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Biomedical subjects

P Boudes

Publications and source records attributed to P Boudes.

At least 19 recordsLinked to original sources
PubMed1998

Drug compliance in therapeutic trials: a review.

Because poor compliance introduces a major risk of bias in the interpretation of the results of a therapeutic trial, it is an important element to consider. At the planning stage, factors known to be associated with poor compliance should be recognized. The different methods of evaluating compliance, either clinical or biological, should be reviewed and the best strategy selected. During the therapeutic trial, the objective is to maintain an appropriate level of compliance. Patients, investigators, and sponsors have different options and responsibilities. The analysis should incorporate compliance as a specific variable in order to help test the robustness of the data. Compliance constitutes by itself a specific outcome measure. Compliance should be an integral part of study reports and publications, but it is frequently not discussed.

Clinical Trials as Topic↗
PubMed1996

A randomized controlled trial of a protease inhibitor (saquinavir) in combination with zidovudine in previously untreated patients with advanced HIV infection.

This study assessed the activity and tolerability of an HIV-protease inhibitor, saquinavir, alone or in combination with zidovudine. A total of 92 previously untreated HIV-infected patients with CD4 cell counts < 300 cells/mm3 participated in a parallel, randomized double-blind study. Patients were randomized to receive one of five treatments, each three times a day: 600 mg of saquinavir; 200 mg of zidovudine; 75, 200 or 600 mg of saquinavir in combination with 200 mg of zidovudine. The primary treatment period was 16 weeks, with monthly extensions in patients who did not show major disease progression or toxicity. The main measures of the efficacy of therapy used were changes in CD4 cell counts and in the concentration of HIV-1 RNA in the plasma (as determined by quantitative polymerase chain reaction). The 600 mg dose of saquinavir in combination with zidovudine induced a 1.6 log (after 4 weeks) and a 0.7 log (after 16 weeks) median reduction in plasma RNA concentration; this reduction was greater than those seen in the other four treatment groups. The combination of 600 mg of saquinavir with zidovudine also resulted in a larger and more sustained improvement in the CD4 cell count than either saquinavir or zidovudine monotherapy or the other combination therapies. In the group receiving 200 mg of saquinavir in combination with zidovudine, the maximal median change in CD4 cell count occurred at week 2 (85 cells/mm3), and by week 16 had fallen to 15 cells/mm3. In the group receiving 600 mg of saquinavir plus zidovudine, the median change in CD4 cell count remained high for the 16-week period (median change of 48 cells/mm3 at week 2 and 61 cells/mm3 at week 16). Saquinavir was safe and very well tolerated, either alone or in combination with zidovudine. The incidence of adverse events was greater in the four groups receiving zidovudine therapy, and all the most commonly reported adverse events have previously been associated with zidovudine therapy. Few changes in laboratory values occurred during the study, except for known zidovudine-associated toxicities. The most frequent abnormalities were raised aspartate aminotransferase and alanine aminotransferase levels, depressed calcium levels, and abnormally high or low phosphate levels. Despite the low oral bioavailability of saquinavir, combined virological and immunological data show definite antiviral activity in vivo for the combination of saquinavir at 600 mg plus zidovudine at 200 mg (each three times daily). The combination of drugs with different mechanisms of action represents an advance in the treatment of HIV infection.

Adult↗
PubMed1991

Multifocal multinucleated giant cell myelitis in an AIDS patient.

A 19-year-old male intravenous drug abuser, was admitted to hospital with a one-week history of lower limb weakness and urinary retention. He was known to have been HIV-seropositive for 3 years and had been treated for cerebral toxoplasmosis. Neurological examination confirmed flaccid paraparesis with weak ankle jerks and bilateral extensor plantar responses. There was no obvious sensory deficit. Neurological examination was otherwise normal. CSF contained 63 mg/dl protein and 10 leucocytes/mm3. Myelography was normal. He died 1 month later from septic peritonitis. Neuropathological examination showed chronic lesions of toxoplasmosis in brain. Small necrotic foci with myelin loss, proliferation of microglia, macrophages and multinucleated giant cells (MGC) were disseminated in the whole spinal cord, mostly in the white matter, but the brain was spared. Immunohistochemistry demonstrated p24 and p17 HIV antigens in macrophages, MGC and microglial cells. These lesions resemble those of so called 'multifocal giant cell encephalitis'. The present case demonstrates that HIV-related multifocal inflammatory changes may be restricted to the spinal cord and may be a cause of myelopathy in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Purely granulomatous Wegener's granulomatosis: a new concept for an old disease.

In summary, PGWG corresponds to an early phase of WG, presenting only with extravascular granuloma. Primarily, ENT, eye, or lung tissues are involved, but any organ may be affected. The diagnosis is made by typical palisading granuloma associated with elevated c-ANCA levels in the patients' serum. The concept of an early granulomatous lesion (PGWG) facilitates the early diagnosis of WG and leads to classification of different forms of disease according to the multistep evolution hypothesis: first PGWG, then localized or limited forms of the disease, and ultimately generalized vasculitis with renal involvement (classical WG). The concept of PGWG forms the basis for future therapeutic trials where folate antagonists are restricted to PGWG, while immunosuppressive treatment is required for the other stages of WG.

Anti-Bacterial Agents↗
PubMed1990

Mediastinal tumour as the presenting manifestation of Wegener's granulomatosis.

A 42-year-old man presented with a mediastinal tumour. On histological examination, tuberculosis was evoked, but no definitive conclusion could be drawn. The patient thereafter developed throat ulcerations and rapidly progressing renal insufficiency due to necrotizing glomerulonephritis. After reviewing the histological material, it was concluded that all of these manifestations were related to Wegener's granulomatosis. The presentation of Wegener's granulomatosis as a mediastinal tumour is very rare, but this form of the disease must be recognized, as early treatment with cyclophosphamide is essential for a favourable outcome.

Adult↗
PubMed1990

[Cytomegalovirus (CMV) and human immunodeficiency virus (HIV) co-infection, of multinucleated giant cells in acquired immunodeficiency syndrome (AIDS) encephalopathy].

A 31-year-old HIV-1-seropositive Haitian male presented with HIV-nephropathy and typical features of subcortical dementia. He died 4 months after the onset of neurological signs. Neuropathological examination revealed HIV encephalitis with diffuse progressive leukoencephalopathy, diffuse poliodystrophy and massive calcifications of white matter, basal ganglia and dentate nuclei probably partly related to renal failure. It was associated with focal, subependymal CMV encephalitis. In the periventricular regions, morphologically characteristic multinucleated giant cells, positive for CD68, and negative for GFAP, contained early CMV antigens (E13) in their nuclei and HIV antigens (gp41 and p24) in their cytoplasm. The co-infection of a single cell by both viruses was confirmed by electron microscopy. The finding that HIV and CMV can co-infect in vivo the same cell raises the question of a direct cooperation of both viruses at the single cell level, and suggests the possibility of a role for CMV as co-factor in the pathogenesis of HIV encephalopathy.

AIDS Dementia Complex↗
PubMed1990

Microscopic Wegener's disease: a particular form of Wegener's granulomatosis.

We describe a case of Wegener's granulomatosis in which the disease was manifested with crescentic glomerulonephritis, upper airway ulcerations, and microangiopathic hemolytic anemia with consumptive coagulopathy. No granuloma was identified but antibodies to cytoplasmic components of neutrophils were strongly positive with a diffuse pattern. Because microscopic vessels were predominantly involved (capillaritis), and granuloma were absent, were refer to this particular form of the disease as "microscopic Wegener's disease."

Aged↗
PubMed1990

[Value of the LDH level in pneumocystis carinii pneumonia in patients infected with human immunodeficiency virus].

LDH levels were measured in 30 AIDS patients with P. carinii pneumonia (PCP), evidenced by bronchoalveolar lavage, and 12 HIV 1-infected patients with P. carinii-negative bronchial or pulmonary manifestations, constituting the control group. Extrapulmonary causes of elevated LDH levels were eliminated. In the case of bronchopneumopathy, the sensitivity and the specificity of an abnormal LDH level for suggesting PCP were both 83%. For an interstitial pneumopathy, the sensitivity was the same but the specificity was 100%. During a one year period, the prevalence of PCP in our department was 69%. The positive and negative predictive values of increased LDH levels in HIV-infected patients were, respectively: 92 and 63% for bronchopneumopathy, and 100 and 73% for interstitial pneumopathy. Furthermore, the lowering and then the normalization of the LDH value were observed in all PCP cases with a favorable outcome. This simple yet highly sensitive laboratory analysis should be used for the diagnosis and monitoring of all bronchopneumopathies in HIV-infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Acute pancytopenia induced by pyrimethamine during treatment of cerebral toxoplasmosis associated with AIDS. Role of dihydrofolate reductase inhibitors].

An AIDS patient with cerebral toxoplasmosis had a folate deficiency-induced acute pancytopenia, which was rapidly reversed by the administration of folic acid. This observation is particularly important as a possible preventive therapy to be given to all HIV-infected patients because of the anti-folic activity of the majority of anti-infectious agents used during the course of this disease and the many potential sites of hematopoietic involvement. The patient's condition is stressed because the undernourished subject is at greater risk for this type of manifestation.

Acquired Immunodeficiency Syndrome↗