[Clinical practice guideline. Diagnosis and treatment of insomnia in the elderly]. / Guía de práctica clínica. Diagnóstico y tratamiento del insomnio en el adulto mayor.

Insomnia is the difficulty to initiate or to maintain sleep. It also has to do with waking up too early at least for a month. A patient with insomnia has daytime consequences such as fatigue, sleepiness, changes in mood, lose of concentration, as well as changes in his social performance and his family relationships, among others. The relationship between this disorder and physical and mental health is important due to the impact that it has on the quality of life and life expectancy of those who suffer from it. Unfortunately, insomnia usually goes unnoticed or untreated, which contributes to the onset or worsening of psychiatric and medical conditions. This exacerbates the problem of insomnia in the elderly people. In relation to the treatment it is recommended: 1) the search and management of secondary causes of insomnia, 2) a non-drug therapy that includes sleep hygiene measures, 3) pharmacotherapy. It is not recommended to start a treatment with a hypnotic drug without rule out medications or diseases that cause or exacerbate insomnia. It is not recommended the use of narcoleptics, melatonin, antihistamines or long half-life benzodiazepines. The consequences include limitations on activities of daily living, loss of functionality, impaired quality of life, increased morbidity and mortality, as well as the worsening of preexisting chronic conditions.

El insomnio es la dificultad para conciliar o mantener el sueño; también consiste en despertar demasiado temprano al menos durante un mes. Un paciente con insomnio presenta consecuencias diurnas como fatiga, somnolencia, deterioro de la memoria, cambios en el estado de ánimo, en la concentración, así como en su desempeño social o familiar, entre otros. La asociación de este padecimiento con la salud física y mental es importante debido al impacto que tiene en la calidad y la esperanza de vida de los que lo padecen. Desafortunadamente, el insomnio suele pasar desapercibido o no tratarse, lo cual contribuye al empeoramiento de condiciones médicas y psiquiátricas. Esto se acentúa más en los adultos mayores, grupo por demás vulnerable. En relación con el tratamiento se recomienda aplicar la siguiente combinación: 1) la búsqueda y el manejo de causas secundarias de insomnio, 2) alguna terapia no farmacológica que incluya medidas de higiene del sueño, 3) tratamiento farmacológico. No es recomendable comenzar el tratamiento con un hipnótico sin haber descartado fármacos o enfermedades que provoquen o exacerben este padecimiento. Tampoco se recomienda el uso de neurolépticos, melatonina, antihistamínicos o benzodiacepinas de vida media larga. Las consecuencias incluyen limitación en las actividades de la vida diaria, pérdida de la funcionalidad, deterioro en la calidad de vida, incremento en la morbimortalidad, además del empeoramiento de las condiciones crónicas prexistentes.

Efficacy of thalidomide in systemic onset juvenile rheumatoid arthritis.

UNLABELLED: Thalidomide is an immunomodulating agent which reverses many of the cytokine disturbances seen in systemic onset juvenile idiopathic arthritis (SoJIA) with inadequate response to other treatments. We report 3 cases of recalcitrant SoJIA which improved dramatically after treatment with thalidomide. PATIENTS: Three children aged 9, 8, and 6 years diagnosed with SoJIA treated with conventional therapy including NSAIDs, corticosteroids, methotrexate and etanercept failed to respond fully and their condition worsened. Thalidomide was begun based on two previous reports showing its efficacy in recalcitrant SoJIA. RESULTS: Thalidomide produced successful remission of the disease in all 3 patients according to the preliminary criteria for inactive disease and clinical remission of JIA. CONCLUSION: Thalidomide may be a viable, alternative corticoid-sparing therapy in patients with recalcitrant, multidrug-resistant SoJIA.

Therapeutic options in autoimmune myasthenia gravis.

Autoimmune myasthenia gravis (MG) is associated with circulating antibodies to AChR, modification of the synaptic cleft, and destruction of the postsynaptic neuromuscular membrane. The hallmark is fluctuating muscular weakness and fatigability of muscles on sustained repeated activity. Various drugs and invasive procedures have been used in the treatment of MG including acetylcholinesterase inhibitors, corticosteroids, azathioprine, cyclosporine, cyclophosphamide, mycophenolate mofetil, tacrolimus, etanercept, intravenous immunoglobulin, plasma exchange and thymectomy. We review the role of each of these drugs and invasive procedures in MG. Although current treatment is highly successful and mortality is almost nil, further trials are required to identify the most suitable treatments for different subgroups of MG patients. In addition, safer and more potent drugs are required as most current drugs have major side effects due to immunosuppression. Therefore, the goal of novel therapies should be increased specificity of the immune-directed agents.

The relationship between the metabolic syndrome and energy-utilization deficit in the pathogenesis of obesity-induced osteoarthritis.

We propose that the pathogenesis of obesity-induced osteoarthritis may be explained by the metabolic changes in the striated muscle induced by the interaction of insulin resistance and systemic inflammation in obese individuals with metabolic syndrome being osteoarthritis the latest consequence by the physiological changes seen in the metabolic syndrome. Increased levels of TH1 cytokines are produced by activated macrophages in the presence of an acute or chronic infectious disease and suppress the sensitivity of insulin receptors on the membrane of muscle cell and adipocytes. Both cells are activated by inflammatory cytokines and contribute to enhance acute inflammation and to maintain a state of chronic, low-grade inflammation in apparently healthy obese individuals. The increased number of macrophage in the adipose tissue of obese individuals acts as an amplifier of inflammation. Patients with osteoarthritis and metabolic syndrome frequently are complaining about hotness and recurrent edema of feet and hands. It is probable that hyperinsulinemia in the presence of insulin resistance and inflammation, induce vasodilation through the TNF mediated-iNOS overexpression. Patients with metabolic syndrome express clinically the consequence of a poor uptake, storage and energy expenditure by the muscle and any other insulin dependent tissue and the consequence of high insulin plasma levels are vasodilation and increased protein synthesis. The fatigue and muscle weakness induced by insulin resistance and inflammation in obese patients with metabolic syndrome increase the frequency and the intensity of traumatic events of peripheral or axial joints that result in stretch and breaking of tenoperiosteal junction and abrasive damage of cartilage and therefore in these patients with metabolic syndrome and pro-inflammatory state the reparative process of cartilage and periarticular tissues would be severely modified by the growth factor activity in presence of high levels of insulin.

Insulin resistance, chronic inflammatory state and the link with systemic lupus erythematosus-related coronary disease.

The association of SLE with atherosclerosis suggests a common pathogenic mechanism. SLE and atherosclerosis are immune complex-mediated diseases. The integration of metabolism and immunity, which under normal conditions is beneficial for the maintenance of good health, can become deteriorative under conditions of metabolic challenge, as exemplified by the immunosuppression characteristic of malnourished or starving individuals. It is now apparent that obesity is associated with a state of chronic inflammation, particularly in white adipose tissue. However, in the absence of obesity, infusion of animals with inflammatory cytokines or lipids can cause insulin resistance. It is possible that the stresses of obesity are similar enough to the stresses of an infection and the body reacts to obesity as it would to an infection. Atherosclerosis can be considered to have a significant chronic inflammatory component. Inflammation also contributes to the typical dyslipidemia associated with SLE that is characterized by elevations of VLDL, LDL and triglycerides as well as reduced HDL. The link between insulin resistance and SLE can be explained by the chronic inflammatory state, and the consequent dyslipoproteinemia.

Pathophysiology of Sjögren's syndrome.

The term Sjögren's syndrome refers to keratoconjunctivitis sicca and xerostomia due to lymphocytic infiltrates of lachrymal and salivary glands. The current used criteria for diagnosis of primary Sjögren's syndrome is the American-European consensus. Primary Sjögren's syndrome is an autoimmune disorder characterized by lymphocytic infiltrates and destruction of the salivary and lachrymal glands and systemic production of autoantibodies to the ribonucleoprotein particles SS-A/Ro and SS-B/La. The infiltrating cells (T- and B-cells, dendritic cells) interfere with glandular function at several points: destruction of glandular elements by cell-mediated mechanisms; secretion of cytokines that activate pathways bearing the signature of type 1 and 2 interferons; production of autoantibodies that interfere with muscarinic receptors; and secretion of metalloproteinases (MMPs) that interfere with the interaction of the glandular cell with its extracellular matrix, which is necessary for efficient glandular function. As the process progresses, the mucosal surfaces become sites of chronic inflammation and the start of a vicious circle. Despite extensive study of the underlying cause of Sjögren's syndrome, the pathogenesis remains obscure. In broad terms, pathogenesis is multifactorial; environmental factors are thought to trigger inflammation in individuals with a genetic predisposition to the disorder.