Cerebrospinal fluid leak after bone marrow biopsy

Immune‐mediated disorders affecting the gastrointestinal (GI) tract may compromise GI integrity, interfere with the absorption of nutrients and cause bleeding and inflammation. All these features contribute to the pathogenesis of anaemia, the most prevalent extra‐intestinal manifestation of immune‐mediated GI disorders. Anaemia is most commonly due to iron deficiency and/or inflammation, but vitamin deficiencies and, more infrequently, autoimmune haemolysis or drug‐induced myelosuppression can be involved. Here we address several issues related to the differential diagnosis and treatment of anaemia in immune‐mediated GI disorders, giving particular relevance to the problem of iron deficiency anaemia associated with inflammation. It is emphasized how, in most cases, anaemias due to iron or vitamin deficiencies are best treated by parenteral administration of the deficient factor(s), and how the available high dose intravenous (IV) iron formulations can reduce ambulatory and social costs of IV iron supplementation, while improving patient's compliance to treatment. Actual and future treatment possibilities for anaemia of inflammation, involving the use of erythropoiesis stimulating agents, biologicals and hepcidin inhibitors are discussed.     

Complications of allergic rhinitis.

With unfortunate high frequency, clinicians consider allergic rhinitis to be more of a nuisance than an illness. When in fact, allergic rhinitis is not only a very common disease process, affecting up to a cumulative frequency of 42% of the U.S. population by age 40, but can lead to significant short-term and long-term medical complications. Poorly controlled symptoms of allergic rhinitis may contribute to sleep loss, secondary daytime fatigue, learning impairment, decreased overall cognitive functioning, decreased long-term productivity and decreased quality of life. Additionally, poorly controlled allergic rhinitis may also contribute to the development of other related disease processes including acute and chronic sinusitis, recurrence of nasal polyps, otitis media/otitis media with effusion, hearing impairment, abnormal craniofacial development, sleep apnea and related complications, aggravation of underlying asthma, and increased propensity to develop asthma. Treatment of allergic rhinitis with sedating antihistamine therapy may result in negative neuropsychiatric effects that contribute to some of these complications. Sedating antihistamines may also be dangerous to use in certain other settings such as driving or operating potentially dangerous machinery. In contrast nonsedating antihistamines have been demonstrated to result in improved performance in allergic rhinitis.     

Cerebrospinal fluid leak and meningitis associated with nasal continuous positive airway pressure therapy

Clear rhinorrhea is a common symptom in patients with obstructive sleep apnea (OSA) and may worsen with continuous positive airway pressure therapy. Clear rhinorrhea can also be the presenting symptom of cerebrospinal fluid (CSF) leak, which is evidence of a communication between the subarachnoid space and the nasal cavity or sinuses. While CSF leak has been reported to occur with nasal continuous positive airway pressure (nCPAP) therapy following trauma to the skull base, its association with OSA and nCPAP therapy in the absence of trauma has not been previously described. We report two patients with OSA in whom CSF leak developed following the institution of nCPAP therapy. In one patient, the rhinorrhea was complicated by meningitis. Both patients underwent successful repair of their defects. One patient successfully restarted nCPAP therapy, while the other refused it.     

Treatment update: allergic rhinitis.

In addition to the introduction of several new pharmacologic agents, two of the most significant recent developments in the management of allergic rhinitis have been the renewed emphasis on preventive measures, such as allergen avoidance and immunotherapy, and the importance of performing an accurate differential diagnosis of the disease. Recently, these evolving management trends were delineated in an algorithm proposed by the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology, which suggests that an initial evaluation be performed by a primary care physician. Based on findings at the initial evaluation, the patient should be treated either empirically in the primary care setting or referred to an allergist-immunologist for consultation. The allergist uses an evidence-based therapeutic approach based on a differential diagnosis of the type of rhinitis, which uses information derived from a detailed medical history, physical examination of the airway, and ancillary tests, particularly skin tests. Rhinitis management by an allergist emphasizes a three-pronged approach that incorporates avoidance, immunotherapy, and pharmacologic therapy. However, because both avoidance and immunotherapy have their limitations, pharmacologic therapy remains the mainstay of rhinitis management, and allergists usually recommend that optimal first-line therapy be broad based and capable of safely alleviating the symptoms of both allergic and nonallergic disease. First generation oral antihistamines, topical corticosteroids and the topical antihistamine azelastine are the most broad-based treatments available. Second-generation oral antihistamines and leukotriene antagonists also are useful in treating allergic rhinitis.     

Childhood allergic rhinitis

Allergic rhinitis is the most common chronic disease in children. This frequency is in strong progress. According to ISAAC' study, it concerns a child (6/7 years) on four and a teenager on two. The seasonal rhinitises are generally well treated. Perennial allergic rhinitises are chronic and often neglected. They are more often complicated or associated to asthma which represents the major evolutionary risk. In a general way, allergic rhinitis are sub-diagnosed and untreated while we have more and more effective therapeutic means. Although allergic rhinitis is not considered as a severe disease, its echo on children's quality of life, physical and psychological well-being, and capacity to learn. It has also important socio-economic consequences. A better coverage is imperative itself as far as the diagnosis based on the symptoms and the allergy cutaneous tests which are easy. The options for treating allergic rhinitis in the child are not so different as those for adult. Complete avoidance of inhalant allergens is not always possible and medication are quite always possible. Intranasal corticosteroids are sometimes prescribed. In persistent disease, allergen immunotherapy may be considered according to the last OMS consensus statement.     

The asthma and allergic rhinitis link.

During the past 10 years, our understanding of asthma and allergic rhinitis (AR) has evolved. The historic perspective of these allergen-induced disorders as distinct and separate entities is being displaced by current thinking that they are described better as a continuum of inflammation involving one common airway. Therefore, traditional therapies originally indicated for AR and asthma are being reassessed to explore their potential value in both upper- and lower-airway diseases. Recently, there has been a renewed interest in the role that histamines play in lower-airway disease, and interest is increasing in the leukotrienes (LTs), which are far more potent inflammatory mediators than histamines, and the role they play in upper-airway disease. Given the pivotal role that LTs play as potent inflammatory mediators in the pathophysiological state of inflammation of both airways, LT receptor antagonists recently have emerged as important therapeutic advances that have potential clinical value in both asthma and allergic rhinitis. The prevalence of asthma and AR is increasing in the general population, and a high proportion of new patients have coexisting upper- and lower-airway disease. Estimates show that 60-78% of patients who have asthma have coexisting AR. The following review discusses the epidemiology of asthma and AR, provides evidence for common pathophysiological mechanisms, and discusses a therapeutic approach that has positive effects on both diseases and may maximize benefits and outcomes for patients with concomitant asthma and AR.     

Mechanisms of allergic rhinitis

The pathogenesis of allergic rhinitis can be better appreciated by understanding the numerous protective mechanisms available for mucosal defense. The system of TH2 lymphocytes, IgE production, mast cell degranulation, eosinophil infiltration, and resident cell responses are central to our understanding and treatment of allergic rhinitis. Histamine remains preeminent in causing the cardinal symptoms of the immediate allergic reaction: itching, watery discharge, and nasal swelling. Recruitment and activation mechanisms responsible for the late-phase allergic response are also reviewed.     

Cerebrospinal fluid lymphocyte transformations in meningitis.

Cerebrospinal fluid lymphocytes from 13 patients with nonsuppurative meningitis were cultured with antigens derived from Mycobacterium tuberculosis, Sporotrichum schenckii, and herpes simplex. When CSF lymphocytes from five patients with infections associated with these organisms were incubated with "correct" antigen there was increased incorporation of thymidine. The levels were higher than those seen when the cells were incubated with different antigens or when CSF lymphocytes from patients with other causes for their meningitis were cultured with these antigens. A compartmentalization of antigen-specific cells was suggested as CSF lymphocytes had greater stimulation than did peripheral blood lymphocytes from the same patient when incubated with the correct antigen. Transformational assays of CSF lymphocytes may provide a valuable diagnostic aid in certain cases of chronic meningitis.     

Inflammatory issues in allergic rhinitis and asthma.

Allergic rhinitis and asthma are both systemic inflammatory disorders with similar pathophysiological mechanisms involving numerous cells and inflammatory mediators. Some airway remodeling also might exist in allergic rhinitis. This review has summarized selected investigative studies from our division and has addressed the effect of various therapeutic agents on nasal fluid, nasal and airway epithelial cells, and the concept of airway remodeling.     

Managing impairment in patients with allergic rhinitis.

Allergic rhinitis is a common medical problem in both the adult and the pediatric population. A main complication of this disease is a reduction in the patient's quality of life. Individuals with either seasonal or perennial allergic rhinitis often are impaired, adversely affecting work and/or school performance. This impairment can result from the disease itself and the treatment thereof. Oral antihistamines are the mainstay of treatment for allergic disease. First-generation antihistamines are considered sedating and frequently are impairing even when sedation is absent. Second-generation antihistamines show some class variability regarding impairment but as a group are clearly less impairing than their first-generation predecessors. Second-generation antihistamines are the preferred medication when antihistamines are necessary.     

Neural expression and increased lavage fluid levels of secretoneurin in seasonal allergic rhinitis

Secretoneurin is a neuropeptide potentially involved in migration of eosinophils, monocytes, and dendritic cells. Whether secretoneurin is present in the human airway mucosa and whether it is released at ongoing allergic airway inflammation is currently unknown. In patients with allergic rhinitis, we have explored the occurrence of secretoneurin in nasal mucosal biopsies and lavage fluids before and during natural allergen exposure. Immunohistochemical analysis revealed an abundance of nerves displaying secretoneurin immunoreactivity, which were distributed predominantly around blood vessels and submucosal glands. A majority of nerve fibers containing vesicular acetylcholine transporter, tyrosine hydroxylase, calcitonin gene-related peptide, and vasoactive intestinal peptide were also secretoneurin-immunoreactive, indicating a localization of secretoneurin in cholinergic, adrenergic, and sensory nerves. Lavage fluid levels of secretoneurin were increased at allergen exposure (p < 0.01-0.05). Levels of secretoneurin did not correlate with eosinophil cationic protein (rho = 0.1, p = 0.7). We conclude that secretoneurin has a widespread occurrence in nasal mucosal nerves of patients with seasonal allergic rhinitis and that increased nasal lavage fluid levels of secretoneurin may characterize ongoing allergen exposure. These data favor a role of secretoneurin in the local traffic of immune cells in human airway mucosa.