treatment for neonatal malignant melanoma. Herein we report a case of giant congenital nodular MM in a newborn, including its clinical, imaging, pathological and molecular pathological features. This case is the largest giant congenital primary nodular malignant melanoma in utero in neonates currently reported in China. CASE PRESENTATION: A female neonatal patient was found to have a 2.97 cm× 1.82 cm×1.50 cm mass with a clear boundary at the right acromion in color Doppler ultrasound examination at 24 weeks of gestation. The mass increased to 3.0 cm×5.0 cm×9.0 cm at birth, and local ulceration was seen. MRI demonstrated that the mass was located on the right shoulder and underarm in a lobulated appearance, and surrounded the right scapula which was deformed. Clinical stage:IV(AJCC 8th Edition (2017)). α-Fetoprofein (AFP) by hematological examination: 1210ng/ml, NSE: 21.28ng/ml, LDH: 842U/L. The patient underwent surgical resection of the tumor, and was pathologically diagnosed as neonatal congenital malignant melanoma; immunohistochemistry (IHC): S-100 (+), HMB45 (+), Melan A (+), and Tyrosinase (+). Molecular pathological examination for BRAF V600E showed no mutations (Quantitative Real-time PCR, qPCR); And so were NRAS, C-kit (exons 9,11,13,14,17,18), and TERT (promoter locus, C228T and C250T) (Sanger sequencing). Non-surgical therapies were not carried out after the surgical resection of the tumor. After 6 months of follow-up, the child developed normally, and color Doppler ultrasound showed no obvious tumor growth or abnormality in the original tumor site. CONCLUSIONS: It is extremely rare to see giant congenital primary nodular MM in utero in neonates. The pathogenesis, treatment and prognosis of congenital MM need further research. The diagnosis mainly depends on histopathology and immunohistochemistry, and it needs to be differentiated from malignant lymphoma and primitive neuroectodermal tumor. The current treatment strategy for MM relies on the surgical excision of the mass. Research directed at molecular detection for genetic mutations would contribute to targeted therapy and better prognosis.

Silencing long non­coding RNA NEAT1 suppresses the tumorigenesis of infantile hemangioma by competitively binding miR­33a­5p to stimulate HIF1α/NF­κB pathway.

Infantile hemangioma (IH) is one of the most common vascular tumors that occurs during childhood, but its pathogenesis is currently not completely understood. Even though lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays vital roles in tumorigenesis of malignant tumors, its roles in IH remain unclear. Therefore, we evaluate the function of lncRNA NEAT1 in IH. Reverse transcription­-quantitative PCR indicated that IH tissues exhibited high expression levels of NEAT1 and hypoxia­inducible factor 1α (HIF1α), and low expression levels of the microRNA (miR)­33a­5p. Small interfering RNA­mediated depletion of NEAT1 suppressed hemangioma endothelial cell (HemEC) proliferation, migration and invasion. The data suggested that NEAT1 positively regulated HIF1α expression by sponging miR­33a­5p in HemECs. miR­33a­5p overexpression or HIF1α silencing also acted to suppress HemEC proliferation, migration and invasion. Furthermore, the results indicated that the NEAT1/miR­33a­5p/HIF1α axis regulated the NF­κB signaling pathway. Collectively, the results revealed that depletion of lncRNA NEAT1 suppressed the tumorigenesis of IH by competitively binding miR­33a­5p and thereby stimulating the HIF1α/NF­κB signaling pathway.

Persistent hyperinsulinemic hypoglycemia of infancy: a clinical and pathological study of 19 cases in a single institution.

OBJECTIVE: To study the clinical and pathological features of persistent hyperinsulinemic hypoglycemia of infancy. METHOD: The clinical and pathological data of 19 cases of persistent hyperinsulinemic hypoglycemia of infancy were retrieved and reviewed from the medical records in Children's Hospital of Fudan University. RESULTS: There were 13 boys and 6 girls. The age interval was from 16 days to 7 months, and the average age was 2.71 ± 2.23 months. The blood glucose concentrations ranged from 0.57 to 3.0 mmol/L (average value 1.60 ± 0.75 mmol/L) and the serum insulin concentrations ranged from 3.1 to 79.4 uIU/ml (average value 27.89 ± 21.81 uIU/ml) at the time of one week before operation. The size of lesion was between 2 cm to 6.5 cm in maximum diameter (average value 4.04 ± 1.18 cm). 19 cases were divided into three types according to the pathological classification criteria: focal type (1 case), diffuse type (17 cases) and atypical type (1 case). The enucleation of the nodule was given for the patient of focal type and subtotal pancreatectomy was administrated for diffuse and atypical type patients. The blood glucose concentrations ranged from 3.0 to 12.4 mmol/L (average value 6.21 ± 2.69 mmol/L) at the time of one month after operation. The difference between the preoperative blood glucose concentrations and the postoperative blood glucose concentrations was statistically significant (1.6037 ± 0.7458 mmol/L vs. 6.2105 ± 2.6882 mmol/L, P<0.05). Insulin was positive for the multiple pancreatic islets, and the ki-67 index was between 5% and 8%. P57(kip2) was negative. 19 patients were followed up for a period of 2 to 38 months. 13 cases recovered well without any complications, and 6 cases had postoperative hyperglycemia and need a medication to control the blood glucose concentrations. CONCLUSION: Persistent hyperinsulinemic hypoglycemia of infancy mainly occurred in infants. Boys had the predominance and the most common pathological type was the diffuse type. The different surgical methods (focal type with lesion enucleation, diffuse and atypical type with subtotal pancreatectomy), were effective for different patients, and most of patients had a good prognosis. Early diagnosis and appropriate treatment to maintain euglycemia remained the mainstay of management to prevent postoperative complications. Therefore, the correct pathological classification could help clinicians to find effective treatment and improve the outcome.