Dutch Paediatric Surveillance Unit

High cardiovascular risk in severely obese young children and adolescents.

Posted by

0


Abstract

Objective To assess the prevalence of cardiovascular risk factors in severely obese children and adolescents.

Methods A nationwide prospective surveillance study was carried out from July 2005 to July 2007 where paediatricians were asked to report all new cases of severe obesity in 2–18-year-old children to the Dutch Paediatric Surveillance Unit. Severe obesity is defined by gender and age-dependent cut-off points for body mass index based on Dutch National Growth Studies corresponding to the adult cut-off point of 35 kg/m2. Paediatricians were asked to complete a questionnaire for every severely obese child regarding socio-demographic characteristics and cardiovascular risk factors (blood pressure, fasting blood glucose and lipids).

Results In 2005, 2006 and 2007, 94%, 87% and 87%, respectively, of paediatricians in the Netherlands responded to the monthly request from the Dutch Paediatric Surveillance Unit and 500 children with newly diagnosed severe obesity were reported. 72.6% (n=363) of paediatricians responded to a subsequent questionnaire. Cardiovascular risk factor data were available in 255/307 (83%) children who were correctly classified as severely obese. 67% had at least one cardiovascular risk factor (56% hypertension, 14% high blood glucose, 0.7% type 2 diabetes and up to 54% low HDL-cholesterol). Remarkably, 62% of severely obese children aged ≤12 years already had one or more cardiovascular risk factors.

Conclusion A high number (2/3) of severely obese children have cardiovascular risk factors. Internationally accepted criteria for defining severe obesity and guidelines for early detection and treatment of severe obesity and comorbidity are urgently needed.

Source: BMJ.

 

 

Mood disorder as a specific complication of stroke

Appraising the impact of Folstein et al’s1 1977 report on ‘Mood disorder as a specific complication of stroke’ is a challenging task for someone who did not enter medical school until the mid-1980s. Stroke changed in the 1970s, and the view in retrospect appears unrecognisable. This was a dramatic change, from an intellectual backwater too dull for neurologists to even bother seeing, to become a hot topic: a disease to be studied in mega trials and a standard bearer for evidence based medicine. Prior to the 1970s, with the exception of dysphasia, neuropsychiatric complications had been given scant thought—it was a disorder that affected how people walked. It was recognised that some elderly patients became depressed after stroke but the prevailing view appeared to be “so what, they’re old and infirm, what do you expect?” It is against this backdrop that the work of researchers at John Hopkins has to be judged.

The importance of the paper was perhaps not the findings but the very fact that they published the study at all. Two years earlier their John Hopkins colleague Robert Robinson published a fascinating study demonstrating that experimentally induced strokes in rats led to alteration in cerebral metabolism of catecholamines that correlated with behavioural changes in the rats that mimicked depression.2 Folstein’s data appeared to be an early example of translational research and were widely disseminated as they appeared to link laboratory based neurobiology with clinical practice. Tantalisingly it seemed to offer a human model for studying the anatomy of depression. Appearing, as it did, contemporaneously with the development of cerebral imaging techniques, this was the impetus researchers had needed. Over the next 2 decades, 143 reports were made on this topic. Sadly, the theory of anatomical location of brain lesions as a simplistic explanation for mood disorder did not stand up to scrutiny.3 It was perhaps too good to be true; a salient reminder of the need for confirmation in humans of findings from animal models.

In critical analysis the paper itself has suffered with the passage of time. Epidemiological techniques have advanced, as has expectation of sample sizes and analysis strategies. Future investigators submitting to the journal are unlikely to get a case control study past peer review without any statistical comparisons! But for all that, it is a well written report that gets its key messages across clearly and succinctly, perhaps because the manuscript was not cluttered with t tests and hazard ratios, and that is something editors welcome in any era.

And the key messages were important—the realisation that depression after stroke was not simply an understandable reaction to disability has stood the test of time. We now know that 33% of stroke patients suffer from depression (95% CI 29% to 36%).4 We now know that this depression leads to increased disability5 and probably increased mortality.6 Most importantly, we now know that antidepressants are effective in treating it.7 Countless patients round the world are benefiting from this knowledge and that is an impact that any researcher can be proud of.

Footnotes

  • Competing interests None.
  • Provenance and peer review Commissioned; not externally peer reviewed.

References

  1. ↵
    1. Folstein MF,
    2. Maiberger R,
    3. McHugh PR

. Mood disorder as a specific complication of stroke. J Neurol Neurosurg Psychiatry 1977;40:1018–20.

[Abstract/FREE Full text]

  1. ↵
    1. Robinson RG,
    2. Shoemaker WJ,
    3. Schlumpf M,
    4. et al

. Effect of experimental cerebral infarction in rat brain on catecholamines and behaviour. Nature 1975;255:332–4.

[CrossRef][Medline]

  1. ↵
    1. Carson AJ,
    2. Machale S,
    3. Allen K,
    4. et al

. Depression after stroke and lesion location: a systematic review. Lancet 2000;356:122–6.

[CrossRef][Medline][Web of Science]

  1. ↵
    1. Hackett ML,
    2. Yapa C,
    3. Parag V,
    4. et al

. Frequency of depression after stroke: a systematic review of observational studies. Stroke 2005;36:1330–40.

[Abstract/FREE Full text]

  1. ↵
    1. Pohjasvaara T,
    2. Vataja R,
    3. Leppavuori A,
    4. et al

. Depression is an independent predictor of poor long-term functional outcome poststroke. Eur J Neurol 2001;8:315–19.

[CrossRef][Medline][Web of Science]

  1. ↵
    1. House A,
    2. Knapp P,
    3. Bamford J,
    4. et al

. Mortality at 12 and 24 months after stroke may be associated with depressive symptoms at 1 month. Stroke 2001;32:696–701.

[Abstract/FREE Full text]

  1. ↵
    1. Hackett ML,
    2. Anderson CS,
    3. House A,
    4. et al

. Interventions for treating depression after stroke. Cochrane Database Syst Rev 2008;4:CD003437.

Search Google Scholar

Source:BMJ