Roberto Patarca-Montero

Roberto Patarca-Montero, MD, PhD. Former Assistant Professor at University of Miami School of Medicine. Former editor of the Journal of Chronic Fatigue Syndrome. Researcher for AIDS and chronic fatigue syndrome.

Books

 * 2004, Medical Etiology, Assessment, and Treatment of Chronic Fatigue and Malaise: Clinical Differentiation and Intervention; What Does the Research Say?
 * 2004, Handbook of Cancer-Related Fatigue: What Does the Research Say?
 * 2003, Chronic Fatigue Syndrome, Genes, and Infection: The ETA-1/OP Paradigm — What Does the Literature Say?
 * 2002, Chronic Fatigue Syndrome and the Body's Immune Defense System: What Does the Research Say?
 * 2002, The Concise Encyclopedia of Fibromyalgia and Myofascial Pain
 * 2001, Treatment of Chronic Fatigue Syndrome in the Antiviral Revolution Era: What Does the Research Say?
 * 2001, Phytotherapy of Chronic Fatigue Syndrome: Evidence-Based and Potentially Useful Botanicals in the Treatment of CFS
 * 2000, Concise Encyclopedia of Chronic Fatigue Syndrome

Notable Studies

 * 2002, The Paul-Bunnell Heterophile Antibody Determinant in Epstein-Barr Virus-Associated Disease"'Abstract - Reactivation of latent herpes viruses (notably Epstein-Barr virus, human herpesvirus-6) is commonly seen in chronic fatigue syndrome and it is believed to contribute to symptom perpetuation. Epstein-Barr virus (EBV), which was first isolated by Epstein, Barr and Achong (1964) from a cultured Burkitts's lymphoma lymphoblast cell line, is the etiological agent for infectious mononucleosis (IM), polyclonal and oligoclonal lymphomas associated with primary and acquired immunodeficiencies, and the complications of X-linked lymphoproliferative syndrome (XLP) (Cantani and Mastrantoni, 1989; Englund, 1988; Ernberg et al., 1990; Jones and Straus, 1987; Okano et al., 1988; Purtilo, 1987; Purtilo et al., 1981; Rowe et al., 1986; Saemundsen et al., 1981) and nasopharyngeal cancer (Pearson et al., 1984). Furthermore, people who have had IM have higher rates of subsequent development of malignant lymphoproliferative disorders (Abo et al., 1982; Snydman et al., 1982) and Hodgkins's disease (Green et al., 1979; Mueller, 1987; Poppema et al., 1985; Weiss et al., 1989), while patients with XLP have a higher incidence of non-Hodgkins's malignant lymphoma (Harrington et al., 1987). The precise role of EBV in these diseases or in CFS is not well understood. Nonetheless, it is known that EBV infection triggers the formation of heterophile antibodies that, for many decades, have formed the basis for serologic diagnosis of IM. In this review, we discuss the discovery, species variation, and structure of the erythrocyte membrane-associated Paul-Bunnell (PB) heterophile antibody determinant, its implications to IM diagnosis, and its potential contribution to defective immune surveillance, such as that seen in chronic fatigue syndrome.'"
 * 2001, Cytokine and Other Immunologic Markers in Chronic Fatigue Syndrome and Their Relation to Neuropsychological Factors
 * 2000, Comparative Analysis of Lymphocytes in Lymph Nodes and Peripheral Blood of Patients with Chronic Fatigue Syndrome"'Abstract - Blood and lymph node samples were obtained from patients with chronic fatigue syndrome (CFS) who had volunteered to undergo a lymph node biopsy while participating in a phase 1 clinical trial of a novel immunomodulatory therapy. The surface marker phenotypes of the peripheral blood and lymph node samples were examined using four-color flow cytometry and compared to published proportions of cells in peripheral blood and lymph nodes from control individuals. While a greater proportion of T lymphocytes from both lymph nodes and peripheral blood of control subjects are immunologically “naive” (CD45RA+), the proportions of lymphocytes with a “memory” phenotype predominate in lymph nodes and peripheral blood of CFS patients. CFS has been proposed to be a disease of autoimmune etiology and in this respect it is interesting to note that decreased proportions of CD45RA+ T (“naive”) cells are also seen in the peripheral blood of patients with autoimmune diseases.'"
 * 2000, Clinical and Immunologic Effects of Autologous Lymph Node Cell Transplant in Chronic Fatigue Syndrome"'Abstract - An open labeled, phase 1, safety and feasibility study using lymph node extraction, ex vivo lymph node cell expansion, followed by autologous cell reinfusion was evaluated as a potential immunomodulatory treatment strategy in patients with chronic fatigue syndrome (CFS). The experimental therapy utilized the cells of the lymph node, activated and grown in culture with defined media, interleukin-2 (IL-2) and anti-CD3 to activate and enhance cellular immunological functions. This procedure was designed to change the cytokine pattern of the lymph node lymphocytes to favor expression of T-helper (Th)l-type over Th2-type cytokines. The mixed population of ex vivo immune-enhanced cells were reinfused into the donor, who was carefully monitored for adverse events and possible clinical benefit. There were no adverse events. There were significant improvements in clinical status in association with a significant decrease in Th2-type cytokine production."
 * 2000, Immunotherapy of Chronic Fatigue Syndrome: Therapeutic Interventions Aimed at Modulating the Th1/Th2 Cytokine Expression Balance"'Abstract - Based on the postulates of viral and autoimmune etiologies of CFS, several interventions have been designed and tested by different research groups around the world, including the United States, Sweden, United Kingdom, Italy, and Japan. This review addresses those interventions aimed at altering the balance of certain cytokines, the mediators of immune responses. Patients with CFS who show evidence of activation of the immune system have poor immune cell function and a predominance of what is called a T-helper (Th)2-type cytokine response when their lymphocytes are activated. A Th2-type response, which is characterized by production of cytokines such as interleukin (IL)−4, −5, and −10, favors the function of B lymphocytes, the cellular factories of immunoglobulins. A predominance of a Th2-type response is therefore consistent with pathologies, such as autoimmunity and atopy, which are based on inappropriate production of immunoglobulins. Many of the CFS therapies discussed decrease the Th2-type predominance seen at baseline in CFS patients, thereby allowing a greater predominance of a Thl-type response, which favors the function of macrophages and natural killer cells. The function of the latter cells, which have the natural ability of directly destroying invading microbes and cancer cells, is defective in untreated CFS patients. Typical Thl-type cytokines include IL-2 and interferon-gamma, and some of the therapies induce their production. The interventions discussed in this review cover a wide spectrum of therapeutic tools ranging from lymph node cell immunotherapy, herbal products, and small molecules to vaccines. Despite the controversies on the etiology of CFS, immunotherapy research is useful and necessary.''"
 * 1998, Interleukin-6 and Disease: Two Case Reports that Point to the Usefulness of Measuring Cytokine Levels in Clinical Settings
 * 1995, Dysregulated Expression of Soluble Immune Mediator Receptors in a Subset of Patients with Chronic Fatigue Syndrome: Cross-Sectional Categorization of Patients by Immune Status - Abstract
 * 1994, Dysregulated expression of tumor necrosis factor in chronic fatigue syndrome: interrelations with cellular sources and patterns of soluble immune mediator expression"'Abstract: Among a group of 70 individuals who met the criteria established by the Centers for Disease Control and Prevention (Atlanta) for chronic fatigue syndrome (CFS), 12%-28% had serum levels exceeding 95% of control values for tumor necrosis factor (TNF) alpha, TNF-beta, interleukin (IL) 1 alpha, IL-2, soluble IL-2 receptor (sIL-2R), or neopterin; overall, 60% of patients had elevated levels of one or more of the nine soluble immune mediators tested. Nevertheless, only the distributions for circulating levels of TNF-alpha and TNF-beta differed significantly in the two populations. In patients with CFS--but not in controls--serum levels of TNF-alpha, IL-1 alpha, IL-4, and sIL-2R correlated significantly with one another and (in the 10 cases analyzed) with relative amounts (as compared to beta-globin or beta-actin) of the only mRNAs detectable by reverse transcriptase-coupled polymerase chain reaction in peripheral-blood mononuclear cells: TNF-beta, unspliced and spliced; IL-1 beta, lymphocyte fraction; and IL-6 (in order of appearance). These findings point to polycellular activation and may be relevant to the etiology and nosology of CFS.'"