Papular-purpuric gloves and socks syndrome associated with B19V infection in a 6-year-old child.

A 6 year-old girl was admitted for evaluation of a fever associated with a petechial rash of 2 days' duration. She was in good general condition with no acute distress. Inspection of the skin revealed an amazing papular and purpuric rash of predominantly acral and symmetrical distribution and sharply demarcated on the ankles. All laboratory tests were found normal. Rash and fever completely resolved in less than 3 days. Serological testing for parvovirus B19 (B19V) antibodies was positive for IgM but negative for IgG. Moreover, B19V DNA was detected in serum with a viral load of 2.24 x 10(8) copies per mL. So we concluded of a paediatric case of popular-purpuric gloves and socks syndrome (PPGSS) associated with B19V infection. PPGSS is an idiosyncratic reaction to viral infection. The syndrome has been associated with several viruses such as HHV6, measles, coxsackie B6, and above all B19V. PPGSS occurs mostly in young adults. It is characterised by a typical papular and purpuric rash with an acral distribution and a sharp demarcation on the wrists and ankles. The rash is often pruritic and can be accompanied by mucosal lesions and/or systemic symptoms such as fever, asthenia and lymphadenopathy. Most of the time, the disease is self-limited with a short course and a benign prognosis. A very similar disease has been described in some children. The distinctive clinical characteristics of PPGSS in children should be recognized by paediatrician in particular at the emergency room in order to avoid superfluous explorations.

Procalcitonin serum levels in children undergoing chronic haemodialysis.

Infections account for considerable morbidity and mortality in patients requiring haemodialysis (HD). Procalcitonin (PCT)-a low molecular weight protein of 13 kDa-helps one to distinguish viral from bacterial infections and to evaluate the severity of bacterial infections. We investigated (1) PCT baseline levels in eight children undergoing chronic HD with high-flux membranes and (2) changes in the serum levels of PCT, C-reactive protein (CRP) and beta-2-microglobulin (beta2-MG)-a peptide with biochemical characteristics similar to those of PCT-before and after haemodialysis sessions. Blood sampling was performed three times in the mid-week session. Serum PCT of the seven uninfected children before HD sessions was increased (0.75+/-0.07 ng/ml), whereas CRP levels were normal. PCT after dialysis decreased significantly by 40% (P<0.0001) compared with initial values, whereas CRP levels before and after HD were not different. beta2-MG decreased by 70%, probably due to different biochemical properties of both proteins. PCT serum levels 15 min and 60 min after the HD session remained unchanged in comparison with those at the end of the HD session, suggesting accumulation of PCT between HD sessions rather than HD-induced production to be responsible for the increased baseline PCT serum levels. We concluded that CRP serum levels were not affected by HD in our group. Moderately elevated baseline PCT serum levels that are presumably due to reduced renal clearance and uraemia and dialysis-ability of PCT should be taken into consideration. However, increase of serum PCT in patients with severe bacterial infections is generally massive (10-fold to 1,000-fold), suggesting a low risk for false negative results in such cases.

Perinatal asphyxia may present with features of neonatal atypical hemolytic uremic syndrome.

Hemolytic uremic syndrome (HUS) is the consequence of platelet consumption at sites of endothelial injury. Perinatal asphyxia (PA) may cause renal failure after birth and can be associated with disseminated intravascular coagulopathy (DIC) with platelet consumption. No biological investigation permits us to distinguish clearly between neonatal HUS and DIC. We report on three neonates with renal failure due to different degrees of PA. They presented biological features compatible with HUS, such as fragmentocytes ( approximately 2%), thrombopenia (<50,000/mm(3)), and anemia (<8 g/dl). One patient required peritoneal dialysis. Haptoglobin was undetectable for all three patients. Factor H and factor I, as well as components of the complement system (C3 and C4) and ADAMTS13 activity, were decreased. Two patients received daily fresh frozen plasma infusions over the first 4 weeks. Renal function improved in two patients; one patient had chronic renal failure. No neurological sequelae were noted. All blood parameters suggestive of thrombotic microangiopathy (TMA) were normal on days 12, 30, and 60. We hypothesize that endothelial cell damage concomitant with PA may lead to a vicious circle that results in consumption of platelets and plasma factors involved in hemostasis and/or fibrinolysis. In conclusion, PA, DIC and HUS are difficult to distinguish, and endothelial cell damage may be their common pathophysiological pathway.