Comparison of dual-energy X-ray absorptiometry and magnetic resonance imaging-measured adipose tissue depots in HIV-infected and control subjects

BACKGROUND: Studies in persons without HIV infection have compared adipose tissue measured by dual-energy X-ray absorptiometry (DXA) and magnetic resonance imaging (MRI), but no such study has been conducted in HIV-infected (HIV+) subjects, who have a high prevalence of regional fat loss. OBJECTIVE: We compared DXA- with MRI-measured trunk, leg, arm, and total fat in HIV+ and control subjects. DESIGN: A cross-sectional analysis was conducted in 877 HIV+ subjects and 260 control subjects in FRAM (Study of Fat Redistribution and Metabolic Change in HIV Infection), stratified by sex and HIV status. RESULTS: Univariate associations of DXA with MRI were strongest for total and trunk fat (r > or = 0.92) and slightly weaker for leg (r > or = 0.87) and arm (r > or = 0.71) fat. The average estimated limb fat was substantially greater for DXA than for MRI for HIV+ and control men and women (all P < 0.0001). Less of a difference was observed in trunk fat measured by DXA and MRI, but the difference was still statistically significant (P < 0.0001). Bland-Altman plots showed increasing differences and variability. Greater average limb fat in control and HIV+ subjects (both P < 0.0001) was associated with greater differences between DXA and MRI measurements. Because the control subjects had more limb fat than did the HIV+ subjects, greater amounts of fat were measured by DXA than by MRI when control subjects were compared with HIV+ subjects. More HIV+ subjects had leg fat in the bottom decile of the control subjects by DXA than by MRI (P < 0.0001). CONCLUSIONS: Although DXA- and MRI-measured adipose tissue depots correlate strongly in HIV+ and control subjects, differences increase as average fat increases, particularly for limb fat. DXA may estimate a higher prevalence of peripheral lipoatrophy than does MRI in HIV+ subjects.     

Tumor immune surveillance defect of X-linked severe combined immunodeficiency is not Epstein-Barr virus specific

Immunodeficient patients are at an increased risk of developing Epstein-Barr virus (EBV) associated lymphomas. We report a patient with X-linked severe combined immunodeficiency (X-SCID), who presented with an EBV-negative, B-cell non-Hodgkin lymphoma. The tumor did not resolve with chemotherapy or rituximab, but only after recovery of functional donor T-cells cell following hematopoietic stem cell transplantation (HSCT). This case illustrates that the cancer predilection associated with immunodeficient hosts may not be a specific immune defect in the recognition of viral specific antigens, and it could be a defect in immune surveillance necessary for elimination of cells with abnormalities in proliferation, function and/or apoptosis.     

Metastases to the oral mucosa: analysis of 157 cases

A review of the English-language literature revealed 157 well-documented cases of metastatic lesions to the oral mucosa. Most (64%) were diagnosed in patients in their fifth to seventh decade. The frequency of the primary site differed between genders: for men it was the lung (35.5%) followed by the kidney (16%) and skin (15%); for women it was the breast (24%) followed by the genital organs (17%). The most common oral site was the gingiva and alveolar mucosa (54.8%) followed by the tongue (27.4%), and with much less frequency by the tonsil, palate, lip, buccal mucosa and floor of the mouth. Of the dentulous patients, 79%) exhibited the metastatic tumor in the attached gingiva. The clinical appearance of the metastatic oral lesion in most cases resembled hyperplastic or reactive lesions.     

Individual differences in children's response to pain: role of temperament and parental characteristics

Sixty-five families were enlisted in a study exploring factors associated with distress behavior in 5-year-old children receiving diphtheria-tetanus-pertussis immunizations. At a home visit 1 month before the immunization, the following measures were obtained: (1) the Behavioral Style Questionnaire, a measure of temperament: (2) parental self-reports of medically related attributes (eg. "good patient"); (3) parental attitudes toward pain in children and responsiveness to their child's pain; and (4) parental prediction of distress at upcoming immunization. The child's distress behavior during the immunization was evaluated using a modification of the Procedure Rating Scale-Revised and, after the procedure, the child's assessment of his or her pain was elicited using the Oucher. Children's mean Procedure Rating Scale-Revised score was 2.57 of a possible 11. Thirty-one (48%) had low (less than or equal to 1) and 7 (11%) had high distress scores (greater than or equal to 2 SD above the mean). Factors positively correlated with distressed behavior included more "difficult child" cluster characteristics, the individual temperamental dimension of adaptability, but few parental attitudes and attributes. Parent's predictions of distress were the strongest correlates. These findings document the variation that children demonstrate in response to pain and offer some insight into associated innate and environmental factors. These results imply that treatment strategies derived from parental knowledge and tailored to individual characteristics of the child may be most effective in alleviating pain-related distress in medical settings.     

Inhibition of adjuvant-induced arthritis by DNA vaccination with the 70-kd or the 90-kd human heat-shock protein: immune cross-regulation with the 60-kd heat-shock protein

OBJECTIVE: Adjuvant arthritis can be induced in Lewis rats by immunization with Mycobacterium tuberculosis (Mt). The mycobacterial 65-kd heat-shock protein (Hsp65) is targeted by arthritogenic T cells. However, Hsp65 and the mycobacterial 71-kd heat-shock protein are also recognized by T cells that can down-regulate adjuvant-induced arthritis (AIA). We have recently demonstrated that vaccination with human Hsp60 DNA inhibits AIA. The present study was undertaken to analyze the role of the T cell responses to self HSP molecules other than Hsp60 in the control of AIA. METHODS: Lewis rats were immunized with DNA vaccines coding for human Hsp70 or Hsp90 (Hsp70 plasmid [pHsp70] or pHsp90), and AIA was induced. The T cell response to Mt, Hsp60, Hsp70, and Hsp90 (proliferation and cytokine release) was studied, and the T cell response to Hsp60 was mapped with overlapping peptides. RESULTS: The Hsp70 or Hsp90 DNA vaccines shifted the arthritogenic T cell response from a Th1 to a Th2/3 phenotype and inhibited AIA. We detected immune crosstalk between Hsp70/90 and Hsp60: both the Hsp70 and Hsp90 DNA vaccines induced Hsp60-specific T cell responses. Similarly, DNA vaccination with Hsp60 induced Hsp70-specific T cell immunity. Epitope mapping studies revealed that Hsp60-specific T cells induced by pHsp70 vaccination reacted with known regulatory Hsp60 epitopes. CONCLUSION: T cell immunity to Hsp70 and to Hsp90, like Hsp60-specific immunity, can modulate the arthritogenic response in AIA. In addition, our results suggest that the regulatory mechanisms induced by Hsp60, Hsp70, and Hsp90 are reinforced by an immune network that connects their reactivities.     

Prospective study of empiric monotherapy with ceftazidime for low-risk grade IV febrile neutropenia after cytotoxic chemotherapy in cancer patients

PURPOSE: It was the aim of this study to evaluate the results of a prospective study in a single medical center using ceftazidime monotherapy in cancer patients with chemotherapy-induced grade IV febrile neutropenia and a low risk for gram-negative bacteremia. SUBJECTS AND METHODS: Thirty-eight patients were admitted with low-risk grade IV febrile neutropenia after chemotherapy for solid tumors. The median patient age was 57 years (range 18-74). Sixteen patients (42%) developed febrile neutropenia after the first cycle of current chemotherapy line, 9 patients (24%) received 2-3 cycles and 13 patients (34%) received more than 3 chemotherapy cycles before manifesting febrile neutropenia. Five patients were treated with prophylactic granulocyte colony-stimulating factor commenced 24 h after completion of the chemotherapy cycle. Empiric monotherapy with intravenous ceftazidime was started on admission and administered 2 g every 8 h. RESULTS: The mean polymorphic nuclear cell count on admission was 231 cells/mm(3). Ceftazidime therapy was well tolerated. Twenty-five (66%) patients responded with clinical improvement and complete resolution of fever within 48 h after initiation of ceftazidime therapy. Thirty-two (84%) patients were afebrile after 72 h of therapy. Thirty-three patients (87%) remained on unmodified ceftazidime therapy throughout their hospitalization. Five patients (13%) subsequently required modification of the treatment regimen for various reasons. Mean duration of fever and neutropenia were 2 (1-10) days and 4 (1-11) days, respectively. None of the patients discontinued therapy because of adverse effects. No positive blood cultures were obtained. No events of septic shock were observed. Mean duration of hospitalization was 6 days (range 3-12). CONCLUSION: In our series, monotherapy with intravenous ceftazidime appears safe and effective in cancer patients with low-risk grade IV febrile neutropenia after cytotoxic chemotherapy and may appreciably reduce antibiotics costs.