Retroperitoneal fibrosis in a patient with human immunodeficiency virus infection.
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Biomedical subjects
Publications and source records attributed to J Pachón.
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We compared two techniques for detecting delayed-type hypersensitivity (DTH) skin responses in 359 patients infected with human immunodeficiency virus (HIV) (mean CD4+ lymphocyte count, 387/microL). DTH responses were assessed with use of two antigenic panels administered simultaneously: tuberculin purified protein derivative (PPD) plus three control antigens (Candida albicans, mumps antigen, and tetanus toxoid) administered by the Mantoux method and by a multiple-puncture device delivering seven antigens percutaneously (MULTITEST CMI; Institut Mérieux, Lyon, France). Eighty-three patients (23%) were anergic, 216 (60%) reacted to both panels, 55 (15%) did not react to MULTITEST CMI but did react to the antigens administered by Mantoux method, and only five (1%) reacted to MULTITEST CMI without reacting to antigens administered by the Mantoux method (P < .001, McNemar's test). Each of the three possible combinations of PPD plus two control antigens administered by the Mantoux method were also superior to MULTITEST CMI for classifying patients as nonanergic (P < .001, McNemar's test). We conclude that the application of antigens by the Mantoux method is more efficient than MULTITEST CMI for detecting DTH skin responses in HIV-infected patients.
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Pneumocystis carinii is a common opportunistic pathogen in patients infected with the human immunodeficiency virus (HIV). Pneumocystis carinii pneumonia is common, while extrapulmonary infections with Pneumocystis carinii have been reported sparingly. The clinical features are frequently nonspecific. The detection of Pneumocystis carinii in cerebrospinal fluid (CSF) has not been reported thus far. In this report, an unusual case of Pneumocystis carinii meningoradiculitis in an HIV-infected patient who had previously received primary prophylaxis with trimethoprim-sulfamethoxazole is presented.
We assessed 10 patients with human immunodeficiency virus (HIV) infection (nine of whom had AIDS) and solitary pulmonary nodules (SPNs) that were detected on roentgenograms. Five of the patients presented with respiratory symptoms. The etiology of the SPN was determined for eight of these patients: six had infections (hydatidosis, mucormycosis, or infection with Nocardia asteroides, Cryptococcus neoformans, cytomegalovirus, or Pneumocystis carinii), one had non-Hodgkin's lymphoma, and the remaining patient had round atelectasis. Sputum studies were of no diagnostic value in any of these cases. Fiberoptic bronchoscopy with bronchoalveolar lavage and transbronchial biopsy was diagnostic in two of seven cases, and percutaneous transthoracic needle biopsy (PTNB) was diagnostic in one of four cases. Several microorganisms that were not the cause of the SPNs were observed in samples of sputum, bronchoscopic specimens, and PTNB specimens. Thoracotomy was diagnostic in the three cases in which it was performed. We conclude that the management of SPNs in HIV-infected patients is complicated by the low sensitivity and specificity of the diagnostic tests used.
The clinical features and the outcomes of eight cases of nosocomial Acinetobacter baumannii meningitis treated with ampicillin/sulbactam are reported. All the patients had fever, neck stiffness or meningeal signs, and a low consciousness level, and in their cerebrospinal fluid (CSF), pleocytosis, a low glucose level, and an elevated protein level were noted. For all CSF isolates of A. baumannii, the MIC of ampicillin/sulbactam was < or = 8/4 microg/mL. The MICs of sulbactam by microdilution in two cases were 4 microg/mL. All isolates were resistant to cefotaxime, ceftriaxone, ceftazidime, ureidopenicillins, ciprofloxacin, and gentamicin. Seven isolates were resistant to imipenem. A. baumannii was isolated from other samples in seven episodes. All patients were treated with ampicillin/sulbactam (seven with 2 g/l g every 6 hours and one with 2 g/l g every 8 hours). Six patients were cured and two patients died of meningitis. There were no side effects with the ampicillin/sulbactam treatment. In conclusion, ampicillin/sulbactam may be effective as therapy for meningitis caused by A. baumanii resistant to imipenem and other beta-lactam drugs.
OBJECTIVES: To describe a large series of patients with vertebral osteomyelitis (VO), and to compare the clinical, biological, radiological, and prognostic features of pyogenic (PVO), tuberculous (TVO), and brucellar vertebral osteomyelitis (BVO). METHODS: A retrospective multicentre study, which included 219 adult patients with VO with confirmed aetiology, who were diagnosed between 1983 and 1995 in two tertiary care centres. Of these patients, 105 (48%) had BVO, 72 (33%) PVO, and 42 (19%) TVO. RESULTS: One hundred and forty eight (67.6%) patients were male and 71 (32.4%) female. The mean (SD) age was 50.4 (16.4) years (range 14-84) and the mean (SD) duration of symptoms before the diagnosis was 14 (16.8) weeks. In 127 patients (57.9%) the vertebral level involved was lumbar, in 70 (31.9%) thoracic, and in 16 (7.3%) cervical. One hundred and nineteen patients (54.4%) received only medical treatment and 100 (45.6%) required both medical and surgical treatment. The presence of diabetes mellitus, intravenous drug abuse, underlying chronic debilitating diseases or immunosuppression, previous infections, preceding bacteraemia, recent vertebral surgery, leucocytosis, neutrophilia, and increased erythrocyte sedimentation rate (ESR) were significantly associated to PVO. A prolonged clinical course, thoracic segment involvement, absence of fever, presence of spinal deformity, neurological deficit, and paravertebral or epidural masses, were significantly more frequent in the group of TVO. The need for surgical treatment and the presence of severe functional sequelae were more frequent in the groups of PVO and TVO. CONCLUSION: There are significant clinical, biological, radiological, and prognostic differences between BVO, PVO, and TVO. These differences can point to the causal agent and orient the initial empirical medical treatment while awaiting a final microbiological diagnosis.
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Brain mass lesions (BML) occurred in 10% of patients infected by the human immunodeficiency virus (HIV), as expression of severe and sometimes treatable diseases. However, the management of them is not well established. We analyzed, retrospectively, 26 brain biopsies (22 estereotaxic) in patients with HIV infection and BML to know their usefulness and safety. The inclusion criteria were: Failure of the anti-Toxoplasma empirical treatment, atypical scan appearance for toxoplasmosis, or severe neurological picture. Brain biopsy yielded a diagnosis in 19 patients (73.1%): Progressive multifocal leukoencephalopathy (n = 8; 30.8%), primary central nervous system lymphoma (n = 6; 23.1%), mycobacteriosis (n = 2; 7.7%), toxoplasmosis (n = 2; 7.7%), criptococcosis (n = 1), cryptosporidiosis (n = 1) and HIV-encephalitis (n = 1). In one case there was a multiple diagnosis: mycobacteriosis, toxoplasmosis, and lymphoma. Brain biopsy results decided a change in therapy in 65.4%, the resolution or improvement of the neurological process in 30.8%, and the determination of the prognosis in 30.8%. In 8 cases (30.7%) there were biopsy complications, with secondary mortality in one. Brain biopsy of BML in HIV-infected patients is a diagnostic method with a high overall diagnostic rentability and uncommon non reversible complications, offering the possibility to prescribe a specific and potentially curative treatment.
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The number of nosocomial infections caused by Acinetobacter baumannii has increased in recent years. During a 12-month study, there were 1.8 episodes of A. Baumannii bacteremia per 1,000 adults admitted to a hospital in Seville, Spain. Seventy-nine patients were included in the study. A. baumannii bacteremia occurred after a mean (+/- SD) hospitalization of 18 +/- 20 days. In all cases the infections were acquired nosocomially; 71% wee acquired in intensive care units. Ampicillin/ sulbactam was found to be the most active agent against A. baumannii. The common source of the bacteremia was the respiratory tract (32 cases [71%]). Twenty patients (25%) had septic shock, and 24 (30%) had disseminated intravascular coagulation (DIC). Treatment with imipenem or ampicillin/sulbactam was most effective (cure rates, 87.5% and 83%, respectively). The deaths of 27 patients (34%) were related to A baumannii bacteremia. The presence of DIC (odds ratio [OR] = 116.4; P < .0001) and inappropriate antimicrobial treatment (OR = 15.2; P < .01) were independently associated with mortality. We conclude that most A. baumannii isolates are multiresistant and that nosocomial A. baumannii bacteremia may cause severe clinical disease that is associated with a high mortality.
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We assayed 229 CSF samples from 180 adults with meningitis of different etiologies for adenosine deaminase activity (ADA) and evaluated the usefulness of this assay in the differential diagnosis of aseptic meningitis. Cases of meningitis were classified as tuberculous meningitis (TBM), pyogenic meningitis, viral meningitis, self-resolving aseptic meningitis without a specific diagnosis, meningitis associated with other infections, and neoplastic meningitis. We also tested 117 CSF specimens for which parameters were normal. We chose a cutoff point of 10 IU/L on the basis of our results and found elevated ADA levels in 50% of the patients with TBM (no differences between patients with AIDS and those who did not have AIDS were observed). Among samples from patients with aseptic meningitis, we observed high ADA levels in only two of five of the patients with neurobrucellosis. Therefore, we concluded that in cases of aseptic meningitis, a CSF ADA level of > or = 10 IU/L has a sensitivity of 48%, a specificity of 100%, a positive predictive value of 1, and a negative predictive value of 0.91 as a diagnostic criterion for TBM or neurobrucellosis. ADA levels were also > 10 IU/L in 30% of the patients with pyogenic meningitis, but this diagnosis was easily excluded on other grounds.
Interleukin (IL)-8 concentrations were analyzed in 70 cerebrospinal fluid (CSF) samples from patients with meningitis of different etiologies and in 34 normal CSF samples. Patient groups included those with pyogenic meningitis, viral meningitis, self-resolving aseptic meningitis without a specific diagnosis, and meningitis of other etiologies and normal CSF from patients with and without neurologic disease. All samples from patients with pyogenic meningitis (18) but only 3 from patients with meningitis of other etiologies and with CSF polymorphonuclear leukocyte (PMNL) counts > or = 80% had IL-8 levels > or = 2.5 ng/mL. IL-8 was above the normal level (< or = 0.5 ng/mL) in samples from 5 of 13 viral and 8 of 23 self-resolving aseptic meningitis patients and in 7 of 13 samples from patients with meningitis caused by other microorganisms. There was a significant relationship between IL-8 levels and CSF PMNL counts in patients with nonpyogenic meningitis. The data suggest a possible role of IL-8 as PMNL chemotactic factor in different infections of the subarachnoid space, not only in pyogenic meningitis.
STUDY OBJECTIVES: To measure interleukin-1 beta (IL-1 beta) levels in pleural effusions of different etiologies and their relationship with several pleural inflammatory parameters, and to verify whether IL-1 beta can be used as diagnostic marker in the differential diagnosis of pleural diseases. MATERIAL AND METHOD: One hundred two pleural effusions were analyzed using a monoclonal antibody enzyme-linked immunosorbent assay. Pleural fluids were classified as follows: transudates (n = 28), empyema (n = 14), parapneumonic (n = 13), tuberculous (n = 19), neoplastic (n = 17), and miscellaneous effusions (n = 11). RESULTS: IL-1 beta was above 200 pg/mL in all the patients with empyema but only in three patients with other etiologies. Two of those three had parapneumonic effusions and the remaining one had a tuberculous pleurisy with a previous bacterial empyema. No significant relationships were found between pleural effusion IL-1 beta levels and the different inflammatory parameters analyzed. As a diagnostic criterion for empyema, pleural IL-1 beta concentration greater than 200 pg/mL had a sensitivity of 100%, a specificity of 96%, and a positive and negative predictive value of 0.82 and 1, respectively. CONCLUSIONS: Our data suggest that IL-1 beta has a significant role in pyogenic infections of the pleural space but not in effusions of other etiologies. It could be used as a diagnostic marker of empyema.