Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical complications associated with narcotic addiction include bacterial endocarditis, pneumonia, pulmonary embolism and renal disease. Renal disorders associated with pentazocine abuse are rarely reported. They vary with method of administration, dosage, and duration of abuse. We describe a 33-year-old male addict, using intravenous pentazocine for 6 years. He has nephrotic syndrome with a rapid deterioration of renal function to a uremic stage within 3 weeks. The laboratory data includes: IgG 1270 mg/dl, IgA 369mg/dl, IgM 326mg/dl, C'3 65.2 mg/dl, C'4 16.3 mg/dl, and serum soluble interleukin-2 receptor level (sIL-2R) greater than 6000U/ml. A renal biopsy revealed membranoproliferative glomerulonephritis (MPGN) type I with tubulointerstitial nephritis. Immunofluorescent (IF) study revealed granular deposition of C'3 and IgM in mesangium and the glomerular capillary wall. The pathogenesis of glomerular disease in drug addicts is discussed, and the literature reviewed.
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PMID:Pentazocine addict nephropathy: a case report. 131 15

We describe the case of pulmonary embolism from metallic mercury after an deliberate intravenous injection in a drug addict. Metallic mercury embolisation is extremely rare and it is very important to remark the role of elementary mercury in chronic poisoning. In most reported cases, including our patient, the clinical pathologic manifestations are not so important. The reported symptoms are chest pain, tachypnea, gastrointestinal-tract disorder and one case of bloody diarrhea. Intravenous injection causes a local endothelial damage. After embolization the mercury may remain within the pulmonary interstitium and the alveoli, where may develop in sterile abscesses and granulomatous foreign body reactions. The mercury may remain localized as a depot of elemental mercury or may be oxidized to the soluble mercuric ion and may be distributed to other body tissues and may produce chronic poisoning. This toxicity causes damages, particularly to the kidneys (glomerular-nephritis), but does not cause changes in renal function (follow-up 10 years).
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PMID:[A case of embolism caused by metallic mercury in a drug addict]. 248 39

The metabolism and urinary excretion of 125I antithrombin III (AT III) was investigated in 2 patients with a nephrotic syndrome caused by minimal chain nephritis and primary amyloidosis, and acquired deficiency of AT III. Increased AT III catabolism was observed in both patients, even after correction for urinary protein loss. Increased AT III catabolism was due to increased influx from the extra- to the intravascular compartment in 1 patient, and to an increased fractional catabolic rate in the other patient who developed later a pulmonary embolism. Analysis of urine samples revealed biologically inactive whole AT III molecules and biologically as well as antigenically inactive fragments, respectively, whereas daily plasma gel filtration showed intact radioactive AT III. These observations reject the hypothesis that AT III deficiency in nephrotic patients is only due to urinary loss of AT III.
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PMID:Antithrombin III metabolism in two patients with a nephrotic syndrome caused by minimal chain nephritis and primary amyloidosis. 366 86

Maternal mortality was examined in a semi-urban Nigerian community over a 10-year period. Maternal mortality was defined as death occurring as the direct result of childbearing and measured per 1000 births. Abortions at below 20 weeks gestation were excluded. From 1966 to 1975, there were 90 maternal deaths out of 13,182, a rate of 6.8/1000. The hospital records of the Baptist Medical Center, located in the western part of Nigeria, were carefully reviewed and cross-checked with obstetric statistical records. Only 13 of the deaths occurred in hospitalized patients. 78 (80%) were due to direct obstetric causes; 12% were from nonobstetric causes. Anemia due to blood loss was the leading casue of death, accounting for 30, or 33%, of the deaths. Anemia, with or without congestive heart failure accounted for 7 deaths. Infection was responsible for 5 deaths. Ruptured uterus, preeclampsia, and eclampsia occurred in equal percentages, 10-11%. Indirect obstetric deaths, such as sudden death, accounted for 10 deaths. 50% of these were anesthetic deaths; the remainder were due to pulmonary embolism. Sickle cell intrapartum crisis was the cause of 1 death. Associated causes included featured pneumonia, nephritis, hepatitis, meningitis, enteritis, and cerebrovascular accident. Parity ranged from 0-11. 25 babies were salvaged in this series. Prevention continues to be the cornerstone in improving maternal mortality figures in developing countries. The Baptist Medical Center's model for providing maternal care is described briefly and is identified as responsible for the encouraging decline in the maternal mortality rate.
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PMID:Maternal mortality in a semi-urban Nigerian community. 720 76

The incidence of renal vein thrombosis (RVT) and other thrombo-embolic phenomena was evaluated in 44 unselected patients with nephrotic syndrome. Renal vein thrombosis was demonstrated by selective renal venography in 10 patients and at post-mortem in one. Extension of the thrombus from the renal veins into the inferior vena cava was seen in 3 patients. Evidence of thrombo-embolism elsewhere in the body was seen in the form of thrombophlebitis in the lower extremities in 4 patients (9.1%), pulmonary embolism in 3 (6.8%) and myocardial infarction in one (2.3%). Of the 11 patients with RVT, renal histology showed membranous glomerulonephritis in 3, minimal change nephritis in 5, membrano-proliferative in one and focal and diffuse proliferative glomerulonephritis in one patient each. The characteristics clinical findings such as gross haematuria and flank pain were noted in only 3 patients with RVT. No significant difference could be detected between the plasma fibrinogen, serum cholesterol, beta-lipoprotein, triglycerides and phospholipid concentration of those who showed RVT and the remainder in whom RVT was not demonstrated. The possible mechanisms involved in the pathogenesis of RVT in nephrotic syndrome are discussed.
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PMID:Renal vein thrombosis in nephrotic syndrome--a prospective study and review. 732 94

We analysed the causes of 67 deaths, over a 4 y period, in our oriental population with systemic lupus erythematosus (SLE). The median disease duration was 48 +/- 60.5 months (range 1-250 months). The mean age at diagnosis and death were 30 and 35.1 y respectively. SLE alone accounted for death in 30 patients (44.8%), infection in 27 (40.3%), pulmonary embolism in 5 (7.5%), malignancy in 4 (5.9%) and rheumatic heart disease in 1 (1.5%). The major organ involvement in those with active disease at death were SLE related thrombocytopenia (n = 23/44, 52.3%), nephritis (n = 21/44), 47.7%), cerebral lupus (n = 16/44, 36.4%), and pulmonary haemorrhage (n = 12/44, 27.3%). As in other series, SLE and infection were the principal causes of death in our population. During this 4 y period, there was no late death due to atherosclerosis.
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PMID:SLE mortality in an oriental population. 911 15

Enteropathy-associated T-cell lymphoma (EATCL) is a high grade, pleomorphic peripheral T-cell lymphoma usually with cytotoxic phenotypes. We describe a first case of patient with EATCL that is remarkable for its fulminant course and invasion of both kidneys manifested as acute renal failure. The patient was a 23 year old woman with a long history of celiac disease. She was presented with acute renal failure and enlarged mononuclear infiltrated kidneys. Diagnosis of tubulointerstitial nephritis and polyserositis was confirmed with consecutive pulse doses of steroid therapy. After recovery, she had disseminated disease two months later. Magnetic resonance imaging showed thickened intestine wall, extremely augmented kidneys, enlarged intra-abdominal lymph nodes with extra-luminal compression of common bile duct. Laparotomy with mesenterial adipous tissue and lymph glands biopsy was done. Consecutive pathophysiological and immunohistochemical analyses confirmed the diagnosis of EATCL: CD45RO+, CD43+, CD3+. The revision of renal pathophysiology substantiated the diagnosis. The patient received chemotherapy, but unfortunately she died manifesting signs of pulmonary embolism caused by tumor cells.
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PMID:A rare case of enteropathy-associated T-cell lymphoma presenting as acute renal failure. 1661 43

The endothelium is a monolayer of cells that covers the inner surface of blood vessels and its integrity is essential for the maintenance of vascular health. Endothelial dysfunction is a key pathological component of antiphospholipid syndrome (APS). Its systemic complications include thrombotic endocarditis, valvular dysfunction, cerebrovascular occlusions, proliferative nephritis, deep vein thrombosis, and pulmonary embolism. In women, APS is also associated with pregnancy complications (obstetric APS). The conventional treatment regimens for APS are ineffective when the clinical symptoms are severe. Therefore, a better understanding of alterations in the endothelium caused by antiphospholipid antibodies (aPL) may lead to more effective therapies in patients with elevated aPL titers and severe clinical symptoms. Currently, while in vivo analyses of endothelial dysfunction in patients with APS have been reported, most research has been performed using in vitro models with endothelial cells exposed to either patient serum/plasma, monoclonal aPL, or IgGs isolated from patients with APS. These studies have described a reduction in endothelial cell nitric oxide synthesis, the induction of inflammatory and procoagulant phenotypes, an increase in endothelial proliferation, and impairments in vascular remodeling and angiogenesis. Despite these lines of evidence, further research is required to better understand the pathophysiology of endothelial dysfunction in patients with APS. In this review, we have compared the current understanding about the mechanisms of endothelial dysfunction induced by patient-derived aPL under the two main clinical manifestations of APS: thrombosis and gestational complications, either alone or in combination. We also discuss gaps in our current knowledge regarding aPL-induced endothelial dysfunction.
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PMID:Mechanisms of Endothelial Dysfunction in Antiphospholipid Syndrome: Association With Clinical Manifestations. 3062 4