Overweight in dogs, but not in cats, is related to overweight in their owners

OBJECTIVE: To quantify the environmental component of aetiology of overweight and obesity by examining the relationship between the degree of overweight in dogs and cats and the degree of overweight in their owners. DESIGN: Cross-sectional study. Main outcome measures of the owners were weight, height (stature) and BMI. Of the animals, weight and divergence from ideal weight were measured by a veterinarian. SETTING: Three veterinary clinics in Amsterdam, The Netherlands. SUBJECTS: Dogs and cats, together with their owners, who visited the veterinary clinic. Dogs and cats had to be older than 1 year, and their owners had to be at least 21 years old. After exclusion, there remained forty-seven pairs of dogs and their owners and thirty-six pairs of cats and their owners. RESULTS: We found a significant relationship between the degree of overweight of dogs and the BMI of their owners (r = 0.31). Correction for length of ownership, gender and age of the animal, and gender, age, education level and activity score of the owner did not materially affect this relationship. However, after correction for the amount of time the dog was being walked each day, this relationship disappeared. No significant relationship was found between the degree of overweight of cats and the BMI of their owners. CONCLUSIONS: The degree to which dogs are overweight is, in contrast to the degree to which cats are overweight, related to the BMI of their owners

Epstein-Barr Virus-Positive Posttransplant Lymphoproliferative Disease After Solid Organ Transplantation: Pathogenesis, Clinical Manifestations, Diagnosis, and Management

Posttransplant lymphoproliferative disease (PTLD) is a potentially fatal complication after (solid organ) transplantation, which is highly associated with Epstein-Barr virus (EBV). The EBV-specific cytotoxic T cell response that is essential in controlling the virus in healthy individuals is suppressed in transplant recipients using immunosuppressive drugs. A primary EBV infection in EBV-seronegative patients receiving an EBV-seropositive donor organ or a reactivation in those who are already latently infected pretransplantation can lead to uninhibited growth of EBV-infected B cells and subsequently to PTLD. Effective preventive strategies, such as vaccines and antiviral agents, are lacking. Because not every transplant recipient with increasing EBV viral load develops PTLD, it is hard to decide how intensively these patients should bemonitored and how and when a preemptive intervention should take place. There is a need for other tools to help predict the development of PTLD in patients at risk to make timing and strategy of preemptive intervention easier and more reliable. The cornerstone of the treatment of patients with PTLD is restoring the host's immunity by reduction of immunosuppressive drug therapy. American and British guidelines recommend to add rituximab monotherapy or rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisolone, depending on histology and clinical characteristics. Although response to these therapies is good, toxicity is a problem, and PTLD still has a relatively high mortality rate. An evolving therapy, especially in PTLD occurring in allogeneic stem cell transplantation, is restoring the host's immune response with infusion of EBV-specific cytotoxic T cells. This may also play a role in the future in both prevention and treatment of PTLD in SO

Anti-citrullinated protein antibody response after primary EBV infection in kidney transplant patients

<div><p>Rheumatoid arthritis (RA) is a chronic inflammatory disease of synovial joints, characterized by the presence of the highly disease-specific anti-citrullinated protein antibodies (ACPA) in approximately 70% of patients. Epstein-Barr virus (EBV) has previously been suggested to be involved in the pathophysiology of RA. However, given the high incidence of EBV in the general population and the difficulty of detecting initial infection, providing a direct link between EBV infection and RA development has remained elusive. We hypothesized that primary EBV infection may be a trigger for the development of the ACPA response <i>in vivo</i>. Using a unique cohort of 26 kidney transplant patients with a primary EBV infection, the presence of ACPA before and following infection was determined. No increase in IgG anti-CCP2 titers was detected following EBV infection. IgG anti-CCP2 antibodies were present in two patients and borderline positive in another. These three patients were HLA-DR4 negative. To test whether EBV infection may trigger a non-class switched anti-CCP2 response, IgM anti-CCP2 antibodies were analyzed. No general trend in the IgM anti-CCP2 response was observed following EBV infection. Since two out of the three IgG anti-CCP2 (borderline) positive patients were diagnosed with IgA nephropathy, 23 additional IgA nephropathy patients were tested for IgG anti-CCP2, regardless of their EBV status. All of these patients were IgG anti-CCP2 negative, indicating that IgG anti-CCP2 is not commonly present in IgA nephropathy patients. Collectively, these data do not support the hypothesis that EBV does trigger the highly RA specific ACPA response.</p></div

Characteristics of the additional IgA nephropathy patients.

<p>Characteristics of the additional IgA nephropathy patients.</p

IgG and IgM anti-CCP2 antibody expression in serum.

<p>Time points are (1) the first available time point before EBV infection, (2) the first time point with a positive EBV viral load or serology, (3) the first available time point after time point 2. (A) IgG anti-CCP2 antibody levels of all tested patients (n = 26) in arbitrary units as defined by the IMMUNOSCAN CCPlus test. Values above 25 U/ml, represented by a dotted line, are considered to be positive. (B) IgM anti-CCP2 antibody levels of all tested patients (n = 26) in arbitrary units.</p

EBV-antibody responses and EBV viral load detection by qPCR.

<p>EBV-antibody responses and EBV viral load detection by qPCR.</p

OD values for the IgG and IgM anti-CCP2 antibodies compared to the IgG and IgM anti-arginine2 antibody controls.

<p>Patients previously tested positive for IgG (n = 2) or IgM anti-CCP2 (n = 10) antibodies were additionally tested for IgG respectively IgM anti-arginine2 antibodies. (A) IgG anti-CCP2 and IgG anti-arginine2 antibody levels. (B) IgM anti-CCP2 and IgM anti-arginine2 antibody levels. Patient numbers are depicted on the x-axis.</p