Maternal mercury exposure and neuro-motor development in breastfed infants from Porto Velho (Amazon), Brazil

Fish is an important item in the diet of Amazonians, and per se is their best single source of essential nutrients. Rapid urbanization and migration are bringing changes in dietary habits of Amazonians. Exposure to fish-Hg during pregnancy and lactation were studied in 100 women and newborns from Porto Velho. Tissue-Hg concentrations and neurodevelopment (Gesell Developmental Schedules) were assessed at birth and at 6 months in exclusively breastfed infants. Maternal mean frequency of fish consumption was low (<2 meals/week; range 0->7 meals/week) compared to Amazonian standards. Women consuming <2 fish meals/week showed less median hair-Hg (3.5 microgg-1) than women that consumed 2 fish meals/week (5.7 microgg). Median total Hg in maternal hair (5.4 microgg-1) was higher than in newborns (1.6 microgg-1). Significant correlation was observed between maternal hair-Hg and infant hair-Hg at birth (r=0.353; p<0.01) and at six months (r=0.510; p<0.01). Placenta-Hg was also significantly correlated to maternal hair-Hg (r=0.321; p<0.01), newborn hair-Hg (r=0.219; p<0.05), maternal blood-Hg (r=0.250; p<0.01) and to umbilical cord-Hg (r=0.857; p<0.01). Most infants (74%) had normal Gesell Schedules but among the 26% showing neuro-motor development delays only six (7%) had multiple (motor, language, and adaptative) delays. The infants with multiple delays were born from mothers with range of hair-Hg comparable to mothers of normally developed infants. Coincidentally, mothers of infants with multiple delays also showed the lowest range of income and level of education. Fish consumption, income, and level of education varied greatly among these breastfeeding urban mothers. It seems that development delays of exclusively breastfed infants are a component of the health inequalities that accompanies socioeconomic disadvantages.     

A model for calculating costs of hospital-acquired infections: an Italian experience

PURPOSE: Many approaches on the economic aspect of hospital acquired infections (HAIs) have two major limitations: first, the lack of distinction between resources attributable to the management of HAI and resources absorbed by the main clinical problem for which the patient was hospitalized, and second, the lack of an adequate method for calculating the relative costs. These assume that the resources used by HAI can be determined by measuring the extra days of length of days (LOS) of infected patients versus non-infected patients and attribute to extra-LOS a value to the mean total cost. The aim of the article is to test a cost-modelling method that could overcome these limitations by applying the appropriateness evaluation protocol to the medical charts of patients with hospital-acquired symptomatic urinary tract infection (UTI) or sepsis, and by using cost-centre accounting. DESIGN/METHODOLOGY/APPROACH: The paper explains and tests a model for calculating costs of HAIs. FINDINGS: The data analysis showed that it is not always true that infections protract LOS: five out of 25 sepsis cases have extra-LOS and eight out of 25 UTI cases have extra-LOS, while the cases of sepsis that arose in surgery ward and intensive care units and urinary tract infections in ICU are without prolongation of LOS. The data analysis also showed that, using the mean total cost, the three cases of sepsis in the general surgery and the six in the ICU did not incur costs, nor did the two cases of UTI in ICU, so that they appear to be infections at zero cost. Moreover, the weight of the cost for the bed, or for the diagnostic services, or for the pharmacological treatment, varied widely depending on the site of the HAI and the ward where the patient was hospitalized. ORIGINALITY/VALUE: The method can be applied in any hospital.     

Prognostic role of sarcopenia in metastatic colorectal cancer patients during first-line chemotherapy: A retrospective study

BACKGROUNDSarcopenia is a condition characterized by decreased skeletal muscle mass due to physiological ageing or to a concomitant disease such as neoplasia. In cancer patients, a low lean body mass is suggested to be a negative prognostic factor for survival and for the development of dose-limiting chemotherapy toxicities irrespective of disease stage. AIMTo evaluate the prognostic role of sarcopenia in patients with metastatic colorectal cancer (mCRC) undergoing first-line chemotherapy.METHODSOur retrospective analysis included 56 mCRC patients who received first-line chemotherapy from 2014 to 2017 at the Medical Oncology Unit of our hospital. Computerized scans were performed before starting chemotherapy and at the first disease reassessment. Sarcopenia was assessed using the skeletal mass index = muscle area in cm²/(height in m²) calculated at the L3 vertebra. Overall survival and objective response rate were evaluated. Toxicities were analyzed during the first four cycles of therapy and graded according to Common Terminology Criteria for Adverse Events version 4.0. A loss of skeletal muscle mass ≥ 5% was considered indicative of deterioration in muscle condition.RESULTSMedian age was 67 years and 35.7% of patients were ≥ 70 years old. Fourteen patients (25%) were sarcopenic at baseline computed tomography (CT) scan (7/33 men; 7/23 women); 5/14 sarcopenic patients were ≥ 70 years old. Median follow-up was 26.8 mo (3.8-66.8 mo) and median overall survival was 27.2 mo (95%CI: 23.3-37.3). Sarcopenia was not correlated to overall survival (P = 0.362), to higher toxicities reported during the first 4 cycles of chemotherapy (P = 1.0) or to response to treatment (P = 0.221). At the first disease reassessment, a skeletal muscle loss (SML) ≥ 5% was found in 17 patients (30.3%) 3 of whom were already sarcopenic at baseline CT scan, while 7 patients became sarcopenic. SML was not correlated to overall survival (P = 0.961). No statistically significant correlation was found between baseline sarcopenia and age (P = 1.0), body mass index (P = 0.728), stage at diagnosis (P = 0.355) or neutrophil/lymphocyte ratio (P = 0.751).CONCLUSIONNeither baseline sarcopenia nor SML affected survival. In addition, baseline sarcopenia was not related to worse treatment toxicity. However, these results must be interpreted with caution due to the limited sample size.     

Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine

To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma beta-endorphin (beta-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 micrograms iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both beta-EP (F = 5.86, p less than 0.002) and cortisol (F = 4.43, p less than 0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for beta-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased beta-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal beta-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p less than 0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.     

The Role of Antisocial, Affective, and Childhood Behavioral Characteristics in Alcoholics' Neuropsychological Performance

Chronic alcoholics demonstrate cognitive deficits when compared with nonalcoholics. These deficits are typically attributed to the direct effects of ethanol and its metabolites on the central nervous system (CNS). There are other factors, however, that differentiate alcoholics from controls, such as personality or behavioral characteristics. These factors may affect neuropsychological performance and thus alter the interpretation of alcoholic cognitive deficits as resulting solely from alcohol's toxic effects. To investigate this question, male and female alcoholics and peer nonalcoholic controls were compared on personality, behavioral, and cognitive measures. Alcoholics had greater numbers of antisocial behaviors, childhood behavioral disorder symptoms (CBD), and affective symptomatology, and had poorer neuropsychological performance than controls. The three personality and behavioral factors were positively intercorrelated with each other, and were negatively related to cognitive performance. The CBD factor proved to be the most consistent predictor of neuropsychological performance for both alcoholics and controls, and males and females. While the behavioral factors differentiated alcoholics from controls and predicted performance, significant differences between the groups in cognitive performance still remained when these factors were taken into account.     

Adolescent Sons of Alcoholics: Neuropsychological and Personality Characteristics

Adolescent sons of alcoholics and nonalcoholics were compared on a battery of intellectual, neuropsychological, personality, and behavioral measures. The former group demonstrated certain neuropsychological deficits in perceptual-motor ability, memory, and language processing. They also had auditory and visual attentional impairments and a lower level of achievement in reading comprehension. In addition, the sons of alcoholics presented a more neurotic personality profile than sons of nonalcoholics. They were, however, less impulsive than the comparison group. More development and familial problems were noted in the alcoholics' offspring as well. The implications of these findings for understanding the causes and consequences of alcoholism are discussed.     

Modifications of cardiac function in cirrhotic patients treated with transjugular intrahepatic portosystemic shunt (TIPS)

OBJECTIVES: The implantation of a transjugular intrahepatic portosystemic shunt (TIPS) has been shown to exacerbate the hyperdynamic circulation and might induce a significant cardiac overload. We investigated cardiac function before and 1, 3, 6, and 12 months after the TIPS procedure in cirrhotic patients. METHODS: Eleven patients with nonalcoholic cirrhosis were evaluated. Cardiovascular parameters were assessed by two-dimensional Doppler echocardiography. RESULTS: After TIPS, the left ventricular diastolic diameter increased from 26.5 +/- 1.8 mm (basal) to 30.0 +/- 2.8 mm (6 months) (p < 0.05), whereas the ejection fraction showed a slight increase (basal, 64.5 +/- 3.3; 6 months, 68.1 +/- 3.2). The left ventricular pre-ejection period and the isovolumetric relaxation time decreased transiently at 1 month (p < 0.05). An increased velocity in all of the components of pulmonary venous flow (systolic, diastolic, and atrial) documented the accelerated fluxes induced by the procedure. The estimated pulmonary systolic arterial pressure also increased at 1 month (29.5 +/- 1.4 vs 44.1 +/- 1.4 mm Hg, p < 0.05). All of these modifications reverted after 6 months. CONCLUSIONS: Our study demonstrates that nonalcoholic cirrhotic patients, without cardiovascular pathologies, show transient modifications in cardiac dimension and function for 3-6 months after TIPS caused by the increased volume load shunted to the heart.     

Transplantation of peripheral blood progenitor cells from HLA-identical sibling donors

Transplantation of peripheral blood progenitor cells (PBPCs) has largely replaced autologous bone marrow transplantation. The same might occur in the allogeneic setting if the favourable initial experience with allogeneic PBPCT is confirmed. We analysed all primary transplants utilizing unmodified PBPC from HLA-identical sibling donors reported to the European Group for Blood and Marrow Transplantation (EBMT) for 1994. 59 patients with a median age of 39 years received myeloablative therapy for acute myelogenous leukaemia (23 patients), acute lymphoblastic leukaemia (13), chronic myelogenous leukaemia (nine), lymphoma (seven), or other diagnoses (seven) mostly of advanced stages followed by transplantation of allogeneic PBPC. Three patients died soon after grafting, the others showed prompt haemopoietic recovery with median times to recover an absolute neutrophil count (ANC) above 0.5 and 1.0×10⁹/l of 15 (range 9–27) and 17 d (range 10–28) respectively. Time to platelet recovery above 20 or 50×10⁹/l was 16 (range 9–76) and 18 d (range 12–100) respectively. 27 patients (46%) developed no or mild acute graft-versus-host disease (GVHD). The incidence of moderate (grade II) disease was 27%; 24% of the patients developed severe acute GVHD (grades III or IV). 55% of patients who were alive 90 d after transplantation developed chronic GVHD, the probability to develop extensive chronic GVHD was 32% (95% confidence interval 22–42) with a median follow-up of 14 months. Overall and event-free survival (EFS) at 1 year were 54% (CI 48–60) and 50% (CI 43–57), respectively, the relapse incidence was 23% (CI 17–29). EFS was 67% (CI 55–79) in patients transplanted for acute leukaemias in first complete remission, chronic myelogenous leukaemia in first chronic phase, or severe aplastic anaemia. Transplantation of allogeneic PBPC resulted in prompt and durable engraftment. The incidence and severity of acute and chronic GVHD seemed comparable to that observed after allogeneic BMT. Overall and event-free survival in this cohort of patients, most of whom suffered from advanced leukaemia or lymphoma, is encouraging, suggesting that the high numbers of T lymphocytes and/or natural killer cells contained in a typical PBPC collection product exert a vigorous graft-versus-leukaemia effect. Further evaluation of allogeneic PBPCT is highly desirable.     

Enhanced Mucosal Interleukin-6 and -8 in Helicobacter pylori-Positive Dyspeptic Patients

Objectives: To determine the concentrations of interleukin-1β, interieukin-6, and interieukin-8 in tissue homogenates of mucosal biopsy specimens from Helicobacter pylori-positive and -negative patients. Methods: In 43 consecutive patients who underwent upper gastrointestinal endoscopy, seven antral biopsies were taken; three specimens were used for cytokine determination and the remaining four biopsies were processed for H. pylori detection. Peripheral venous blood was collected and IgG to H. pylori was assayed by an ELISA technique. Results: Twenty-nine of 43 patients (67%) were histologically positive for H. pylori; all had chronic gastritis. The mucosal levels of interleukin-6 and interleukin-8 were significantly higher in H. pylori-positive patients than in the negative patients p < 0.001). A significantly higher percentage of interleukin-8 was found in patients colonized by H. pylori with active superficial chronic gastritis (85.7%), compared to quiescent superficial gastritis (12.5%) ( p < 0.01), and the median and range were, respectively, 400 (0–1000) and 0 (0–200) pg/mg protein (p < 0.001). In patients with active superficial gastritis, a significant correlation between interleukin-6 and -8 was found ( p 0.01). No difference was found regarding the mucosal levels of interleukin-lβ according to the presence of H. pylori. Conclusions: These results suggest a possible pathogenetic role for interleukin-6 and interleukin-8 in H. pylori -associated gastritis.     

Report from the Rockefellar Foundation Sponsored International Workshop on reducing mortality and improving quality of life in long-term survivors of Hodgkin's disease: July 9–16, 2003, Bellagio, Italy

Abstract:  A workshop, sponsored by the Rockefellar Foundation, was held between 9 to 16 July, 2003 to devise strategies to reduce mortality and improve quality of life of long-term survivors of Hodgkin's disease. Participants were selected for their clinical and research background on late effects after Hodgkin's disease therapy. Experts from both developed and developing nations were represented in the workshop, and efforts were made to ensure that the proposed strategies would be globally applicable whenever possible. The types of late complications, magnitude of the problem, contributing risk factors, methodology to assess the risk, and challenges faced by developing countries were presented. The main areas of late effects of Hodgkin's disease discussed were as follows: second malignancy, cardiac disease, infection, pulmonary dysfunction, endocrine abnormalities, and quality of life. This report summarizes the findings of the workshop, recommendations, and proposed research priorities in each of the above areas.