Less severe retinopathy of prematurity induced by surfactant replacement therapy

To assess the effect of surfactant replacement therapy (SRT) on the prevalence and severity of retinopathy of prematurity (ROP), we compared data from 160 SRT-treated preterm infants with data from 230 historic controls. The prevalence of ROP was 30.6% in the treatment group and 23.4% in the control group. Severe ROP (stages 3-4) was seen in 6.1% of the infants with ROP in the treatment group and 20.3% of the ROP patients in the control group. Surfactant therapy had no influence on the prevalence of ROP (odds ratio 1.4, 95% confidence interval 0.797-2.459, p = 0.242). However, SRT was associated with a decreased risk for severe ROP, compared to mild ROP (odds ratio 0.226, 95% confidence interval 0.056-0.905, p = 0.036). These data suggest that SRT is associated with a decreased risk for severe ROP.     

Influence of clinical status on the association between plasma total and unbound bilirubin and death or adverse neurodevelopmental outcomes in extremely low birth weight infants

Objectives: To assess the influence of clinical status on the association between total plasma bilirubin and unbound bilirubin on death or adverse neurodevelopmental outcomes at 18–22 months corrected age in extremely low birth weight infants. Method: Total plasma bilirubin and unbound bilirubin were measured in 1101 extremely low birth weight infants at 5 ± 1 days of age. Clinical criteria were used to classify infants as clinically stable or unstable. Survivors were examined at 18–22 months corrected age by certified examiners. Outcome variables were death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death prior to follow‐up. For all outcomes, the interaction between bilirubin variables and clinical status was assessed in logistic regression analyses adjusted for multiple risk factors. Results: Regardless of clinical status, an increasing level of unbound bilirubin was associated with higher rates of death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss and death before follow‐up. Total plasma bilirubin values were directly associated with death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death before follow‐up in unstable infants, but not in stable infants. An inverse association between total plasma bilirubin and death or cerebral palsy was found in stable infants. Conclusions: In extremely low birth weight infants, clinical status at 5 days of age affects the association between total plasma bilirubin and death or adverse neurodevelopmental outcomes at 18–22 months of corrected age. An increasing level of UB is associated a higher risk of death or adverse neurodevelopmental outcomes regardless of clinical status. Increasing levels of total plasma bilirubin are directly associated with increasing risk of death or adverse neurodevelopmental outcomes in unstable, but not in stable infants.     

OBSERVER VARIATION IN THE SCINTIGRAPHIC DIAGNOSIS OF SOLITARY COLD THYROID LESIONS

In order to evaluate the reproducibility of the diagnosis of solitary cold thyroid lesions, two specialists in nuclear medicine and two specialists in endocrinology independently twice read 240 thyroid 99mTc pertechnetate scintigrams. No significant difference or interaction between the results obtained from the right and the left lobe was found. A solitary cold lesion was diagnosed in 100 of the 480 lobes; however, in only 30 did all four observers agree upon the diagnosis. Interobserver variation was determined by pairwise comparison of observers. The observed agreement was between 0.91 and 0.94. After adjusting for expected chance agreement, kappa values between 0.57 and 0.70 were found. Intraobserver variation was smaller than interobserver variation, revealing agreement rates of 0.93-0.96 and kappa values between 0.71 and 0.77. Agreement was related to large lesions, lesions located centrally in the lobe, and ovoid-shaped lesions. Clinicians should be aware to what extent they can rely on the information they use in their decisions. The considerable inconsistency in the evaluation of cold lesions on thyroid scintigrams should be taken into consideration, and calls in question the value of using thyroid scintigrams for deciding whether a patient should be referred for operation or biopsy.     

Energy intake and physical activity during pregnancy in relation to maternal fat accretion and infant birthweight

Summary. During the second pregnancy of 56 Swedish women resulting in a term birth, energy intake and physical activity were measured for 3 days at weeks 17 and 33. The values were related to maternal lean body mass, pregnancy weight gain, maternal fat accretion and infant birth-weight by multiple linear regression analyses. A significant regression coefficient was found for energy intake at week 17 on maternal fat accretion. Energy intake was not significantly correlated with infant birthweight, not even when physical activity and maternal lean body mass were taken into account. Thus in a well-nourished Swedish population, energy intake is positively related to maternal fat accretion but not to the birthweight of term infants.     

脾切除对结直肠癌切除术后的影响：一项多中心、嵌入式、配对队列研究

目的探讨医源性脾脏损伤脾切除对结直肠癌切除患者术后长期生存的影响。方法对1990年1月1日至1999年12月31日10年间行结直肠癌手术切除并附带脾切除患者进行病例配对回顾研究。分析患者年龄、性别、依据美国麻醉学医师协会（ASA）标准评估的身体状况、疾病分期、手术类型及预后等资料。配对病例来自同一医疗中心，性别、年龄、疾病分期及手术类型完全相同。手术附带脾切除患者为试验组，未切脾者为对照组。结果55例患者行医源性脾切除术，对照组在年龄、性别、身体状况、疾病分期及手术类型上与之匹配。随访时间（从手术开始到患者死亡或者最后一次随访1为2～205个月（中位随访时间为43个月）。Cox比例危险度模型进行Kaplan-Meier法生存分析发现两组间差异有显著性意义，不切除脾脏对患者生存有利（危险度1．8，95％可信区间为1-3．3，P=0．0399），未切脾组与切脾组5年生存率分别为70％和47％，10年生存率分别为55％和38％。结论结直肠癌患者在行结肠或直肠切除时，因医源性脾脏损伤而切除脾脏者，预后较差。     

Familial Dysalbuminemic Hyperthyroxinemia

ABSTRACT. Jensen IW, Faber J (Department of Endocrinology, Aalborg Hospital North, Aalborg, and Departments of Internal Medicine and Clinical Chemistry, Frederiksberg Hospital, Copenhagen, Denmark). Familial dysalbuminemic hyperthyroxinemia. Acta Med Scand 1987; 221:469–73. A family with familial dysalbuminemic hyperthyroxinemia is described. The syndrome is inherited as an autosomal dominant trait and is characterized by marked elevation of serum thyroxine, due to increased binding of thyroxine to albumin, whereas serum triiodothyronine is normal. Serum free thyroxine is normal when measured with ultrafiltration or equilibrium dialysis, but artefactually high when measured with an analogue assay. The importance of the condition, which is harmless, lies in the misinterpretation of values with subsequent erroneous treatment of thyrotoxicosis. By using an ultrasensitive TSH method it is possible to discriminate between euthyroid and hyperthyroid patients and thereby to avoid incorrect diagnosis in subjects with euthyroid hyperthyroxinemia.     

Differential effects of secretin-fragments imply a dual mechanism of action for secretin

The effects of synthetic peptides, representing different parts of the secretin molecule in isolated mouse pancreatic islets have been investigated in perifusion studies. In the presence of 10 mM D-glucose the C-terminal nonapeptide Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH₂ (S_19–27) showed a 2-fold higher activity than that earlier shown for S_22–27 and had the same effect on the dynamic pattern of insulin release as secretin, while the elongating sequence Leu-Gln-Arg (S_19–21) had no effect on the insulin release. The nonapeptide Leu-Ser-Arg-Leu-Arg-Asp-Ser-Ala-Arg (S_10–18) had no influence on the insulin release. Glu-cagon release seen after intact secretin could not be shown for any of the smaller fragments. Accumulation of CAMP in the islets as seen with secretin, could at 10mmol/L D-glucose only be demonstrated with S_22–27 or S_19–27 but not with S_10–18 or S_1–6. Our results indicate that full size secretin has to be present to stimulate glucagon release while insulin-releasing activity can be confined to the C-terminal part of the hormone.     

Mode of regulation of natural killer cell activity by interferon

Whereas xenogeneic tumors such as baby hamster kidney or HeLa cells grow in nude mice, the same cells persistently infected with a variety of viruses are rejected. Spleen cells from normal nude mice were found to be induced to produce interferon and to exert natural killer (NK) activity on virus persistently infected (PI) tumor cells, and not on uninfected parental cells in vitro. The phenotype of the interferon-producing cells and the NK effector cells was found to be the same namely, Qa 5(+), Ly 5(+), ganglio-N- tetraosylceramide, with 35 percent of the NK cells also expressing Thy 1.2. NK activity against virus PI tumor cell lines could be nonspecifically augmented both in vivo and in vitro by prior contact with virus PI tumor cells. It was unambiguously demonstrated with chemically homogeneous mouse interferon that interferon, and not a contaminant, was responsible for the augmentation of NK activity in vitro. Studies on the mode of interferon action in augmenting NK activity revealed that the target cell for interferon action was serologically distinct from the NK effector cell. Anti-Ly 5 + complement (C)-treated spleen cells were depleted of NK activity and the ability to produce interferon, but, upon incubation with interferon for 1-3 h, regained both NK activity and susceptibility to anti-Ly 5 + C. Treatment with anti-Qa 5 + C eliminated NK activity, which could not be restored by the addition of interferon. We conclude that interferon produced by Ly 5(+) cells in response to virus PI tumor cells acts on Ly 5(-) precursor cells and induces their differentiation into functional Ly 5(+) NK effector cells.     

The effect of gastrin on basal and aminoacid-stimulated insulin and glucagon secretion in man

Abstract. The effect of gastrin on basal and aminoacid-stimulated glucagon and insulin secretion was studied in eleven normal young subjects. The concentrations of glucagon, insulin and gastrin in plasma or serum were measured radioimmunochemically. The results of amino-acid-stimulation were compared to those obtained during a protein-rich meal.
Intravenous injection of synthetic human gastrin-17 in doses from 15.6 ng to 1 μg/kg increased the concentration of glucagon and insulin in peripheral venous blood to a maximum within 5 min. In spite of the enhanced concentrations of insulin induced by gastrin, corresponding concentrations of glucose were either unchanged or increased. Infusion of a mixture of fifteen aminoacids increased the concentrations of glucose, glucagon and insulin. While the increases in glucose and insulin concentrations were similar to those obtained after a protein-rich meal, the glucagon response was much larger after the infusion. Injection of gastrin-17 after 30 min of infusion of aminoacids did not potentiate either the glucagon or the insulin response.
The results indicate that gastrin, besides stimulating insulin secretion, can also stimulate glucagon secretion in a dose-dependent manner. The concentrations of gastrin necessary to stimulate glucagon secretion significantly correspond to the concentrations found in diseases with endogenous hypergastrinaemia (achlorhydria and Zollinger-Ellison syndrome). While gastrin potentiates the glucose-induced insulin secretion, it does not potentiate neither the aminoacid-induced insulin nor glucagon secretion.