Resuppression of virus load after interruption in treatment with nevirapine and 2 nucleoside reverse-transcriptase inhibitors.

This retrospective chart review evaluated the effectiveness of reinitiation of treatment with nevirapine and dual nucleoside-analogue reverse-transcriptase inhibitors (NRTIs) after an interruption in antiretroviral therapy in 135 patients with human immunodeficiency virus type 1 RNA levels of <400 copies/mL who were receiving the same regimen. Reinitiation of a nevirapine regimen resulted in resuppression of virus load to <400 copies/mL in most patients who adhered to the regimen. Direct interruption of a non-NRTI regimen could lead to easier and more efficient structured protocols for treatment interruption.

Effectiveness and tolerability of nevirapine, stavudine, and lamivudine in clinical practice.

BACKGROUND: Recent studies reveal patients on protease inhibitor (PI)-based regimens achieve viral suppression less often in clinical practice than in clinical trials. Nonnucleoside reverse transcriptase inhibitors (NNRTIs) can provide an equally effective and more convenient alternative. PURPOSE: This retrospective chart review examines the effectiveness, tolerability, and convenience of a nevirapine (NVP), stavudine (d4T), and lamivudine (3TC)-containing regimen in an urban HIV clinical practice. METHOD: Chart review of patients from September 1996 to April 2000 yielded 73 patients on NVP+d4T+3TC; 83.6% were treatment experienced. RESULTS: By 16 weeks, 86.4% (57/66) had viral loads (VL) <400 in an as-treated (AT) analysis, while 78.1% (57/73) had VL <400 in an intent-to-treat (ITT) analysis. By 24 weeks, 84.6% (33/39) had VL <50 (AT). Beyond 48 weeks, 88.9% (16/18) had VL <50. The mean CD4 increase was 170 cells/mm(3). Rash was the most common adverse event (13.7%) in this review. CONCLUSION: Consistent with other studies, this NVP+d4T+3TC regimen appears effective in both treatment-experienced and -naive patients, regardless of baseline viral loads, in a clinical practice setting.

D-xylose absorption as a measurement of malabsorption in poult enteritis and mortality syndrome.

Severe wasting of body tissues, diarrhea, high morbidity and mortality, and stunting are all characteristics of poult enteritis and mortality syndrome (PEMS). The wasting of musculature and loss of nearly all adipose tissue suggested that even though the PEMS-infected poults were eating some feed, nutrient intake was not sufficient to meet body requirements for maintenance and growth. Because epithelial cells in the gastrointestinal tract appeared to be a target of the undefined etiological agent (or agents) that causes PEMS, a study was conducted in which PEMS-infected poults were evaluated for malabsorption through 3 wk of age. D-Xylose, a poorly metabolized pentose, was given per os as a bolus, and blood samples were obtained from the ulnar vein in the wing of control and PEMS-infected poults over a 3-h period to estimate intestinal absorption. D-Xylose absorption in control poults peaked 30 to 60 min after the oral treatment, similar to results reported earlier. The PEMS-infected poults did not show a peak in absorption. The PEMS-infected poults showed significant delays in D-xylose absorption at 4, 7, and 11 d after PEMS challenge. The severe malabsorption and metabolic deficiency problem associated with PEMS was postulated to be a direct effect of the undefined infectious agent or agents that cause the disease.

Influence of BioChrome on the response of metabolic hormones in PEMS-infected poults.

Poult enteritis and mortality syndrome (PEMS), a disease that affects turkeys between 7 and 28 d of age, causes a severe inflammation of the intestinal tract and is characterized in poults by severe diarrhea, high morbidity, mortality, and stunting. The PEMS-associated mortality and growth depression is related to malabsorption and decreased metabolic activity caused, in part, by a possible insulin deficiency or insensitivity. Insulin receptors are stimulated by the glucose tolerance factor (GTF) that incorporates Cr. Body Cr deficiency can be exacerbated by dietary deficiency and by increased excretion due to stress associated with a diarrheal disease such as PEMS. BioChrome (BC) contains natural, preformed GTF, the bioactive form of Cr. Experiments were conducted in which BC was blended into poult starter feed at 400 ppb during the first 21 d posthatch. Body weights were determined at 1, 7, 14, and 21 d of age, and weekly feed conversions were calculated for each treatment group (control, BC, PEMS, and BC+PEMS). At 6 d post-hatch, each PEMS-designated poult was given a 0.1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. Blood samples were taken via cardiac puncture from four birds per treatment group at 7, 10, 14, 17, and 21 d of age. Radioimmunoassays were conducted for plasma insulin, glucagon, thyroxine (T4), and triiodothyronine (T3). Plasma insulin levels were depressed in PEMS-infected poults from Days 10 through 17, but plasma glucagon levels in the PEMS-infected poults were significantly elevated at 14 and 17 d, after which they returned to control levels in both of the PEMS-infected groups. The T3 and T4 levels were depressed through Day 21 in PEMS-infected poults, but with BC treatment these blood hormone levels rebounded by Day 21. Body weights of PEMS-infected poults were increased significantly by the BC treatment but not to the level of noninfected controls.

Hypothermia, hypoglycemia, and hypothyrosis associated with poult enteritis and mortality syndrome.

A metabolic dysfunction contributes to the poor performance and mortality associated with Poult Enteritis and Mortality Syndrome (PEMS). Within 2 d after contact-exposed poults were removed from the presence of PEMS-infected poults and returned to their respective treatment rooms to infect experimental poults, the experimental poults began to huddle together and show signs of the disease. When separated from the huddle, body temperatures of exposure poults were depressed significantly. Body temperatures decreased progressively through 8 d after exposure with a maximum depression of 2 C and returned to a normal level at 18 d after PEMS exposure. Similar decreasing patterns in serum glucose, inorganic phosphorus, triiodothyronine, and thyroxine were observed, with maximum decreases in these serum constituents being found between 8 and 13 d after PEMS exposure. There were significant correlations among decreasing body temperatures, decreasing serum constituents, and mortality in the PEMS-exposed poults. Daily mortality rates associated with PEMS began at 6 d and peaked at 9 d after PEMS exposure. Mortality rates decreased from 9 to 15 d after experimental PEMS exposure. Depressions in serum constituents, body temperature, and increased mortality rates did not coincide with decreased feed intake associated with PEMS. Therefore, it was concluded that the agent(s) causing PEMS may have a direct effect on energy metabolism in afflicted poults.