For personal use. Only reproduce with permission from Elsevier Ltd Comment www.thelancet.com Vol 365 April 16, 2005 1367 2 Solime na M, F olli F , Denis -Sonini S, et al. Aut oantib odies t o gluta mic aci d decarboxylase in a patient with stiff-man syndrome, epilepsy and type I diabetes mellitus. N Engl J Med 1988; 318: 1012–20. 3 Folli F, Sol imena M , Cofie ll R, et al. Aut oantib odies t o a 128 k D synaptic protein in stiff-man syndrome with breast cancer. N Engl J Med 1993; 328: 546–51. 4 Wessig C, Kl ein R, Schnei der MF, To yka K V, Na umann M, So mmer C. Neuropathology and binding studies in anti-amphiphysin-associated stiff- person syndrome. Neurology 2003; 61: 195–98. 5 Yoshid a Y, Kinuta M, Abe T , et al. The st imulat ory ac tion of amphi phys in on dynamin function is dependent on lipid bilayer curvature. EMBO J 2004; 23: 3483–91. 6 Dinkel K, Meinck HM, J ury K M, Karges W, Richter W. Inhibi tion of gamma- aminobutyric acid synthesis by glutamic acid decarboxylase autoantibodies in stiff-man syndrome.Ann Neurol 1998; 44: 194–201. 7 Lohmann T, Hawa M, L eslie RDG, Lane R, Picard J, Lo ndei M. Immune reactivity to glutamic acid decarboxylase 65 in stiff-man syndrome and type 1 diabetes mellitus. Lancet 2000; 356: 31–36. 8 Atk ins on MA. The $6 4 000 que sti on in di abe tes co nti nue s . . . Lancet 2000; 356: 4–6. 9 Dalak as MC , Li M, Fujii M, Jacobo witz D M. St iff p erson s yndr ome: quantification, specificity, and intrathecal synthesis of GAD 65 antibodies. Neurology 2001; 57: 780–84. 10 Brashe ar HR, Phi llips L H. Auto antib odies to G ABAerg ic neuron s and response to plasmapheresis in stiff-man syndrome. Neurology 1991; 41: 1588–92. 11 Koerner C, Wielan d B, Richt er W, Meinck H -M. Stif f-per son synd romes: motor cortex hyperexcitability correlates with anti-GAD autoimmunity. Neurology 2004; 62: 1357–62. 12 Burns TM , Jones H R, Phill ips LH, B ugawan T L, Erli ch HA, Le nnon VA . Clinically disparate stiff-person syndrome with GAD65 autoantibody in a father and daughter. Neurology 2003; 61: 1291–93. 13 Burns TM, Jones HR, Ph illips LH . Stiff per son synd rome doe s not alway s occur with maternal passive transfer of GAD65 antibodies. Neurology 2005; 64: 399–400. 14 Pittock SJ, Kryzer TJ, Lenn on VA. Paran eoplas tic anti bodies coexist and predict cancer, not neurological syndrome.Ann Neurol 2004; 56: 715–19. 15 Antoin e JC, Absi L, Hon norat J, et al. Antiamphip hysin an tibod ies are associated with various paraneoplastic neurological syndromes and tumors.Arch Neurol 1999; 56: 172–77. 16 Saiz A, Dalmau J, Husta Bu tler M, et al. A nti-amphiph ysin I antib odies in patients with paraneoplastic neurological disorders associated with small cell lung cancer.J Neurol Neurosurg Psych 1999; 66: 214–17. 17 Graus F, De lattr e JY, Antoi ne JC, et al. Rec omme nded dia gnostic criteria for paraneoplastic neurological syndromes. J Neurol Neurosurg Psych 2004; 75: 1135–40. Pre-eclampsia remains one of the most complex challenges for perinatal clinicians and researchers. As a major cause of maternal and perinatal mortality and morbidity worldwide, this condition lacks an effective prevention strategy or curative treatment. Furthermore, the efforts to develop screening tests have been disappointing for potential use in clinical practice. Agustin Conde-Agudelo and co-workers recently published a systematic review of screening tests for pre- eclamp sia, derived from 87 studie s in 211369 women. 1 On the basis of a comprehensive review of clinical, biophysical, and biochemical tests, the authors conclude that there is currently no clinically useful screening test to predict the development of pre-eclampsia. Why do we need an efficient screening tool for pre- eclampsia? In general, risk screening is justified when a test is able to define a population that will benefit from an effective preventive treatment (primary prevention), or when earlier diagnosis will lead to more timely intervention that will decrease disease morbidity (secondary prevention). 2 For pre-eclampsia, primary prevention with low-dose aspirin or calcium supplementation is disappointing. 3 A possible reason for this lack of effect is that the large trials that tested interventions recruited low-risk to moderate-risk women, or women judged at high-risk solely on the basis of clinical risk factors. Given that pre-eclampsia is likely to be a heterogeneous condition, potentially involving several separate pathophysiological pathways, it is not surprising that simple clinical indicators are ineffective in identifying women who would benefit from a pathway-specific treatment. Screening for pre-eclampsia: the quest for the Holy Grail? S c i e n c e P h o t o L i b r a r y Rights were not granted to include this image in electronic media. Please refer to the printed journal
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2 Solimena M, Folli F, Denis-Sonini S, et al. Autoantibodies to glutamic aciddecarboxylase in a patient with stiff-man syndrome, epilepsy and type Idiabetes mellitus. N Engl J Med 1988; 318: 1012–20.
3 Folli F, Solimena M, Cofiell R, et al. Autoantibodies to a 128 kD synapticprotein in stiff-man syndrome with breast cancer. N Engl J Med 1993; 328:546–51.
4 Wessig C, Klein R, Schneider MF, Toyka KV, Naumann M, Sommer C.Neuropathology and binding studies in anti-amphiphysin-associated stiff-person syndrome. Neurology 2003; 61: 195–98.
5 Yoshida Y, Kinuta M, Abe T, et al. The stimulatory action of amphiphysinon dynamin function is dependent on lipid bilayer curvature. EMBO J 2004;23: 3483–91.
6 Dinkel K, Meinck HM, Jury KM, Karges W, Richter W. Inhibition of gamma-aminobutyric acid synthesis by glutamic acid decarboxylaseautoantibodies in stiff-man syndrome. Ann Neurol 1998; 44: 194–201.
7 Lohmann T, Hawa M, Leslie RDG, Lane R, Picard J, Londei M. Immune
reactivity to glutamic acid decarboxylase 65 in stiff-man syndrome andtype 1 diabetes mellitus. Lancet 2000; 356: 31–36.
8 Atkinson MA. The $64 000 question in diabetes continues . . .Lancet 2000; 356: 4–6.
9 Dalakas MC, Li M, Fujii M, Jacobowitz DM. Stiff person syndrome:quantification, specificity, and intrathecal synthesis of GAD65 antibodies.Neurology 2001; 57: 780–84.
10 Brashear HR, Phillips LH. Autoantibodies to GABAergic neurons andresponse to plasmapheresis in stiff-man syndrome. Neurology 1991; 41:1588–92.
12 Burns TM, Jones HR, Phillips LH, Bugawan TL, Erlich HA, Lennon VA.Clinically disparate stiff-person syndrome with GAD65 autoantibody in afather and daughter. Neurology 2003; 61: 1291–93.
13 Burns TM, Jones HR, Phillips LH. Stiff person syndrome does not alwaysoccur with maternal passive transfer of GAD65 antibodies. Neurology2005; 64: 399–400.
14 Pittock SJ, Kryzer TJ, Lennon VA. Paraneoplastic antibodies coexist andpredict cancer, not neurological syndrome. Ann Neurol 2004; 56: 715–19.
15 Antoine JC, Absi L, Honnorat J, et al. Antiamphiphysin antibodies areassociated with various paraneoplastic neurological syndromes and
tumors. Arch Neurol 1999; 56: 172–77.16 Saiz A, Dalmau J, Husta Butler M, et al. Anti-amphiphysin I antibodies in
patients with paraneoplastic neurological disorders associated with smallcell lung cancer. J Neurol Neurosurg Psych 1999; 66: 214–17.
1 Conde-Agudelo A, Villar J, Lindheimer M. World Health Organizationsystematic review of screening tests for preeclampsia. Obstet Gynecol2004; 104: 1367–91.
2 Dekker G, Sibai B. Primary, secondary, and tertiary prevention of pre-eclampsia. Lancet 2001; 357: 209–15.
3 Sibai BM. Prevention of preeclampsia: a big disappointment. Am J Obstet Gynecol 1998; 179: 1275–78.
4 Chappell LC, Seed PT, Briley AL, et al. Effect of antioxidants on theoccurrence of pre-eclampsia in women at increased risk: a randomisedtrial. Lancet 1999; 354: 810–16.
5 Roberts JM, Cooper DW. Pathogenesis and genetics of pre-eclampsia.Lancet 2001; 357: 53–56.
6 Harrington K, Carpenter RG, Goldfrad C, Campbell S. Transvaginal Dopplerultrasound of the uteroplacental circulation in the early prediction of pre-eclampsia and intrauterine growth retardation. Br J Obstet Gynaecol 1997;104: 674–81.
suspicious bruising, one of the first tasks is to find out
whether the bruises are the result of abuse or merely a
side-effect of normal childhood activity. If an injury is
found to be a result of abuse, the next question will
invariably be a request about the age of the bruise.
These are the most frequent questions posed to
physicians evaluating maltreated children. How these
questions are answered can determine if a child is
removed from their home or if a parent or caregiver is
criminally prosecuted. The weight of the response
should be balanced by the knowledge of the science:
bruises are one of the most common manifestations of
child abuse. Bruises in active mobile children are very
common.
Recently, Sabine Maguire and colleagues summarised
the current literature about patterns of bruising and
ageing of bruises. In their first article,1 a review of the
literature on bruising in infants and children in general,
they describe their methods. When 6984 papers
spanning 53 years were reviewed, they found 23 papers
met their criteria for full analysis by 15 reviewers. Seven
papers addressed bruising in non-abused children while
two more discussed both abused and non-abused
children. No differences were noted between children
of various socioeconomic groups. Increased bruisingwas noted as age and development advances, during
summer months, and with increased family size. Also,
lack of bruising in children not yet independently
mobile was noted. There was a strong correlation in
areas of bruising in non-abused children: forward, bony
prominences. Abusive bruises had a typical pattern and
distribution as bruises were seen on soft parts of the
body. Fourteen papers covered bruising in abused
children alone and two more discussed both abused
and non-abused children. The head was the most
common site for bruises in abused children.The conclusions are clinically intuitive, but provide a
more empiric literature-based review that provides an
essential framework for any clinician attempting to
determine the cause of bruising. Jenny cautions that
“the aging of bruises is an inexact process” and that
“soft tissue injury is extremely uncommon” in younger
children and the distribution of bruises in abused and
non-abused children differed by development and
age.2 Jenny and colleagues also noted that in infants,
bruising might be an ominous indicator of more
serious maltreatment, namely abusive head injury.
Indeed, when apparently minor bruising was
overlooked in a non-mobile infant, serious and even
fatal injury could follow.3
Maguire and colleagues have done a comprehensive
review of the medical literature for evidence-based
medicine about bruising. Their findings on patterns of
Bruising in children
7 Salomon LJ, Benattar C, Audibert F, et al. Severe preeclampsia is associatedwith high inhibin A levels and normal leptin levels at 7 to 13 weeks intopregnancy. Am J Obstet Gynecol 2003; 189: 1517–22.
8 Florio P, Reis FM, Pezzani I, Luisi S, Severi FM, Petraglia F. The addition of activin A and inhibin A measurement to uterine artery Dopplervelocimetry to improve the early prediction of pre-eclampsia.Ultrasound Obstet Gynecol 2003; 21: 165–69.
9 Audibert F, Benchimol Y, Benattar C, Champagne C, Frydman R. Prediction
of preeclampsia or intrauterine growth restriction by second trimesterserum screening and uterine Doppler velocimetry. Fetal Diagn Ther 2005;20: 48–53.
10 Audibert F, Dommergues M, Benattar C, Taieb J, Thalabard JC, Frydman R.Screening for Down syndrome using first-trimester ultrasound andsecond-trimester maternal serum markers in a low-risk population: aprospective longitudinal study. Ultrasound Obstet Gynecol 2001; 18:26–31.