Erythropoietin levels in children and adolescents with inflammatory bowel disease

Iron deficiency anemia (IDA) and anemia of chronic disease (CDA) are often encountered in patients with inflammatory bowel disease (IBD). Inadequate intake or loss of iron is a clear cause of IDA, but mechanisms of CDA induction are multifactorial and involve erythropoiesis disturbance due to circulating inflammation mediators. The authors investigated erythropoietin (Epo) levels in children and adolescents with IBD and correlated them to disease activity, with the aim of gaining an improved understanding of the role of Epo in CDA. Thirty-three patients with IBD were examined (18 boys, 15 girls) ages 4 to 15 years (median 11 years). Two study groups related to the disease activity were formed: group A, those with active disease (n = 21), and group B, those in remission (n = 12). Epo levels were measured using a two-site chemiluminescence immunoassay. Predictive Epo values in response to the degree of anemia were calculated by the equation: logEpo = (3.48 - 0.20) x Hb. According to the results, CDA anemia was present only in patients with active disease. These patients also had a significantly higher possibility of altered Epo levels than expected compared with patients with inactive disease (16/21 vs. 4/12, P < 0.05). It was also interesting that most of the patients with anomalous Epo concentrations presented with an elevated Epo value compared with that expected from the calculation (14/20). It seems that disturbed Epo concentrations are correlated with disease activity in children and adolescents with IBD. It is possible that failure of the bone marrow to respond to increased Epo levels leads to further incremental response. These in turn lead to the high Epo concentrations detected in most of the authors' patients. Impaired Epo production is another mechanism of CDA development and is the one mainly expressed in patients with low Epo values.     

Bithalamic infarcts: embolism of the top of basilar artery or deep cerebral venous thrombosis?

Bithalamic infarcts are usually attributed to thromboembolism of the top of the basilar artery. However, in some cases, deep cerebral venous thrombosis and thrombosis of cerebral venous sinuses was proved to be the cause. The case of a 47-year-old female with ischemic thalamic and mesencephalic lesions is reported, that was attributed to thrombosis of internal cerebral veins. In cases of bithalamic infarcts, apart from the top of the basilar artery syndrome, deep cerebral venous thrombosis should be taken into consideration. Neuroimaging findings such as generalized cerebral edema, multiple infarcts or hemorrhages, hyperdense appearance of cerebral sinuses or veins and filling defects in the cerebral venous sinuses in contrast-CCT, can lead to the proper diagnosis.     

Testicular descent related to growth hormone treatment

An 8.7 year-old boy with cryptorchidism and growth hormone (GH) deficiency due to septooptic dysplasia presented testicular descent related to the commencement of hGH treatment. This case suggests a role for GH in testicular descent.     

Selection of obstetrics and gynecology residents on the basis of medical school performance

OBJECTIVE: The purpose of this study was to determine whether United States Medical Licensing Examination scores during medical school predict resident-in-training examination scores and whether other criteria of medical student performance correlate with the faculty's subjective evaluation of resident performance. STUDY DESIGN: United States Medical Licensing Examination step I and II scores for 24 residents were compared to their scores on in-training examinations. Faculty evaluated 20 graduated residents by rating both their cognitive and noncognitive clinical performance. Scores from these evaluations were compared with several criteria of their medical school performance. Statistical analysis for all comparisons was linear regression. RESULTS: United States Medical Licensing Examination scores positively correlated with in-training examination scores. United States Medical Licensing Examination scores, honor grades in student clinical rotations, and student interview scores did not correlate with the faculty evaluation of resident performance. CONCLUSION: Standardized tests of medical student cognitive function predict the resident's performance on standardized tests. Selection criteria that are based on other medical school achievements do not necessarily correlate with overall performance as residents in obstetrics and gynecology.     

High prevalence of decreased cortisol reserve in brain-dead potential organ donors

OBJECTIVE: To investigate the adrenocortical function in brain-dead patients, potential organ donors. DESIGN: Prospective study. SETTING: Intensive care units in two teaching hospitals. PATIENTS: A total of 37 patients (28 men, nine women) with severe brain injury, having a mean age of 42 +/- 18 yrs, were included in the study. Group A consisted of 20 brain-injured patients who did not deteriorate to brain death. Group B included 17 brain-injured patients who were brain dead; of these, ten patients developed brain death during ICU stay and seven patients were admitted to the ICU after clinical brain death. INTERVENTIONS: In all patients (group A and group B), a morning blood sample was obtained at admission to the ICU to determine baseline plasma cortisol. Subsequently, 1 microg of corticotropin (adrenocorticotropic hormone, Synacthen) was administered intravenously, and a blood sample was taken 30 mins after the injection. In group B patients who became brain dead while being treated in the ICU (n = 10), the same procedure was repeated the morning after the confirmation of brain death. Patients having a cortisol level of at least 18 microg/dL after the administration of adrenocorticotropic hormone were defined as responders. MEASUREMENTS AND MAIN RESULTS: After the occurrence of brain death, group B patients had significantly lower values for baseline (8.5 +/- 6.2 vs. 17.0 +/- 6.6 microg/dL, p <.001) and stimulated (16.9 +/- 6.3 vs. 23.9 +/- 5.7 microg/dL, p =.001) plasma cortisol compared with group A patients. Thirteen group B patients (76%) and two group A patients (10%) were nonresponders to adrenocorticotropic hormone (p <.001). In group B patients, baseline and stimulated cortisol concentrations were significantly related (r =.71, p =.001), whereas there was no correlation between baseline cortisol and the increment in cortisol (r = -.37, p =.15). Mean hormonal data of the ten brain-dead patients studied at admission in the ICU and after the occurrence of brain death were the following: baseline plasma cortisol (23.5 +/- 11.4 vs. 6.8 +/- 4.2 microg/dL, p =.003) and stimulated serum cortisol (28.8 +/- 9.9 vs. 16.3 +/- 4.3 microg/dL, p =.008). CONCLUSIONS: Adrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors.     

Association of polymorphisms of the estrogen receptor alpha gene with bone mineral density and fracture risk in women: a meta-analysis.

The contribution of genetic polymorphisms to bone mineral density (BMD) and fracture risk in women is a controversial topic. We evaluated the effect of the XbaI and PvuII polymorphisms of the estrogen receptor a to BMD and fracture risk in a meta-analysis, including published data and additional information from investigators. Five thousand eight hundred thirty-four women from 30 study groups were analyzed with fixed and random effects models. The PvuII polymorphism was not associated with BMD at any skeletal site examined and 95% CIs exclude effects over 0.015 g/cm2 for both the femoral neck and the lumbar spine. Conversely, XX homozygotes (women carrying two copies of the gene variant without an XbaI restriction site) consistently had higher BMD than other subjects. The magnitude of the effect was similar in the femoral neck and lumbar spine (0.014 g/cm2 [95% CI, 0.003-0.025] and 0.015 g/cm2 [95% CI, 0.000-0.030], respectively; no between-study heterogeneity for either). Total body BMD was also significantly higher in XX homozygotes (by 0.039 g/cm2 and 0.029 g/cm2 compared with Xx and xx, respectively). Available data on fractures suggested a protective effect for XX (odds ratio [OR], 0.66 [95% CI, 0.47-0.93] among 1591 women), but not PP (OR, 0.93 [95% CI, 0.72-1.18] among 2,229 women). In summary, we have found that XX homozygotes may have higher BMD and also a decreased risk of fractures when compared with carriers of the x allele, whereas the PvuII polymorphism is not associated with either BMD or fracture risk.