Nasal inflammation and chronic ear disease in Australian Aboriginal children

Objective : Chronic middle ear disease is common in Aboriginal children, and may be linked to nasal inflammation and Eustachian tube dysfunction. The pattern of nasal inflammation is unknown. The study reported here was performed to define the role of allergy and infection in causing nasal inflammation in Aboriginal children with chronic middle ear disease.
Methodology : Thirty-one Aboriginal children aged between 3 and 7 years underwent clinical assessment, audiometry and allergy skin tests. Nasal swabs for bacterial culture and cytology were performed during the winter and again in spring to identify any seasonal variation. A randomized trial of nasal beclomethasone for 8 weeks was conducted in children with abnormal tympanometry to identify the effect of therapy upon nasal cytology.
Results : Twenty-six of the 31 children had abnormal tympanograms. Average hearing levels were reduced in nine children. Pathogenic organisms were isolated from most children: Streptococcus pneumoniae (82%), Haemophilus influenzae (79%), Moraxella catarrhalis (39%) and Staphylococcus aureus (29%). Eight of the 31 children (26%) were atopic. Nasal cytology disclosed a marked neutrophil infiltrate (80% of cells) during the winter, which fell significantly in spring to 52% of cells. Only two subjects had nasal eosinophilia of >10%. There was no effect of beclomethasone on nasal cytology.
Conclusions : Chronic ear disease in Aboriginal children is associated with nasal inflammation, neutrophil infiltration and the presence of bacteria. These features suggest respiratory infection as the main cause of chronic nasal inflammation in Aboriginal children with middle ear disease. There is a seasonal variation in the severity of the nasal infiltrate, consistent with increased infections during winter. Despite a high prevalence of atopy, allergic nasal disease was uncommon.     

Pericardial effusion complicating a percutaneous central venous line in a neonate

A premature infant developed pericardial effusion four days after the insertion of a 25-gauge silastic percutaneous central venous catheter. The effusion contained parenteral nutrition fluid and resolved rapidly after withdrawal of the catheter. Pericardial effusion is a potential complication of percutaneous, as well as surgically placed, central venous catheters.     

Mental health and psychosocial functioning in adolescents with congenital heart disease. A comparison between adolescents born with severe heart defect and atrial septal defect

Twenty-six adolescents, aged 13–18 years, with severe congenital heart disease were matched for sex, age and living area with 26 adolescents with repaired atrial septal defect and regarded as physically fit. These two groups were compared according to somatic condition, psychopathology, psychosocial functioning and chronic family difficulties. A higher rate of psychiatric problems in the complex group, an association between psychosocial functioning and physical capacity, as well as an association between psychosocial functioning and chronic family difficulties were observed. These findings suggest that physical capacity is of crucial importance for mental health and functioning of adolescents with congenital heart disease. The association with chronic family difficulties also suggests that a comprehensive biopsychosocial approach is necessary in the treatment and rehabilitation of these patients.     

Auxology and response to growth hormone treatment of patients with intrauterine growth retardation or Silver-Russell syndrome: analysis of data from the Kabi Pharmacia International Growth Study

Using the database from the Kabi Pharmacia International Growth Study, 105 patients with intrauterine growth retardation (IUGR) (82 males, 23 females) and 45 with Silver-Russell syndrome (SRS) (32 males, 13 females) with persistent postnatal growth failure were studied. Patients with IUGR had a birth length and birth weight more than 2 SD below the mean for gestational age. Their height deficit at the start of GH treatment was -3.0 SDS at a median chronological age of 8.7 years and a median bone age of 7.0 years. Mean paternal and maternal heights were 166 and 153 cm, respectively. The median dose of GH was 0.5 IU/kg/week, given at a median frequency of five injections/week. The median height SDS for chronological age after 1, 2 and 3 years of GH treatment were -2.5, -2.1 and -1.9, respectively. In the 45 patients with SRS, median chronological age and median bone age at the start of treatment were 6.7 and 3.2 years, respectively, and mean paternal and maternal heights were 167.5 and 160 cm, respectively. The median dose of GH was 0.7 IU/kg/week, given at a median frequency of six injections/week. The median height SDS for chronological age at the start of treatment and after 1, 2 and 3 years were -3.5, -2.9, -2.8 and -2.2, respectively. Although the criteria used by physicians when diagnosing SRS were not controlled or verified in this study, it appears that patients with SRS can be differentiated from those with IUGR with persistent growth failure by their reduced bone age for chronological age at the start of treatment, and by the fact that patients with SRS tended to be born to parents of normal height. GH treatment in both groups induced catch-up growth, though long-term follow-up studies will be required to assess the effects of treatment on final height.     

Urinary albumin excretion and transcapillary escape rate of albumin in malignancies

Transcapillary escape rate of albumin was determined in 22 patients with different malignancies. In addition, urinary albumin excretion rate was measured in 24-h urine samples using a sensitive immunoassay. Increased urinary albumin excretion was defined as ≥20 μg/min according to conventional standards. Renal glomerular filtration and tubular function was estimated by⁵¹Cr-EDTA plasma clearance and urinary beta 2-microglobulin, respectively. Median urinary albumin excretion rate was 15.0 μg/min (range 6–510 μg/min) and the frequency of increased urinary albumin excretion was 41%. This agrees with other studies showing increased albuminuria in several types of malignant diseases. Patients with advanced disease (tumour, node, metastasis (TNM) stage II–IV) had a significantly higher urinary albumin excretion rate than patients with localized disease (TNM stage I). Serum creatinine, glomerular filtration rate and urinary beta 2-microglobulin were all within normal limits. Median transcapillary escape rate of albumin was 5.5%/h (range 2–8%/h) and this level is comparable with values in healthy subjects. There was no significant difference in transcapillary escape rate between patients with elevated urinary albumin excretion and the normoalbuminuric group. Median value of the absolut outflux of albumin was 10.6 g/h with similar levels in patients with increased urinary albumin excretion and patients with normoalbuminuria. Our results indicate a high prevalence of minor glomerular dysfunction with a slightly elevated urinary albumin excretion in patients with malignancies. The normal endothelial function, as estimated by the transcapillary escape rate of albumin, suggests an overal unaffected capillary permeability and increased urinary albumin loss appears to be an isolated renal phenomenon in cancer patients.     

Circadian changes in PACAP type 1 (PAC1) receptor mRNA in the rat suprachiasmatic and supraoptic nuclei

A receptor for pituitary adenylate cyclase activating polypeptide (PACAP), denoted as PAC₁, is expressed in the suprachiasmatic nuclei (SCN). Since the circadian clock demonstrates phase-dependent sensitivity to PACAP, we have used in situ hybridization histochemistry to examine whether PAC₁ mRNA is differentially expressed in the rat SCN across the 24-h cycle. There was a significant variation in PAC₁ mRNA within the SCN and supraoptic nuclei during the light–dark cycle and in constant darkness, with peaks at the middle of both the real and subjective day and night; no significant variation was observed in the cingulate cortex. The results suggest that the phase-dependent actions of PACAP on the clock may involve phase-specific changes in the availability of PAC₁ receptors within the SCN.     

Target definition in prostate, head, and neck

Target definition is a major source of errors in both prostate and head and neck external-beam radiation treatment. Delineation errors remain constant during the course of radiation and therefore have a large impact on the dose to the tumor. Major sources of delineation variation are visibility of the target including its extensions, disagreement on the target extension, and interpretation or lack of delineation protocols. The visibility of the target can be greatly improved with the use of multimodality imaging. Both in the head and neck and the prostate, computed tomography (CT)-magnetic resonance imaging coregistration decreases the target volume and its variability. CT-positron emission tomography delineation is promising for delineation in head and neck cancer. Despite the better visibility, a different interpretation of the target extension remains a major source of error. The use of coregistration of CT with a second modality, together with improved guidelines for delineation and an online anatomical atlas, increases agreement between observers in prostate, lung, and nasopharynx tumors. Delineation errors should not be treated differently from other geometrical errors. Similar margin recipes for the correction of setup errors and organ motion should be adapted to incorporate the effect of delineation errors. A calculation of a 3-dimensional clinical target volume-planning target volume margin incorporating delineation errors for the head and neck is around 6.1 to 9.7 mm. Given the good local control of IMRT with smaller margins and smaller pathological specimens, it is likely that the delineated CTV frequently overestimates the actual volume.     

Homocysteine and the kidney

Plasma homocysteine concentration exhibits a strong relationship with (indices of) renal function. Hyperhomocysteinemia has been implicated in the high vascular event rate in patients with chronic renal failure. The precise pathophysiological explanation for the occurrence of hyperhomocysteinemia in renal failure is not yet elucidated. A defective intrinsic renal metabolism of homocysteine seems unlikely. There are several indications that whole body homocysteine metabolism is altered in renal insufficiency. Stable isotope studies in dialysis patients have shown a decreased homocysteine clearance by transsulfuration and decreased homocysteine remethylation and methionine transmethylation. Several, but not all, prospective studies have linked hyperhomocysteinemia to adverse cardiovascular outcomes in renal failure patients. Treatment of hyperhomocysteinemia in renal insufficiency is based on folic acid-containing regimens, but so far, none of the regimens has been shown to successfully normalize plasma homocysteine concentration. Intervention studies have not yet demonstrated beneficial vascular effects of homocysteine-lowering treatment in dialysis patients.