Risk factors for physical child abuse in infants and toddlers.

BACKGROUND: We examined the risk factors and injuries in physical child abuse between November 2003 and February 2007. PATIENTS AND METHODS: The uptake area of the University Hospital of Turku, Finland, consists of about 700 000 inhabitants. Forty-eight cases of physical child abuse were examined. The median age of the abused children was 2.2 years, for children with skull fractures it was 0.5 years. The incidence of child physical abuse increased during the study period; it was 0.6/month in 2004 and 1.7/month in 2006. Mortality in the study group was 2.1 %. RESULTS: Depression, overactivity, crying and prematurity were risk factors in the physically abused children. Parental risk factors were alcohol and drug abuse. Most often the perpetrator was the father or stepfather; when the perpetrator was unknown, the children were mostly in their mothers' care. The average delay of 3 weeks until starting the investigation into abuse was mostly due to delays by health centers or homes. Radiographs were the cornerstones of the medical examination but magnetic resonance examinations were essential for the examination protocol. CONCLUSIONS: All levels of public health services, day care facilities and schools must be aware of possible physical child abuse and initiate an investigation as soon as possible by contacting the authorities. Physically abused children and their families must be followed up and supported for a sufficiently long period by social pediatric outpatient wards. The general information on child maltreatment provided to the public needs to be increased to prevent abuse. A child welfare report must be made to social workers in every maltreatment case examined in hospital, and in most cases the offence must also be reported to the police. Nevertheless, in certain cases even permanent custody of the child cannot be avoided.

Radiographic follow-up of pneumonia in children.

This study assessed the clinical value of routine follow-up chest radiographs in hospitalized children with community-acquired pneumonia. The study population consisted of 196 children hospitalized for community-acquired pneumonia diagnosed between 1993-1995. Seventeen infective agents (10 viruses and 7 bacteria) were sought. Chest radiographs were taken on admission and 3-7 weeks later. All children were treated with antibiotics. Data on the course of illness over the following 8-10 years were obtained from patient files and questionnaires sent to parents. A potential causative agent was found in 165 (84%) of 196 cases. On follow-up chest radiographs, residual or new changes were seen in 30% of cases. The residual changes tended to be more common after mixed viral-bacterial infection (43%) than after sole viral (25%) or sole bacterial (20%) infection. Interstitial infiltrates (66%), atelectasis (46%), and enlarged lymph nodes were the most common sequelae seen on follow-up. Residual findings on follow-up radiographs did not affect the treatment of the children. No further chest radiographs were taken. During the 8-10-year follow-up of 194 children, no illnesses appeared that were associated with previous pneumonia. Twenty-six children had a new episode of pneumonia, 7 of them had asthma, and 6 had different underlying illnesses. In conclusion, routine follow-up chest radiographs are not needed in childhood community-acquired pneumonia if the child has a clinically uneventful recovery.

Differentiation of bacterial and viral pneumonia in children.

BACKGROUND: A study was undertaken to investigate the differential diagnostic role of chest radiographic findings, total white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and serum C reactive protein (CRP) in children with community acquired pneumonia of varying aetiology. METHODS: The study population consisted of 254 consecutive children admitted to hospital with community acquired pneumonia diagnosed between 1993 and 1995. WBC, ESR, and CRP levels were determined on admission. Seventeen infective agents (10 viruses and seven bacteria) were searched for. Chest radiographs were retrospectively and separately reviewed by three paediatric radiologists. RESULTS: A potential causative agent was found in 215 (85%) of the 254 cases. Bacterial infection was found in 71% of 137 children with alveolar infiltrates on the chest radiograph, while 72% of the 134 cases with a bacterial pneumonia had alveolar infiltrates. Half of the 77 children with solely interstitial infiltrates on the chest radiograph had evidence of bacterial infection. The proportion of patients with increased WBC or ESR did not differ between bacterial and viral pneumonias, but differences in the CRP levels of >40 mg/l, >80 mg/l, and >120 mg/l were significant although the sensitivity for detecting bacterial pneumonia was too low for use in clinical practice. CONCLUSIONS: Most children with alveolar pneumonia, especially those with lobar infiltrates, have laboratory evidence of a bacterial infection. Interstitial infiltrates are seen in both viral and bacterial pneumonias.

Clinical profile of serologically diagnosed pneumococcal pneumonia.

OBJECTIVE: To describe the characteristics of serologically diagnosed pneumococcal pneumonia and compare them with those of respiratory syncytial virus (RSV) pneumonia and bacteremic pneumococcal pneumonia. METHODS: IgG antibodies to pneumococcal pneumolysin and C-polysaccharide as well as immune complexes containing IgG antibodies to pneumolysin and C-polysaccharide were measured from acute and convalescent sera of 254 children with community-acquired pneumonia. Evidence of pneumococcal infection was found in 93 children. Clinical and laboratory data were retrospectively collected from the records of 38 children with sole (all tests for 16 other microbes negative) pneumococcal pneumonia and compared with 26 sole RSV-induced pneumonia from the present series and with the data of our 85 bacteremic pneumococcal pneumonia cases reported earlier. RESULTS: Serologically diagnosed sole pneumococcal pneumonia clinically overlapped with RSV pneumonia, but RSV pneumonia was more often associated with tachypnea (45% vs. 17%, P < 0.05) and low white blood cell counts (means, 12.0 x 109/l vs. 20.8 x 109/l; P < 0.001) as well as low serum C-reactive protein levels (means, 28 mg/l vs. 137 mg/l; P < 0.001). Alveolar infiltrates were found in 15% of chest radiographs of children with RSV pneumonia compared with 76% of those in children with sole pneumococcal pneumonia (P < 0.001). Patients with bacteremic pneumonia more often appeared ill (79% vs. 50%, P < 0.001) and more often had typical pneumococcal pneumonia with high fever, leukocytosis and lobar infiltrates in their chest radiographs (70% vs. 34%, P < 0.05) than those with serologically diagnosed pneumococcal pneumonia. CONCLUSIONS: Serologically detected pneumococcal pneumonia differs significantly from RSV pneumonia in laboratory and chest radiography findings, but the clinical signs and symptoms overlap considerably. Bacteremic pneumococcal pneumonia is a more severe illness than the serologically diagnosed one.

Streptococcus pneumoniae and Mycoplasma pneumoniae coinfection in community acquired pneumonia.

The characteristics of nine children with community acquired pneumonia with evidence of Streptococcus pneumoniae and Mycoplasma pneumoniae coinfection are described.

Serum procalcitonin, C-reactive protein and interleukin-6 for distinguishing bacterial and viral pneumonia in children.

OBJECTIVE: Serum procalcitonin (PCT), C-reactive protein (CRP) and interleukin-6 (IL-6) concentrations were measured in 126 children hospitalized for community-acquired, radiologically confirmed pneumonia to assess whether these host response values could be used to distinguish bacterial from viral pneumonia. METHODS: The samples for PCT, CRP and IL-6 measurements were obtained on admission or the first day of hospitalization. The etiology of pneumonia was studied with an extensive panel of methods that detected 6 bacteria and 11 viruses. RESULTS: In all, 54% had evidence of bacterial pneumonia, and 32% had evidence of sole viral pneumonia. In 14% of the cases the etiology could not be determined. Children with bacterial pneumonia had significantly higher PCT (median 2.09 ng/ml vs. 0.56 ng/ml, P = 0.019) and CRP concentrations (96 mg/l vs. 54 mg/l, P = 0.008) than those with sole viral etiology. However, the values markedly overlapped. No significant difference in IL-6 concentrations was seen between the two patient groups. Using PCT > or = 2.0 ng/ml, CRP > or = 150 mg/l or IL-6 > or = 40 pg/ml, the specificity was > or =80% for bacterial pneumonia. The sensitivities with these cutoff values were 50% for PCT, 31% for CRP and 34% for IL-6. CONCLUSIONS: The results indicate that the measurement of serum PCT, CRP and IL-6 has little value in the differentiation of bacterial and viral pneumonia in children. However, in some patients with very high serum PCT, CRP or IL-6 values, bacterial pneumonia is probable.

Etiology of community-acquired pneumonia in 254 hospitalized children.

BACKGROUND: Childhood community-acquired pneumonia is a common illness, but there have been relatively few comprehensive studies of the viral and bacterial etiology in developed countries. The aim of the present investigation was to determine the etiology of community-acquired pneumonia in hospitalized children by several laboratory methods. METHODS: In a 3-year prospective study a nasopharyngeal aspirate for viral studies and acute and convalescent serum samples for viral and bacterial serology were taken from 254 children with symptoms of acute infection and infiltrates compatible with pneumonia in the chest radiograph. The role of 17 microbes was investigated. RESULTS: A potential causative agent was detected in 215 (85%) of the 254 patients. Sixty-two percent of the patients had viral infection, 53% had bacterial infection and 30% had evidence of concomitant viral-bacterial infection. Streptococcus pneumoniae (37%), respiratory syncytial virus (29%) and rhinovirus (24%) were the most common agents associated with community-acquired pneumonia. Only one patient had a positive blood culture (S. pneumoniae) of 125 cultured. A dual viral infection was detected in 35 patients, and a dual bacterial infection was detected in 19 patients. CONCLUSIONS: The possible causative agent of childhood community-acquired pneumonia can be detected in most cases. Further studies are warranted to determine what etiologic investigations would aid in the management of pneumonia. With effective immunization for S. pneumoniae and respiratory syncytial virus infections, more than one-half of the pneumonia cases in this study could have been prevented.

Oral prednisolone is an effective adjuvant therapy for acute otitis media with discharge through tympanostomy tubes.

OBJECTIVE: To determine the efficacy of a short course of oral prednisolone as an adjuvant therapy for acute otitis media draining through tympanostomy tubes. STUDY DESIGN: In a randomized, double-blind, placebo-controlled study, children with acute discharge (<48 hours) through tympanostomy tubes received either prednisolone (2 mg/kg/d; n = 23) or placebo (n = 27) for 3 days. All children received amoxicillin/clavulanate (40/10 mg/kg/d) for 7 days. The children were examined daily at the study clinic until the drainage ceased. RESULTS: The median duration of otorrhea in the prednisolone group was 1.0 days (25% to 75% range, 1.0 to 2.0 days), compared with 3.0 days (25% to 75% range, 2.0 to 4.0 days) in the children receiving placebo (P <.001). The duration of otorrhea was

Wild type p53 can mediate sequence-specific transactivation of an internal promoter within the mdm2 gene.

The p53 tumor suppressor gene product can complex with polypeptides encoded by the mdm2 putative protoncogene. In addition, mdm2 mRNA levels have been shown to increase following the activation of wild type (wt) p53. To determine the basis for the effect of wt p53 on mdm2 mRNA, we studied the interaction of the mdm2 gene with p53. We report that wt p53 can bind sequence-specifically to a DNA region residing downstream to exon 1 of the mdm2 gene. This is correlated with a pronounced p53-dependent transcriptional activation. Efficient p53-dependent transactivation can be obtained with an mdm2 genomic DNA fragment lacking the putative mdm2 promoter. These findings suggest that p53 can induce transcription from an internal promoter located within the mdm2 gene. These findings raise the possibility that, in addition to increasing the overall levels of mdm2 mRNA, wt p53 may also modulate the repertoire of mdm2 transcripts present within the cell.

mdm2 expression is induced by wild type p53 activity.

We have recently characterized a 95 kDa protein, p95, which exhibits enhanced binding to temperature-sensitive p53 (ts-p53) when cells are shifted down to 32.5 degrees C, a temperature at which ts-p53 possesses wild-type (wt)-like activities. In the present study we show that p95 is a product of the mdm2 putative proto-oncogene. The enhanced complex formation of mdm2 with ts-p53 in cells maintained at 32.5 degrees C is due to an elevation in total mdm2 protein levels following the temperature shift. We further demonstrate that the induction of mdm2 expression by t p53 activity is at the mRNA level. The induction occurs with very rapid kinetics and does not require de novo protein synthesis, suggesting a direct involvement of p53 in the process. Based on these data and on recent findings implicating p53 as a transcription factor, we suggest that the mdm2 gene is a target for activation by wt p53. In view of the ability of mdm2 to act as a specific antagonist of p53 activity, this induction process may serve to tightly autoregulate p53 activity in living cells.