Empirically supported treatments in pediatric psychology: disease- related pain

OBJECTIVE: To evaluate psychological literature addressing interventions for disease-related pain in children. METHODS: We conducted a literature review of all studies using psychological interventions for pain stemming directly from disease process as well as pain secondary to disease treatment. RESULTS: Few empirically validated psychological approaches to the treatment of disease pain were found. Although existing intervention studies do not meet Chambless criteria, some promising strategies were identified. CONCLUSIONS: Clinical evidence suggests that cognitive-behavioral strategies for the management of disease pain in children are promising and manualized, controlled intervention studies are needed.      

Is there heterozygote expression of growth hormone receptor deficiency?

Expression of heterozygosity for the defect in the growth hormone (GH) receptor has been proposed to be reflected in stature, and in GH binding protein (GHBP) and insulin-like growth factor I (IGF-I) levels in parents and other relatives of patients with GH receptor deficiency (GHRD; Laron syndrome). The Ecuadorean population with GHRD, in which heterozygosity can be accurately determined in clinically unaffected relatives of probands, offers a unique opportunity to consider this issue. It has previously been demonstrated that 17 parents heterozygous for the Ecuadorean mutation of the GH receptor differed little in biochemical measures (GHBP, IGF-I, IGF-II, IGFBP-2 and IGFBP-3) from Ecuadorean controls. Mean height SDS of 24 non-carrier siblings (−1.3 ± 0.95 SD) and 41 heterozygote siblings or offspring of probands (−1.8 ± 1.15) did not differ significantly ( p = 0.08). Thus, although there may be slight heterozygote expression of the defective gene for the GH receptor, there is no rationale for counselling based on such minimal variation.     

Heart rate increases in patients with growth hormone receptor deficiency treated with insulin-like growth factor I

Cardiac function was measured in 16 prepubertal Ecuadorean patients with growth hormone receptor deficiency given insulin-like growth factor I (IGF-I) during part of a clinical trial. The IGF-I was given subcutaneously twice daily at a dose of 40 μg/kg on days 1 and 2, 80 μg/kg on days 3 and 4, and 120 μg/kg thereafter. Heart rate was determined at baseline (pretreatment) and on days 1–7 by repeated palpation of the radial artery and at baseline and on days 2, 4 and 7 by continuous portable Holter monitoring. Heart rate measured by both methods rose progressively with increasing doses of IGF-I. The mean palpated pulse exceeded baseline on each treatment day and was significantly higher on day 5 than day 4 and significantly higher on day 3 than day 2. The mean Holter heart rate was significantly higher on day 4 than on day 2 and significantly higher on day 2 than at baseline. Non-significant glucose and electrolyte changes did not appear to be associated with the cardiac events.     

Effects of insulin-like growth factor I treatment on the molecular distribution of insulin-like growth factors among different binding proteins

The molecular distribution of insulin-like growth factor I (IGF-I) and IGF-II among the IGF binding proteins (IGFBPs) was studied before and during IGF-I therapy in Ecuadorean adults with growth hormone receptor deficiency (GHRD). Of the total circulating IGF-I and IGF-II, 70% was carried by the 150 kDa complex in normal subjects, while in patients with GHRD, 50% of serum IGF-I, but only 30–35% of serum IGF-II, was measured within the 150 kDa IGFBP-3 region. Administration of IGF-I altered the concentration of IGF-I and IGF-II, although the percentage of total IGF measured within each IGFBP region was not affected, as the increase in IGF-I and the decrease in IGF-II were proportional. Similarly, serum concentrations of IGFBP-3 and the acid-labile subunit, measured by radioimmunoassay, were unaltered. Thus, administration of IGF-I to patients with GHRD was unable to correct the aberrant distribution of IGFs among the IGFBPs.     

Transperitoneal laparoscopic radical nephrectomy for bulky renal tumors

Laparoscopic management of kidney cancer is becoming accepted as an alternative to open radical nephrectomy. Technical considerations have limited the application of laparoscopic radical nephrectomy to relatively small, clinically localized tumors. At the National Cancer Institute, we have broadened the indications to include bulky tumors. Herein, we describe the operation with attention to the technical caveats that have been gained with experience.     

Specimen morcellation after laparoscopic radical nephrectomy: confirmation of histologic diagnosis using needle biopsy

BACKGROUND AND PURPOSE: Laparoscopic radical nephrectomy (LRN) is being increasingly offered for the management of renal-cell carcinoma (RCC). Specimen removal may be performed through a small or hand-port incision or by specimen morcellation. Limited studies exist addressing the accuracy of histopathologic diagnosis in morcellated renal tumors. Because of concerns about the lack of a diagnosis secondary to the morcellation process, we performed premorcellation needle biopsies to obtain nondisrupted tissue for pathologic analysis. Herein, we compare the histopathologic diagnosis achieved via needle biopsy prior to morcellation with that of the final specimen. PATIENTS AND METHODS: Following successful laparoscopic resection, specimens were entrapped in a Lapsac. Needle biopsies were performed manually through the mouth of the Lapsac, and morcellation was then done in some patients using manual and mechanical methods. The histopathologic diagnoses in the needle biopsy specimens and the morcellated material were compared. RESULTS: Laparoscopic radical nephrectomy with specimen morcellation was performed in 15 patients. Nine patients had premorcellation needle biopsies. Eight of these biopsies had sufficient tissue for diagnosis of RCC. This finding correlated with final diagnosis from the morcellated material. Perinephric fat invasion was identified in three morcellated specimens. CONCLUSIONS: Needle biopsy prior to specimen morcellation confirmed the histologic diagnosis of the morcellated specimen. This finding suggests that such histopathology material is adequate for diagnosis and may make premorcellation needle biopsy redundant.     

Family conflict and slow growth

AIMS: Having previously observed that slow growth in childhood is associated with subsequent labour market disadvantage, an attempt was made to determine whether family conflict is associated with slow growth to age 7 years, independently of material disadvantage. METHODS: A total of 6574 children born between 3 and 9 March 1958 who were members of the British National Child Development Study were used in these analyses. Slow growth at age 7 years was indicated by short stature defined as the lowest fifth of the height distribution. In multivariate analysis, adjustment was made for fully attained adult height as a measure of genetically predetermined height. RESULTS: A total of 31.1% of children who had experienced family conflict were of short stature compared with 20.2% of those who had not, representing relative odds of 1.79 (95% confidence interval (CI) 1.39 to 2.30). After adjustment for social class, crowding, sex, and predetermined height, the relative odds were slightly reduced to 1.62 (95% CI 1.18 to 2.23). A total of 44.0% of children from the most crowded households were of short stature compared with 16.4% of those from the least crowded. The unadjusted relative odds were 3.99 (95% CI 2.94 to 5.41) and after adjustment for the potential confounding variables they were 3.07 (95% CI 2.08 to 4.51). Low social class was also a risk for short stature at age 7 years, but this was not statistically significant after adjustment for the other confounding factors. CONCLUSIONS: Family conflict during childhood was independently associated with slow growth to age 7 years.     

Analysis of 7-methylbenz[a]anthracene-DNA adducts formed in SENCAR mouse epidermis by 32P-postlabeling

The present study has analysed the DNA adducts formed in SENCAR mouse epidermis following topical application of 7-methylbenz[a]anthracene (7- MBA). Mice were treated with 400 nmol of 7-MBA, which represents an initiating dose of this hydrocarbon for SENCAR mice. DNA adducts were analysed 24 h after topical application of the hydrocarbon by 32P- postlabeling coupled with either HPLC analysis or an improved TLC procedure giving better resolution of DNA adducts through the use of a D6 solvent [isopropanol:4N NH4OH (1:1)] following D5. Twenty-four hours after topical application of 400 nmol 7-MBA, the level of total covalent binding was 0.37 +/- 0.07 pmol/mg DNA as determined by 32P- postlabeling. This level of binding correlated well with the relative tumor initiating activity of this hydrocarbon compared to 7,12- dimethylbenz[a]anthracene (6.4 +/- 0.01 pmol/mg DNA) and dibenz[a,j]anthracene (0.03 +/- 0.01 pmol/mg DNA). Analysis of the 32P- labeled 3',5'-diphosphodeoxyribonucleosides by HPLC and TLC revealed the presence of deoxyguanosine (dGuo) and deoxyadenosine (dAdo) adducts formed from both the anti- and syn-bay-region diol-epoxides of 7-MBA (anti- and syn-7-MBADEs). The major DNA adduct derived from 7-MBA in mouse epidermis was tentatively identified as (+) anti-7-MBADE-trans-N2- dGuo. In addition, a minor dGuo adduct derived from the bay-region syn- diol-epoxide of 7-MBA was detected as well as a minor dAdo adduct from this diol-epoxide. Another minor dAdo adduct was also detectably present which arose from either the anti- or syn-diol epoxide. Furthermore, several unidentified DNA adducts were present in both HPLC and TLC chromatograms of DNA samples from 7-MBA-treated mice. These results are discussed in terms of the role of specific 7-MBA-DNA adducts in tumor initiation by this hydrocarbon.      

Role of gastro-oesophageal reflux in infant irritability

Gastro-oesophageal reflux (GOR) disease may cause excessive crying in infants. The role of GOR was evaluated in infant irritability and an attempt was made to define clinical predictors of pathological reflux. Seventy consecutively admitted infants with irritability and presumptive GOR were retrospectively reviewed. All had undergone prolonged oesophageal pH monitoring. Pathological GOR was defined as a fractional reflux time of > or = 10% and was significantly less common in infants under 3 months (one of 24; 4.2%) than in older infants (10 of 46; 21.7%). All infants with pathological GOR presented with frequent vomiting, and 'silent' pathological reflux did not occur. Poor weight gain, feeding refusal, backarching, and sleep disturbance were not significantly associated with pathological GOR. The results suggest that pathological GOR is an unlikely cause of infant irritability under the age of 3 months.