Cases reported "Pneumonia, Pneumocystis"

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1/587. Bilateral upper-lobe cavitary pneumocystis carinii pneumonia in a patient on dapsone prophylaxis.

    pneumocystis carinii pneumonia (PCP) presenting as bilateral upper-lobe cavitary disease is rare. Isolated upper-lobe involvement has traditionally been associated with aerosolized pentamidine prophylaxis. dapsone is a cheap and effective prophylactic agent against P carinii in patients who cannot tolerate trimethoprim-sulfamethoxazole. This is a case of a man who presented with bilateral upper-lobe cavitary P carinii pneumonia despite being on dapsone prophylaxis. bronchoalveolar lavage was negative for P carinii. Transbronchial biopsy was positive for P carinii. The patient improved significantly with radiological resolution on specific treatment for P carinii. PCP should be included in the differential diagnosis of upper-lobe cavitary lung disease, and a transbronchial biopsy should be performed when the diagnosis is suspected. ( info)

2/587. bronchiolitis obliterans organizing pneumonia associated with pneumocystis carinii infection in a liver transplant patient receiving tacrolimus.

    We report on a case of bronchiolitis obliterans organizing pneumonia (BOOP) associated with pneumocystis carinii pneumonia (PCP) after liver transplantation and tacrolimus based immunosuppression. Radiologically, bilateral diffuse interstitial shadowing and patchy alveolar infiltrates developed after switching the patient from cyclosporin A to tacrolimus for persistent rejection. bronchoalveolar lavage (BAL) fluid showed inflammatory cells but no pathogenic organisms. Open lung biopsy revealed BOOP with granulomatous PCP. Thus, even in the case of negative BAL the possibility of an atypical P. carinii infection has to be considered for differential diagnosis of pneumonia in immunocompromised patients after organ transplantation. The combination of BOOP with PCP after liver transplantation and tacrolimus medication has not been reported previously. ( info)

3/587. Management of opportunistic infections in acquired immunodeficiency syndrome. I. Treatment.

    A case report of a patient infected with human immunodeficiency virus (hiv) is described. The patient presents with a multitude of medical complaints that are of acute or subacute onset. The medical examination of these complaints is described and includes algorithms for the diagnosis and treatment of the most common hiv-related opportunistic infections, including pneumocystis carinii pneumonia, toxoplasmosis, mycobacterium avium complex, cytomegalovirus infection, and cryptococcal meningitis. ( info)

4/587. University of Miami Division of Clinical pharmacology therapeutic rounds: drug-induced hyperkalemia.

    Drug-induced hyperkalemia is an important but often overlooked problem encountered commonly in clinical practice. It may occur in the ambulatory as well as the impatient setting. Every evaluation of a hyperkalemic patient should include a careful review of medications to determine if a drug capable of causing or aggravating hyperkalemia is present. Medications generally produce hyperkalemia either by causing redistribution of potassium (beta2 -adrenergic blockers, succinylcholine, digitalis overdose, hypertonic mannitol) or by impairing renal potassium excretion. Drugs cause impaired renal potassium excretion by (1) interfering with the production and/or secretion of aldosterone (nonsterodial anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin-II receptor antagonists, heparin, cyclosporine, and FK 506) or (2) blocking the kaliuretic effects of aldosterone (potassium-sparing diuretics, trimethoprim, pentamidine, and nefamostat mesilate). Because severe renal insufficeiency is generally required to cause hyperkalemia, an elevated serum potassium concentration in a patient with mild-to-moderate renal failure should not be ascribed to renal failure alone. A careful search for "hidden" potassium loads and for causes of impaired tubular secretion of potassium (including drugs) is necessary. Finally, it is important to recognize that the causes of hyperkalemia may be additive. patients may have more than one cause of hyperkalemia at the same time. Therefore, all potential causes of hyperkalemia, including drugs, should be systematically evaluated in every hyperkalemic patient. ( info)

5/587. Apparent hemolysis in an AIDS patient receiving trimethoprim/sulfamethoxazole: case report and literature review.

    OBJECTIVE: To describe a case of acute hemolysis associated temporally with administration of trimethoprim/sulfamethoxazole (TMP/SMX) in a patient with AIDS, review the available literature on TMP/SMX-induced hemolytic anemia, and discuss possible drug- and disease-related factors that may have contributed to the episode of hemolysis. CASE SUMMARY: A precipitous decrease in red blood cell count, hemoglobin, and hematocrit occurred shortly after a black woman with AIDS received a single intravenous dose of TMP/SMX for pneumocystis carinii pneumonia. Following drug discontinuation and repeated transfusions, the patient's hematologic indices returned to baseline. literature SOURCES: References were obtained using medline searches, the bibliographies of articles identified during the searches, review articles, and standard textbooks. DATA SYNTHESIS: Of the two different mechanisms of TMP/SMX-induced hemolytic anemia, the reaction is most likely to occur via dose-related oxidative disruption of the erythrocyte membrane in subpopulations deficient in glucose-6-phosphate dehydrogenase (G6PD) activity. In the US, G6PD deficiency most frequently is encountered among blacks. The potential for hemolysis may be further increased in G6PD-deficient AIDS patients, who also appear to lack adequate intracellular glutathione, which is essential for protecting the erythrocyte membrane from oxidative damage. Although an assay for G6PD activity was not conducted, the case circumstances were consistent with TMP/SMX-induced hemolysis in a G6PD-deficient patient. CONCLUSIONS: Black patients with AIDS who are receiving relatively high (greater than or equal to 50 mg/kg/d) dosages of TMP/SMX should be monitored closely for signs and symptoms of hemolytic anemia. ( info)

6/587. Autoimmune enteropathy with distinct mucosal features in T-cell activation deficiency: the contribution of T cells to the mucosal lesion.

    BACKGROUND: Autoimmune enteropathy is normally characterised by crypt hyperplastic villous atrophy with enterocyte autoantibodies, activation of mucosal lymphocytes and increased epithelial HLA-DR. This case involved a severely affected Portuguese infant who was found to have lymphocyte activation deficiency and demonstrated correspondingly distinct mucosal features. methods: A female infant of nonconsanguineous parents was treated for vomiting and diarrhoea, first with milk exclusion and then with parenteral nutrition. lymphocyte subsets and immunoglobulin concentrations were normal, but in vitro testing showed no activation in response to phytohaemagglutinin, candida, or purified protein derivative, although the response to interleukin (IL)-2 was intact. interleukin-2 deficiency was excluded. Analysis of jejunal biopsy specimens revealed only mild villous blunting with absent goblet cells, normal epithelial proliferation, and no crypt hyperplasia. The dense infiltrate of CD8 and CD4 T lymphocytes showed normal CD2 and CD3 expression but no activation or proliferation markers. HLA-DR was not increased on epithelium or lymphocytes. Thus, in addition to in vitro evidence for lymphocyte activation deficiency, the mucosal specimens showed no evidence of in situ T-cell activation. RESULTS: After development of overwhelming septicaemia, the patient died at 18 months, just before a planned bone marrow transplant. CONCLUSIONS: These findings confirm significant heterogeneity within autoimmune enteropathy. Formal immune function testing should be performed in all affected infants to identify T-cell activation deficiencies. The distinct mucosal findings suggest that activated T cells usually induce the crypt hyperplastic villous atrophy characteristic of classic autoimmune enteropathy. ( info)

7/587. Concurrent infection with legionella pneumophila and pneumocystis carinii in a patient with adult T cell leukemia.

    A 48-year-old woman was admitted to our hospital with high fever, chills, cough, and exertional dyspnea. On admission, the chest roentgenogram and computed tomography scan showed bilateral alveolar infiltration in the middle and lower lung fields. Microscopic examination of the bronchial lavage fluid showed flower cells typical for adult T-cell leukemia (ATL) and cysts of pneumocystis carinii, and legionella pneumophila serogroup 1 grew on buffered charcoal yeast extract (BCYE)-alpha agar. The patient was successfully treated with antibiotics including trimethoprim/sulfamethoxazole, erythromycin, and sparfloxacin. Remission of ATL was achieved after three courses of antileukemic chemotherapy. Mixed infection of opportunistic pathogens should be considered in patients with ATL. ( info)

8/587. Enteroviral meningoencephalitis as a complication of X-linked hyper IgM syndrome.

    We describe 5 children from 2 families with mutations in the cd40 ligand (CD40L) gene leading to absent expression of CD40L on activated CD4 cells. All subjects presented with interstitial pneumonia with low serum IgG and normal serum IgM. One child had normal and one child had elevated serum IgA. Four had confirmed pneumocystis carinii pneumonia. In spite of intravenous immunoglobulin treatment yielding therapeutic serum immunoglobulin levels, 3 children had enteroviral encephalitis. When assessed by flow cytometry, the 3 surviving affected male children had absent CD40L expression on activated CD4( ) T cells. The affected children from both families were shown to have the same single nucleotide insertion (codon 131) resulting in frameshift and early termination within exon 4 (extracellular domain). This observation demonstrates that persistent enteroviral infection is not only observed in X-linked agammaglobulinemia but may also occur in patients with X-linked hyper IgM syndrome. ( info)

9/587. Therapeutic failure of trimethoprim/sulfamethoxazole in the treatment of pneumocystis carinii pneumonia.

    OBJECTIVE: To report a case of failure of treatment of pneumocystis carinii pneumonia (PCP) with trimethoprim/sulfamethoxazole (TMP/SMX) in a patient with hiv infection, despite an adequate serum SMX concentration. CASE SUMMARY: A 52-year-old white man was treated with TMP/SMX for PCP. After discharge he returned to the hospital with worsening of the PCP despite a serum SMX concentration of 60 micrograms/mL 18 hours after his last dose of TMP/SMX. DISCUSSION: PCP is one of the most common complications of hiv infection. TMP/SMX is the drug of choice for prophylaxis and treatment. The causes of therapeutic failure with this agent are not well documented. CONCLUSIONS: Alternative therapies to TMP/SMX should be seriously considered if the serum concentrations are therapeutic and the patient is not clinically improved. ( info)

10/587. Concurrent pneumocystis carinii and cytomegalovirus pneumonia after autologous peripheral blood stem cell transplantation.

    A 46-year-old woman developed concurrent CMV and pneumocystis carinii pneumonia (PCP) 140 days after autologous peripheral blood stem cell transplantation (APBSCT) for AML. She was seropositive for CMV before undergoing APBSCT and had required prednisone for immune thrombocytopenia and allergic dermatitis for 9 weeks prior to the onset of pneumonia. She had also been receiving PCP prophylaxis with pentamidine aerosol every month for 3 months before developing symptoms. The pneumonia was complicated by severe hypoxia, requiring ventilator support and pneumothorax requiring chest tube thoracostomy. She recovered following treatment with trimethoprim-sulfamethoxazole (TMP-SMX), prednisone, gancyclovir and intravenous immunoglobulin. Although the overall incidence of severe CMV disease is low after APBSCT, preventive measures such as surveillance culture and secondary prophylaxis with gancyclovir may be warranted in patients whose cellular immune response is further compromised by corticosteroid use or other factors. ( info)
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