Periapical infection may affect birth outcomes via systemic inflammation.

OBJECTIVES: Maternal dental periapical infections are associated with preterm birth and intrauterine growth restriction. This study investigates whether the association is mediated through bacterial spread from periapical lesions to placenta (direct pathway) or systemic inflammatory reaction (indirect pathway). MATERIALS AND METHODS: We compared birth outcomes in Malawian mothers with and without periapical infection. As markers of a direct pathway, we identified placental bacteria using a 16S rDNA approach and assessed histological evidence of inflammation in the placenta and amniotic membranes. We measured C-reactive protein, alpha-1-acid glycoprotein, and salivary cortisol as markers of an indirect pathway. We used regression models to associate the predictor variables with duration of pregnancy and newborn size. RESULTS: Of 1,024 women, 23.5% had periapical infection. There was no association of periapical infection with either bacterial DNA or histological inflammation in placenta or membranes. Periapical infection was associated with C-reactive protein, alpha-1-acid glycoprotein, and cortisol concentrations in a dose-dependent manner at 36 weeks. Addition of alpha-1-acid glycoprotein or cortisol concentration into regression models attenuated the association between periapical infection and pregnancy outcomes. CONCLUSION: There was no evidence of direct spread of periapical bacteria to the placenta. Periapical infections and adverse pregnancy outcomes are in part mediated through systemic inflammation.

Ward round--A rare tumor of the kidney resulting in hypertension, renal failure and a cerebrovascular accident in a young female.

A 17-year-old girl was admitted to our hospital with severe refractory hypertension evolving over approximately 4 years. Despite not having the resources to identify plasma-renin levels and using standard imaging techniques, a juxtaglomerular cell tumor was suspected and was histologically confirmed after surgical excision. This is a potentially lethal condition if left untreated and surgical excision is curative. The benign nature of the tumor is emphasized and its chemical, radiological and microscopic appearance discussed according to the literature. To the best of our knowledge, this is the first reported case of a patient surviving a cerebrovascular accident associated with a juxtaglomerular cell tumor.

Endemic Burkitt lymphoma: a 28-day treatment schedule with cyclophosphamide and intrathecal methotrexate.

BACKGROUND: Endemic Burkitt lymphoma (eBL) is the most common childhood cancer in equatorial Africa and there is a need for affordable, effective treatment. AIM: To record the morbidity of treatment and event-free survival after 1 year using relatively high doses of cyclophosphamide at short intervals combined with intrathecal methotrexate. METHODS: Forty consecutive patients with a mean age of 6.9 (range 2-15) years were treated at Queen Elizabeth Central Hospital, Blantyre between 10th April and 17th November 2006. The initial diagnosis was made clinically and confirmed by fine-needle aspiration in 73%. Abdominal ultrasound, bone marrow aspirate and CSF analysis were undertaken routinely. Chemotherapy consisted of cyclophosphamide, 40 mg/kg on day 1 and 60 mg/kg on days 8, 18 and 28. Intrathecal methotrexate 12.5 mg and hydrocortisone 12.5 mg were administered on days 1, 8, 18 and 28. Allopurinol was commenced before chemotherapy, and a high urinary output was maintained to prevent tumour lysis. RESULTS: St Jude stage distribution was stage I, 1; II, 9; III, 24; and IV, 6. An equal number (70%) presented with abdominal and facial disease, and 15% with paraplegia. Twenty patients (50%) were below the 5th NCHS centile for weight-for-age. Two patients died during treatment, three had chemotherapy-resistant disease and 35 (88%) achieved complete clinical remission by day 28. Sixteen required antibiotic treatment for presumed infection and nine received a blood transfusion. Relapse occurred in 16 patients after 65-311 days (median 137). Nineteen patients (48%) have been in continued remission for 265-670 days (median 454). CONCLUSION: This short, inexpensive treatment schedule (<50 US$) cured almost 50% of eBL patients in a setting of very limited resources.

Rescue chemotherapy for patients with resistant or relapsed endemic Burkitt's lymphoma.

Patients with endemic Burkitt's lymphoma who failed primary treatment with the Malawi 2002 or 2003 Burkitt's lymphoma treatment protocols, consisting of high frequency cyclophosphamide 40 mg/kg and intrathecal methotrexate, were offered rescue chemotherapy. Twenty-eight patients (14 boys and 14 girls; age range 3-13 years) with resistant disease (n=8) or relapse (n=20) presented to the Queen Elizabeth Central Hospital, Blantyre, Malawi. Treatment consisted of cyclophosphamide 60 mg/kg and vincristine 1.5 mg/m(2) i.v. on Days 1, 8 and 15, plus intrathecal methotrexate on the same days in those patients treated for a relapse. The majority of patients (81%) had St Jude stage III or IV disease. Twenty patients (71%) achieved a complete clinical remission. Day 8 treatment was delayed in eight children and Day 15 treatment in five patients, both for a median of 7 days, mainly due to neutropenia. Ten patients relapsed after 42-311 days (median 105 days). Ten patients (36%) remained in remission for 353-712 days (median 487 days). Patients whose first relapse occurred after 6 months as well as those with limited disease had the best outcome. This simple 15-day chemotherapy schedule salvaged 36% of patients and significantly increased the overall cure rate of our Burkitt's lymphoma patients.

Plasmodium falciparum-infected erythrocytes induce tissue factor expression in endothelial cells and support the assembly of multimolecular coagulation complexes.

BACKGROUND: Plasmodium falciparum malaria infects 300-500 million people every year, causing 1-2 million deaths annually. Evidence of a coagulation disorder, activation of endothelial cells (EC) and increase in inflammatory cytokines are often present in malaria. OBJECTIVES: We have asked whether interaction of parasitized red blood cells (pRBC) with EC induces tissue factor (TF) expression in vitro and in vivo. The role of phosphatidylserine-containing pRBC to support the assembly of blood coagulation complexes was also investigated. RESULTS: We demonstrate that mature forms of pRBC induce functional expression of TF by EC in vitro with productive assembly of the extrinsic Xnase complex and initiation of the coagulation cascade. Late-stage pRBC also support the prothrombinase and intrinsic Xnase complex formation in vitro, and may function as activated platelets in the amplification phase of the blood coagulation. Notably, post-mortem brain sections obtained from P. falciparum-infected children who died from cerebral malaria and other causes display a consistent staining for TF in the EC. CONCLUSIONS: These findings place TF expression by endothelium and the amplification of the coagulation cascade by pRBC and/or activated platelets as potentially critical steps in the pathogenesis of malaria. Furthermore, it may allow investigators to test other therapeutic alternatives targeting TF or modulators of EC function in the treatment of malaria and/or its complications.