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Query: UMLS:C0019693 (HIV)
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Serum lactate dehydrogenase levels, alveolar-arterial oxygen gradient, and percentage of neutrophils in bronchoalveolar lavage correlate most strongly with early mortality in Pneumocystis carinii pneumonia (PCP) in HIV-infected patients. However, the individual outcome can not be predicted by these parameters due to a considerable overlap between survivors and nonsurvivors. We prospectively investigated a PCP severity score, which has been developed earlier based on a retrospective analysis. Seven of 94 consecutively examined HIV-infected patients died within 14 days after diagnosis of PCP. A PCP severity score greater than 7 had a positive predictive value for early fatal outcome of 66.7 percent (6/9) and a negative predictive value of 98.8 percent (84/85). The overall diagnostic accuracy was 95.7 percent (90/94). The positive predictive value for early fatal outcome of a P(A-a)O2 > 35 mm Hg was 24 percent (6/25); the negative predictive value was 98.6 percent (68/69). However, the overall diagnostic accuracy was only 78.7 percent (74/94). The PCP severity score is a valuable tool for clinical decision making, for the early identification of patients with a prognostic unfavorable course, and for the comparison of patient populations in future studies of HIV-associated PCP.
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PMID:Prospective evaluation of a prognostic score for Pneumocystis carinii pneumonia in HIV-infected patients. 139 41

To determine if the use of aerosolized pentamidine prophylaxis decreases the clinical severity or the sensitivity of diagnostic tests for Pneumocystis carinii pneumonia (PCP), we conducted a retrospective matched cohort comparison study of patients admitted to San Francisco General Hospital with PCP from August 1, 1989, to June 30, 1990. Patients who had received pentamidine prophylaxis during at least the 2 months prior to the diagnosis of PCP were matched with patients who had not received the drug. Matching was based on the number of prior episodes of PCP, sex, age, and risk factors for human immunodeficiency virus infection. As markers of clinical severity, we chose alveolar-arterial oxygen difference, serum lactate dehydrogenase levels, outpatient versus inpatient treatment, length of hospitalization, length of intravenous anti-pneumocystis treatment, development of respiratory failure, in-hospital mortality, and chest radiographic appearance. Although, of the 27 matched pairs identified, significantly fewer of the pentamidine cohort were treated as inpatients, and significantly more of this cohort had upper lobe dominant disease on chest radiograph, we found no other significant differences between markers of clinical severity for the two cohorts. In addition, we found no significant differences in the rate of sputum or bronchoalveolar lavage positivity for P. carinii between the two cohorts. We conclude that, although hospitalization is less common in patients with a history of prophylactic pentamidine use, aerosolized pentamidine prophylaxis does not decrease the clinical severity or the sensitivities of sputum induction or bronchoalveolar lavage as diagnostic tests for PCP.
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PMID:Effect of aerosolized pentamidine prophylaxis on the clinical severity and diagnosis of Pneumocystis carinii pneumonia. 141 8

It has been previously demonstrated that serum lactate dehydrogenase is elevated among HIV patients with pneumocystis carinii pneumonia (PCP). To evaluate the clinical utility of this test we analyzed the admission LDH levels of patients hospitalized for the first time due to the secondary complications of AIDS. Among 76 patients without a prior history of PCP, 41 (54%) had PCP diagnosed during their hospitalization while 35 (46%) did not have PCP. Serum LDH was significantly higher among PCP patients than in patients without PCP (mean = 423 IU/L vs 234 IU/L). Receiver operating characteristic curve analysis demonstrated that at an optimal cutoff point of LDH greater than or equal to 240 IU/L, the test sensitivity and specificity were 0.78 and 0.74 respectively among all hospitalized patients. However, when only patients with dyspnea were considered, the optimal test sensitivity and specificity improved to 0.94 and 0.78 at a cutoff point of LDH greater than or equal to 220 IU/L. Comparing the areas under fitted ROC curves, serum LDH was a significantly better discriminator among patients with dyspnea than among those who were not short of breath. We conclude that while serum LDH is strongly associated with the presence of PCP among AIDS patients, it is a poor screening test for PCP when applied to all hospitalized AIDS patients with and without respiratory complaints. Serum LDH is no substitute for appropriate microbiological studies. However, with further evaluation, it may prove to be a useful test in guiding the clinical management of dyspneic patients in whom sputum or bronchial examinations are negative or not immediately available.
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PMID:The clinical utility of serum lactate dehydrogenase in diagnosing pneumocystis carinii pneumonia among hospitalized AIDS patients. 151 88

We report the development of severe hepatotoxicity in a patient on zidovudine therapy who received 3.3 g of acetaminophen in less than 36 hours. Three days later, the patient's serum aspartate aminotransferase level was 5,724 U/L, alanine aminotransferase was 3,124 U/L, lactate dehydrogenase was 12,675 U/L, alkaline phosphatase was 84 U/L, and total bilirubin was 20 mumol/L. These values substantially improved over the ensuing 4 days. Serologic results for hepatitis B, hepatitis A, and cytomegalovirus were all negative. The pattern and time sequence of transaminase elevation in this patient are consistent with acute acetaminophen hepatotoxicity, especially since zidovudine-induced hepatotoxicity is described as producing cholestasis rather than acute hepatitis. We hypothesize that our patient's susceptibility to acetaminophen-dependent hepatotoxicity may have been augmented by competitive utilization of glucuronidation by other drugs such as zidovudine and/or trimethoprim-sulfamethoxazole with subsequent increased cytochrome P450-dependent metabolism of acetaminophen. Additionally, due to malnutrition and/or to human immunodeficiency virus infection per se, our patient may have had decreased hepatic reserves of glutathione with which to conjugate the toxic acetaminophen product of the P450 system. Although severe acetaminophen-associated hepatotoxicity has not previously been reported in patients receiving zidovudine, we suggest that clinicians be aware of this potential interaction and counsel malnourished patients, especially those with concomitant hepatic disease, to exercise caution when taking both these medications.
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PMID:Severe hepatotoxicity in a patient receiving both acetaminophen and zidovudine. 836 34

Four out of eleven patients--none of them HIV positive--who received treatment for non-Hodgkin lymphoma by the MACOP-B protocol between June 1989 and February 1990 were taken ill during or shortly after the conclusion of the course with fulminant pneumonia necessitating artificial ventilation. In three cases Pneumocystis carinii was identified as the pathogen, and in one patient the diagnosis of pneumocystosis seemed probable. The mean cumulative doses given before the outbreak of pneumonia were as follows: cyclophosphamide 2753 +/- 1161 mg, methotrexate 1590 +/- 667 mg, bleomycin 36 +/- 16.8 mg and prednisone 4378 +/- 1734 mg. The mean haemoglobin concentration was 10.7 +/- 0.5 g/dl, leucocyte count 5250 +/- 2100/microliters, lymphocyte count 1300 +/- 300/microliters and lactate dehydrogenase 227 +/- 34 U/l. The cumulative doses and laboratory findings in the seven patients not affected by pneumocytosis were not significantly different. The patients with pneumonia were supported by mechanical ventilation for 6-26 days and treated with large doses of corticosteroids and co-trimoxazole. One patient died after 17 days' ventilation. Three patients were successfully weaned from the ventilator. Chemotherapy protocols such as MACOP-B predispose to acute Pneumocystis pneumonia. The risk of infection is independent of the cumulative doses of the drugs employed. For this reason, prophylaxis with co-trimoxazole is normally mandatory.
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PMID:[Acute pneumocystosis during polychemotherapy following the MACOP-B protocol]. 169 17

Pneumonia caused by common pyogenic bacteria occurs frequently in HIV-infected patients. Its clinical presentation has been described as being similar to that seen in non-immunosuppressed hosts but clearly different to that of opportunistic pneumonias. An atypical presentation has rarely been seen. In a 10-month period, we saw 12 HIV-infected patients who presented with Haemophilus influenzae pneumonia which was clinically and radiologically indistinguishable from Pneumocystis carinii pneumonia. Ten of the patients were intravenous drug users and were in different stages of HIV disease. The clinical picture was characterized by a prolonged course (median 4 weeks), non-productive cough, dyspnoea, and absence of findings usually present in bacterial pneumonia. Laboratory data frequently showed absence of leukocytosis, increased lactate dehydrogenase levels, hypoxaemia, and decreased CD4+ cell counts. All presented with interstitial or mixed bilateral infiltrates. Resistance to ampicillin and trimethoprim-sulphamethoxazole were each found in seven cases. Eleven patients were cured with antibiotic therapy, although five relapsed. H. influenzae pneumonia should be considered in HIV-infected patients who present with pulmonary symptoms and bilateral infiltrates of subacute or chronic onset. Clinical resolution of pneumonia is the usual outcome, but recurrences of infection are frequent.
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PMID:Latent Haemophilus influenzae pneumonia in patients infected with HIV. 177 77

A case study is given of a 25-year old woman with rhabdomyolysis associated with HIV infection. The presenting symptoms were a 1-week history of backache, gross swelling of both hands and feet, and weakness and marked pain in most muscle groups; 3 days before admission the urine was black and she was unable to walk. Multiple, firm 1-2 cm lymph nodes were revealed during examination. White blood cell count (WBC) was 22,000/microliter with 12 pc lymphocytes, 7.3 pc monocytes, and 80.5 pc polymorphonuclear leukocytes. Hemoglobin concentration was 15.8 g/deciliter; platelet count was 124,000/microliter with a Westergren ESR of 109 mm/h. An antinuclear antibody test was negative. Serum concentration of urea was 3.8 mmol/liter, creatinine 42 microliter/liter, sodium 128 mmol/liter, and potassium 5.9 mmol/liter. Microscopic examination of urine revealed WBC 100/HPF, red blood cells 20/HBF, and granular casts. The dipstick test showed blood land protein in the urine. Electromyography showed inflammatory myopathy. Creatine Kinase (CK) concentration was 2359 IU/liter and lactate dehydrogenase concentration 1000 IU/liter. Hemolysis was present from clinical or laboratory signs. The patient tested HIV positive by ELISA (Abbott) and Western blot (Dupont). Treatment consisted of administration of 60 mg/day of prednisolone orally. Over 2 weeks, swelling of limbs was reduced and CK concentration was reduced to 931 IU/liter. The patient was discharged and did not keep a follow-up appointment. The patient did not have a history of other predisposing conditions, only HIV infection and persistent muscle weakness and inflammatory myopathy. There is evidence from other patient studies of myopathy associated with HIV infection and polymyositislike illness. In this case study, the patient may have had a acute form of polymyositis, or acute viral myositis such as occurs with echo, influenza, coxsackie, and other viral infections. A detailed viral investigation was not performed. HIV infection may have directly infected myocytes or immunosuppression predisposing to acute myositis by other pathogens. HIV-related muscle disease should include rhabdomyolysis.
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PMID:Rhabdomyolysis associated with human immunodeficiency virus (HIV) infection. 180 50

Because the beneficial effects of zidovudine in human immunodeficiency virus infection-associated psoriasis have recently been observed, this study focused on the drug's action on the rapidly proliferating human HaCaT keratinocyte line as an in vitro model for epidermal hyperproliferation. Cultures in log growth phase were exposed to zidovudine for 2 days. Zidovudine slowed proliferation in a dose-dependent fashion as evidenced by 50% inhibition concentrations of 33 mumol/L (cell number), 30 mumol/L (protein content), 0.9 mumol/L (protein synthesis), and 0.7 mumol/L (DNA synthesis). Significant (p less than 0.01) reduction of cell viability to 94.6% and 87.2%, as well as morphologic manifestations of cytotoxicity, were first evident after 2 days' exposure to maximal drug concentrations of 10 and 100 mumol/L, respectively. Control viability, assayed by trypan blue exclusion, was 98.0%. Direct cytotoxic plasma membrane injury could be ruled out by the absence of any increase in cytoplasmic lactate dehydrogenase release into supernatants at least during the 1 day of maximal dosage exposure. The drug-induced inhibition of proliferation was reversible within 7 days after a 2-day exposure to 100 mumol/L zidovudine. Two days of treatment with a 10 mumol/L dose did not alter the pattern and synthesis of keratins in vitro. Thus the known antipsoriatic efficacy of zidovudine might be explained, at least partly, by the drug's cytostatic potency.
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PMID:Antiproliferative potential of zidovudine in human keratinocyte cultures. 191 88

All reported clinical characteristics of acute retroviral illness with the human immunodeficiency virus (HIV) are nonspecific. Signs and symptoms described are associated with a variety of acute infections. We report the cases of three patients in whom the acute retroviral illness was characterized by transient oral candidiasis and unexplained high lactate dehydrogenase values, with or without transient pulmonary infiltrate, in the context of an acute febrile illness. The clinical findings correlated with a severe reduction in the number of CD4 cells. We believe that thrush could be a marker of acute retroviral infection, as it is not a feature of any other heterophil-negative mononucleosis-like syndrome. We propose that in any patient having transient thrush and acute viral syndrome, the possibility of HIV infection should be aggressively pursued serologically, regardless of the patient's HIV risk status, provided that the usual causes of candidiasis (eg, diabetes mellitus, antibiotic use, and dentures) can be excluded.
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PMID:Oral candidiasis as a marker of acute retroviral illness. 205 63

The clinical presentation of 60 consecutive Pneumocystis carinii pneumonias in 58 HIV-infected patients (48 men, 10 women, mean age 34 [22-53] years) was prospectively evaluated from April to August 1989 and compared with 60 consecutive P. carinii pneumonias in 59 HIV-infected patients (55 men, 4 women, mean age 37.5 [22-60] years) between 1981-88. Mortality rates within 14 days after diagnosis of P. carinii pneumonia were 50% (8 of 16 patients) until 1985, 20.5% (9 of 44) between 1986 and August 1988, and 1.7% (one of 60) in 1989. The degree of severity of the pneumonias at time of diagnosis was markedly lower in 1989, as shown by following parameters (averages of 1989, compared with averages of 1981-88): lactate dehydrogenase 540 (250-1419) U/l versus 680 (235-1920) U/l (not significant); alveolo-arterial difference of partial oxygen tension (pA-aO2) 22.9 (0.5-73.5) mmHg versus 39.7 (19-70) mmHg (P less than 0.001); score of radiological findings 1.4 (0-3) versus 2.7 (0-4) (P less than 0.001). In 1989, mainly clinical symptoms (dry cough: 57 of 60 cases, dyspnea: 44 of 60 cases, fever: 43 of 60 cases) initiated the diagnostic procedure: chest radiographs, lactate dehydrogenase and pA-aO2 were normal in 13, 25 and 33 episodes, respectively. The lower mortality rate of P. carinii pneumonia could not primarily be explained by therapeutical progress since the treatment of choice did not change fundamentally since 1981. Above all, early diagnosis fundamentally determined the probability of survival.
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PMID:[Pneumocystis carinii pneumonia in HIV infection: better prognosis because of early diagnosis]. 222 63


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