Efectividad de la técnica de resolución de problemas aplicada por enfermeras: disminución de la ansiedad y la depresión en cuidadoras familiares

ObjectiveTo determine the effectiveness of Problem Solving Technique in reducing anxiety and depression, and increased perceived well-being in women family caregivers of chronic patients.DesignA clinical trialField of studyHealth centres in Tarragona, Spain, during 2007-2011.ParticipantsA sample 122 caregivers of patients in home care programs that met the inclusion criteria, were assigned to intervention or control group according to a simple random process.InterventionsIn the experimental group, the nurses applied the Problem Solving Technique to the caregiver according to a four-session protocol. The nurses provided the usual care to the caregivers In the control group. One month after intervention, the dependent vriables were measured again in both groups.Principal measurementThe dependent variables of anxiety and depression were measured using the Goldberg scale, and the emotional well-being variable by the scale of emotional health of the primary caregiver.ResultsA statistically significant improvement was detected in the anxiety and depression symptoms, as well as the perceived well-being in the intervention group compared to the control group.ConclusionsImplementation of the Problem Solving Technique is a useful therapeutic tool for reducing symptoms of distress in family caregivers of chronic patients.     

Meningococcal meningitis with ‘normal’ cerebrospinal fluid

A prospective study was made of all patients with normal CSF counts and positive cultures for Neisseria meningitidis diagnosed in “El Vallés” County, Barcelona between January 1987 and December 1990. Meningococcal meningitis was documented in 82 patients, eight of whom (seven children, five boys and two girls with a mean age of 5·6 ± 3·3 years, and a 69-year-old male patient) had no apparent CSF abnormalities in the initial lumbar puncture. At the time of admission all patients had fever (mean 39·1 °C) of 10·8 ± 5·6 hour duration and petechial rash which had been present for a mean of 3·6 ± 3·3 hours. Signs of meningeal irritation were not found. A 4-month-old infant with symptoms of circulatory collapse, intracranial hypertension and impairment of consciousness subsequently died of septicemia in 48 hours. Group B N. meningitidis was isolated in six cases (reduced penicillin-susceptibility in two cases) and group C N. meningitidis in the remaining two (reduced penicillin-susceptibility in one case). Patients without pleocytosis did not differ in a statistically significant fashion from the patients with high pleocytosis in the duration of temperature, and petechial rash, leukopenia, positive blood culture and fatal outcome.     

Brief Report: Educational attainment does not influence brain aging

Education has been related to various advantageous lifetime outcomes. Here, using longitudinal structural MRI data (4,422 observations), we tested the influential hypothesis that higher education translates into slower rates of brain aging. Cross-sectionally, education was modestly associated with regional cortical volume. However, despite marked mean atrophy in the cortex and hippocampus, education did not influence rates of change. The results were replicated across two independent samples. Our findings challenge the view that higher education slows brain aging.     

Activation of the NF-kB pathway downregulates TFF-1 in gastric carcinogenesis

Trefoil factor 1 (TFF1) is expressed in the normal superficial epithelium of the stomach and is implicated in the maintenance of gastric epithelial structure and function. During gastric carcinogenesis, in which pro-inflammatory cytokines play a crucial role, its expression level decreases suggesting a role as tumor suppressor factor. We have compared expression of TFF1 in gastric mucosa from cancer patients, in which several degrees of inflammatory infiltrate are present, with that in normal mucosa from non-cancer patients without infiltrating inflammatory cells. TFF1 is less expressed in the superficial gastric epithelium from cancer patients than in that from normal individuals in which the nuclear factor (NF)-κB pathway is not activated. We analyzed TFF1 expression in ex vivo samples of gastric mucosa from cancer patients, and in MKN45 gastric cancer cell line after exposure to proinflammatory cytokines interleukin (IL)-1β or tumor necrosis factor (TNF)-α, that activate the NF-κB pathway. We found that IL-1β and TNF-α activate the NF-κB pathway, as reflected in the nuclear expression of p65 and the activation of p-IκBα, and downregulate TFF1 expression after 1 or 2 h of exposure. Moreover, cells in the superficial gastric epithelium in ex vivo samples co-expressed TFF1/p65 at cellular level, whereas tumor cells did not. In summary, downregulation of TFF1 expression during gastric neoplastic transformation is associated with activation of the NF-κB pathway through IL-1β or TNF-α, but other regulatory mechanisms might also be involved.     

Rituximab‐induced interleukin‐15 reduction associated with clinical improvement in rheumatoid arthritis

Rituximab therapy alters all aspects of B‐cell participation in the disturbed immune response of rheumatoid arthritis patients. To determine the impact of B‐cell depletion on other immune compartments, we analysed levels of soluble and surface interleukin‐15 (IL‐15) along with the frequency of IL‐15‐related subsets after rituximab treatment. We then studied the correlation of observed changes with clinical activity. Heparinized blood samples from 33 rheumatoid arthritis patients were collected on days 0, 30, 90 and 180 after each of three rituximab cycles. Serum cytokine levels were determined by ELISA. Interleukin‐15 trans‐presentation was analysed by cytometry. Flow cytometry with monoclonal antibodies was performed to analyse circulating cell subsets. Interleukin‐15 was detected in the serum of 25 patients before initiating the treatment. Rituximab then progressively reduced serum IL‐15 (138 ± 21 pg/ml at baseline, 48 ± 18 pg/ml after third cycle, P = 0·03) along with IL‐17 (1197 ± 203 pg/ml at baseline, 623 ± 213 pg/ml after third cycle, P = 0·03) and tended to increase the frequency of circulating regulatory T cells (3·1 ± 1 cells/μl at baseline, 7·7 ± 2 cells/μl after third cycle). Rituximab also significantly decreased IL‐15 trans‐presentation on surface monocytes of patients negative for IL‐15 serum (mean fluorescence intensity: 4·82 ± 1·30 at baseline, 1·42 ± 0·69 after third cycle P = 0·05). Reduction of serum IL‐15 was associated with decrease in CD8⁺ CD45RO⁺/RA⁺ ratio (1·17 ± 0·21 at baseline, 0·36 ± 0·06 at third cycle, P = 0·02). DAS28, erythrocyte sedimentation rate and C‐reactive protein correlated significantly with CD8⁺ CD45RO⁺/RA⁺ ratio (R = 0·323, R = 0·357, R = 0·369 respectively, P < 0·001). Our results suggest that sustained clinical improvement after rituximab treatment is associated with IL‐15/memory T‐cell‐related mechanisms beyond circulating B cells.     

How Many Have Died from Undiagnosed Human Immunodeficiency Virus–Associated Histoplasmosis,A Treatable Disease? Time to Act

Human immunodeficiency virus (HIV)–associated disseminated Histoplasma capsulatum capsulatum infection often mimics tuberculosis. This disease is well know in the United States but is dramatically underdiagnosed in Central and South America. In the Amazon region, given the available incidence data and the regional HIV prevalence, it is expected that, every year, 1,500 cases of histoplasmosis affect HIV patients in that region alone. Given the mortality in undiagnosed patients, at least 600 patients would be expected to die from an undiagnosed but treatable disease. The lack of a simple diagnostic tool and the lack of awareness by clinicians spiral in a vicious cycle and made a major problem invisible for 30 years. The HIV/acquired immunodeficiency syndrome community should tackle this problem now to prevent numerous avoidable deaths from HIV-associated histoplasmosis in the region and elsewhere.In the Guianas and the Amazon Basin, the prevalence of human immunodeficiency virus (HIV) is approximately 1%. There have been some decreases in incidence in some states in this region, but recent increases in incidence in northern states of Brazil have been reported.^1–3 The population of the Amazon basin is estimated to be approximately 10 million persons,⁴ which would imply that approximately 100,000 persons are HIV positive in the Amazon Basin.The Amazonian environment is suitable for the growth of Histoplasma capsulatum.⁵ For immunocompetent patients, this organism causes mostly benign infections, but in severely immunodepressed HIV-infected patients, infection with this organism leads to a fatal disease in the absence of diagnosis and treatment. There lies the problem. Clinical symptoms are unspecific and often mimic those of tuberculosis.^6,7 Diagnosis is difficult and requires invasive procedures (biopsies, bone marrow smears), and trained staff to detect H. capsulatum, often after weeks of culture.⁸ Severe infections are often fatal within days.⁹ However, death often occurs after long delays in which patients are unsuccessfully treated for unconfirmed tuberculosis. Patients die because they are not treated for a treatable disease and because there is no diagnosis test. With no diagnosis, this possibility is not included in the diagnostic and treatment algorithms of clinicians who, despite unknowingly encountering this disease on a regular basis, have never seen a case because it was never diagnosed. In this context, then why give presumptive treatment of a disease that is not present?It is tragic but it makes total sense. It is even frighteningly tragic when one crunches the numbers to estimate what it means that after 30 years of the HIV epidemic, one of the leading causes of acquired immunodeficiency syndrome (AIDS) in the Amazon¹⁰ still goes largely unrecognized and evolves under the radar of national plans and international funding efforts.The only incidence data available for this region suggests that the incidence of histoplasmosis during the highly active antiretroviral therapy era was 1.5 cases/100 person-years.¹⁰ The historical mortality rate of disseminated histoplasmosis was > 30% despite mycology expertise.^7,8 This finding indicates that for 100,000 HIV patients, there would be 1,500 cases of histoplasmosis/year and 600 deaths/year, and probably more if undiagnosed. This finding also indicates that for more than 30 years the cumulated death rate in the region must have been huge, in the tens of thousands.A rational sceptic could rightly doubt this claim from the generalization of data from the smallest South American territory to the entire Amazon and elsewhere. However, when one reviews the literature, it becomes evident that histoplasmosis is present throughout the region, this fact has been known for decades, and that we should have been paying more attention.⁵ The high prevalence of histoplasmin test reactivity in the region was known even before AIDS was identified in 1981.¹¹ Histoplasmosis has been an AIDS-defining illness since 1993. We should have connected the dots earlier.How could something so huge escape the attention of the HIV/AIDS community in the region? One explanation for this dramatic blind spot is that in the region, the diagnostic capacity for mycology has been insufficient. It has been long argued that medical mycology is a neglected area of biology, and that the often low incidence of mycoses is caused by a lack of medical mycologists rather than the absence of the mycoses.¹² Another explanation is that the standard conceptualization of HIV/AIDS, the usual indicators, and the Joint United Nations Programme on HIV/AIDS terminology and framework did not explicitly entail disseminated histoplasmosis or the regional AIDS-defining illnesses. The anesthetic effect of the familiarity of vertical concepts and vertical programs can make it difficult to reframe the problem and see what was always there.For better diagnostic and treatment, we should know what AIDS is to direct diagnostic hypotheses when caring for individual patients. Misdiagnosing histoplasmosis as tuberculosis, not only delays a life-saving treatment of the individual patient, but it can confound tuberculosis statistics (incidence, resistance, mortality) and make it difficult to evaluate tuberculosis program results.The current financial difficulties should not stand in the way of building the diagnostic capacity for detection of histoplasmosis. It does not necessarily cost much to do the diagnosis. Treatment relies on amphotericin B for severe forms and itraconazole for non-severe forms and prophylaxis.⁷ Both drugs are generic drugs that are perfectly affordable. The toxicity of amphotericin B leads industrialized countries to use the costly liposomal version of the drug. However, The Drugs for Neglected Disease Initiative is releasing a cheap alternative that was developed for treatment of cryptococcosis.¹³ This is an opportunity for resource-limited countries in disease-endemic areas for treatment of histoplasmosis. We should not wait any longer. Every year wasted to build capacity for diagnosis and treatment of histoplasmosis in the Amazon Basin and elsewhere leads to hundreds of deaths that could have been avoided. This is not acceptable.     

Tuberculosis and Histoplasmosis among Human Immunodeficiency Virus–Infected Patients: A Comparative Study

In disease-endemic areas, histoplasmosis is the main differential diagnosis for tuberculosis among human immunodeficiency virus (HIV)–infected patients. However, no study has compared the two diseases. Thus, the objective of this study was to compare tuberculosis and histoplasmosis in HIV-infected patients. A population of 205 HIV-infected patients (99 with tuberculosis and 106 with histoplasmosis) hospitalized in Cayenne, French Guiana during January 1, 1997–December 31, 2008 were selected retrospectively from the French Hospital Database on HIV. Multivariate analysis showed that tuberculosis was associated with cough (adjusted odds ratio [AOR] = 0.20, 95% confidence interval [CI] = 0.05–0.73) and a C-reactive protein level > 70 mg/L (AOR = 0.98, 95% CI = 0.97–0.99). Variables associated with disseminated histoplasmosis were a γ-glutamyl transferase level > 72 IU/L (AOR = 4.99, 95% CI = 1.31–18.99), origin from French Guiana (AOR = 5.20, 95% CI = 1.30–20.73), disseminated localization (AOR = 6.40, 95% CI = 1.44–28.45), a concomitant opportunistic infection (AOR = 6.71, 95% CI = 1.50–29.96), a neutrophil count < 2,750 cells/mm³ (AOR = 10.54, 95% CI = 2.83–39.24), a CD4 cell count < 60 cells/mm³ (AOR = 11.62, 95% CI = 2.30–58.63), and a platelet count < 150,000/mm³ (AOR = 19.20, 95% CI = 3.35–110.14). Tuberculosis and histoplasmosis have similarities, but some factors show a greater association with one of these diseases. Thus, adapted therapeutic choices can be made by using simple clinical and paraclinical criteria.