Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor-reactive antibodies coupled to ricin or its A-chain (immunotoxins) have been used in rodents and humans to treat a variety of neoplastic diseases. Side-effects of such treatment include hepatotoxicity, vascular leak syndrome, myalgia and low grade fever. At high doses, severe toxicities include liver damage, pulmonary edema, aphasia, rhabdomyolysis and kidney failure. There have been a limited number of toxicologic studies on uncoupled ricin or its A-chain and none on deglycosylated A-chain. Since the latter has been utilized in "second generation" immunotoxins, the current studies were carried out to evaluate the toxicities induced by deglycosylated ricin A-chain (dgA) in mice. The administration of dgA to normal BALB/c mice causes early (24 h) weight loss and late (10 day) accumulation of ascites. These effects could be partially altered by changing the route of injection of dgA from i.v. to i.p. Thus, i.p. administration caused weight loss but not ascites, whereas i.v. administration caused both. Weight loss was associated with reduced fluid intake by the treated mice, and was not associated with increased levels of serum TNF-alpha. SCID mice injected with the same dose of dgA as normal BALB/c mice developed ascites, but it was of lesser severity, suggesting that a functional immune system, differences in microbial flora, or strain differences may be involved in the development of ascites.
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PMID:The toxicity of chemically deglycosylated ricin A-chain in mice. 162 27

Findings on chest radiographs of 18 patients with the eosinophilia-myalgia syndrome were compared and correlated with peak eosinophil counts. Nine patients had normal chest radiographs. Of the nine patients with abnormal chest radiographs, three had fine, irregular linear opacities in the lungs (the opacities were most noticeable at the bases); three had similar irregular linear opacities and pleural effusions; and three had pleural effusions and confluent opacities. One patient demonstrated an enlarged heart; no pulmonary edema was seen in this patient or in any others. Although the mean recorded eosinophil cell counts were higher in those patients with abnormal chest radiographs (6,340 vs 5,454/mm3 [6.3 vs 5.4 x 10(9)/L]), the difference was not statistically significant.
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PMID:Eosinophilia-myalgia syndrome: findings on chest radiographs in 18 patients. 183 Dec 75

Fifteen patients with refractory B-cell lymphoma were treated in a Phase I dose escalation clinical trial with a highly potent immunotoxin consisting of the Fab' fragment of a monoclonal anti-CD22 antibody (RFB4) coupled to chemically deglycosylated ricin A chain. All patients had low, intermediate, or high grade non-Hodgkin's lymphoma. The immunotoxin was administered i.v. in two to six doses at 48-h intervals. The peak serum concentration and the t1/2 were not dose dependent among patients and averaged 1.3 micrograms/ml and 86 min, respectively. Three patients made antibody against A chain, and a fourth made antibody against both A chain and mouse immunoglobulin. Antibody responses were low (less than or equal to 85 micrograms/ml) in three patients and were not detected until 1 mo after treatment. The maximum tolerated dose of the immunotoxin was 75 mg/m2. Dose-related toxicities included vascular leak syndrome, fever, anorexia, and myalgia. Dose-limiting toxicities included pulmonary edema and/or effusion, expressive aphasia, and rhabdomyolysis (resulting in reversible kidney failure). There was no evidence of liver dysfunction. Partial responses were achieved in 38% of evaluable patients, and in those patients who had greater than 50% CD22+ tumor cells, 50% of the patients achieved a partial response. Clinical responses were not related to tumor grade and were generally transient, lasting between 1 and 4 mo.
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PMID:Phase I immunotoxin trial in patients with B-cell lymphoma. 185 19

Twenty-two patients who had been bitten by a Russell's viper were studied. Neurological manifestations and generalized myalgia were observed, respectively, in 86.4% and 72.7%. Renal failure did not occur in three patients who received antivenin within 5 hours of the bite, and it is suggested that administration of antivenin within the first few hours following the bite could prevent renal failure. Of 19 patients who were in acute renal failure, seven responded to conservative management while 12 needed peritoneal dialysis. Nine patients developed pulmonary edema and four had grand mal seizures. Five patients died. Autopsy revealed massive pulmonary edema, thought to be the immediate cause of death, in four of them and extensive cortical and tubular necrosis in three.
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PMID:Russell's viper bite in Sri Lanka. A study of 22 cases. 673 82

Rocky Mountain spotted fever occurs during seasonal tick activity. A history of exposure to tick-containing habitats within the 3- to 12-day incubation period is a key epidemiological factor. The signs of fever, headache, myalgia, nausea, vomiting, and anorexia at onset of infection are difficult to distinguish from those of self-limited viral infections. Rash usually appears later and, if present, progresses through a sequence of stages and distribution that are never pathognomonic. The effects of disseminated Rickettsia rickettsii infection of endothelial cells include increased vascular permeability, edema, hypovolemia, hypotension, prerenal azotemia, and, in life-threatening cases, pulmonary edema, shock, acute tubular necrosis, and meningoencephalitis. In severe cases, fluid management is a challenge. The clinical diagnosis, which is difficult, is rarely assisted by laboratory findings because antibodies are usually detected only in convalescence, and immunohistologic methods for detection of rickettsiae are unavailable in most clinics. Doxycycline is the treatment of choice except for pregnant or allergic patients, who are treated with chloramphenicol.
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PMID:Rocky Mountain spotted fever: a seasonal alert. 761 84

Twenty-six patients, whose B-cell lymphoma had relapsed after conventional therapies, were treated in a phase I dose escalation study with an immunotoxin consisting of a mouse CD22 monoclonal antibody (RFB4:IgG1K) coupled to chemically deglycosylated ricin A chain (dgA). Two to 12 doses of the immunotoxin were infused intravenously at 48-hour intervals. The peak serum concentration and half-life (T1/2) did not correlate directly with the dose and averaged 3.8 micrograms/mL and 7.8 hours, respectively. The main dose-limiting toxicity was caused by the vascular leak syndrome (VLS) consisting of weight gain, edema, serum albumin decrease, and critically by pulmonary edema. Myalgia occurred frequently and was only dose limiting in one patient who developed rhabdomyolysis. The presence of lymphoma cells in the blood (> or = 10(10)/L) and clinically detectable splenomegaly were associated with reduced toxicity and a shorter T1/2. Nine of 24 evaluable patients (37.5%) made antibody to either mouse Ig or dgA. There were five partial responses (PR) and one complete response (CR) lasting 30 to 78 days. High peak concentrations of immunotoxin in the serum, a long T1/2, and large areas under the curve (AUC) correlated with both clinical response and toxicity. None of three patients with CD5+ lymphomas (including two CLL patients) had more than mild toxicity or responded to the immunotoxin.
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PMID:A phase I study of an anti-CD22-deglycosylated ricin A chain immunotoxin in the treatment of B-cell lymphomas resistant to conventional therapy. 821 17

Toxic oil syndrome is a multisystemic, epidemic disease that appeared in Spain in 1981, related to the intake of rapeseed cooking oil sold in bulk. It affected 19,748 people, of whom 457 died. The toxic substance was never identified. We report the 8-year follow-up of a cohort of 332 patients. The disease was usually severe and disabling during the first 2 years, but the clinical condition of most of the patients improved thereafter. The acute phase lasted 2 months, and was characterized by pulmonary edema, rash, eosinophilia, and myalgia. During the intermediate phase (second to fourth months), severe myalgia, skin tenderness, subcutaneous edema, altered liver function, and pulmonary hypertension developed. Later on, an early chronic phase developed, from the fourth month to the end of the second year. It was marked by scleroderma, sicca syndrome, polyneuropathy, joint contractures, weight loss, and functional limitations. The clinical manifestations improved during the late chronic phase. Its most prominent clinical features were muscle cramps, chronic musculoskeletal pain, chronic lung disease, Raynaud phenomenon, carpal tunnel syndrome, and psychologic disturbances. Only 9% of the patients achieved remission after the acute phase, the rest developing late clinical manifestations of the disease. The severity of the chronic manifestations was rather variable. At the end of the 8-year follow-up, there were 10 TOS-related deaths (3%), 47% of the patients had some kind of complaint, albeit subtle in most cases, and 16% showed organic involvement related to TOS. The most important pathologic features of TOS were widespread interstitial infiltrates, non-necrotizing angiitis, endothelial proliferation, and tissue fibrosis. Toxic oil syndrome is a dramatic example of an induced scleroderma-like syndrome, similar to the eosinophilia-myalgia syndrome. Patients with EMS may develop some of the late clinical features of TOS in the years to come.
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PMID:Toxic oil syndrome. A long-term follow-up of a cohort of 332 patients. 841 42

Plasmodium falciparum malaria is endemic in the northern KwaZulu areas of South Africa. The clinical morbidity produced by this parasite has not been studied since the institution of the present malaria control programme. Fifty-nine patients were prospectively studied at a peripheral clinic during the peak malaria season; symptoms and signs of the infection, parasite loads, haemoglobin values and leucocyte counts were recorded in all patients. Haemoglobin and leucocyte counts were also measured in 37 control subjects without malaria. The commonest symptoms were persistent headache (100%), rigors (98%) and myalgia (93%). None of the patients presented with coma, pulmonary oedema, hypoglycaemia or algid malaria. Splenomegaly was found in 49%, hepatomegaly in 20% and mental confusion in 5% of patients. Mean parasite load was 1.71% and 57% of patients had parasite loads of < 1%. Anaemia of < 10 g/dl was significantly more frequent (P < 0.0001) in the patient group than in the control group. Leucopenia (white cell count < 4.0 x 10(9)/l) was present in 12 of 50 patients in whom it was measured compared with 2 controls (P = 0.0175). The results show a wide range of morbidity, without severe complications as presenting manifestations. Symptomatic infection in the presence of low parasite loads suggests that there may be little or no immunity in this population.
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PMID:Morbidity from falciparum malaria in Natal/KwaZulu. 845 85

An outbreak of louse-borne relapsing fever, due to the return of soldiers to their original recruitment areas, after the end of thirty years of fighting in northern Ethiopia, was reported in Arsi region, southern Ethiopia. The epidemic spread to different members of the community and eventually the schools. We studied 389 patients affected by the epidemic and who were admitted to Asella Hospital between June 1991 and May 1992. Twenty-seven per cent of the patients were ex-soldiers; 28% were students, who were admitted to the hospital since the schools were opened after the summer vacations. The common clinical features of the disease were fever (99%), headache (92%), hepatosplenomegaly (66%), myalgia (55%), arthralgia (51%), petechial rash (43%), epistaxis (24%) and jaundice (23%). Observed complications were pneumonia (10%), pulmonary edema (6%), myocarditis (3%) and 6 abortions in 15 pregnancies. Patients were treated with low dose penicillin and i.v. fluids. The in-hospital case fatality rate was 3.6%. Jarisch-Herxheimer reaction occurred in 43% of the patients. 1.8% of the patients had relapses after treatment.
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PMID:Louse-borne relapsing fever. A clinical and an epidemiological study of 389 patients in Asella Hospital, Ethiopia. 794 Oct 15

Rhabdomyolysis was diagnosed in two dogs with babesiosis. The first animal presented with muscle pain and caramel-coloured urine, and had markedly elevated serum myoglobin and muscle enzymes. Acute renal failure complicated the clinical picture. The second dog exhibited muscle pain and tremors, together with neurological signs and pulmonary oedema, and died soon after admission. Muscle necrosis and haemorrhage were found at necropsy. In human malaria, a disease clinically similar to canine babesiosis, rhabdomyolysis is unusual, but clinically silent muscle damage appears to be common. Likewise, biochemical evidence of muscle damage is readily found in experimental bovine babesiosis. Muscle enzymes were mildly elevated in three dogs with severe babesiosis and pigmenturia but there was no obvious muscle damage, indicating that this might also apply to canine babesiosis. The pathogenesis of infection-associated rhabdomyolysis and acute renal failure remains unclear, but inflammatory cytokines and nitric oxide could play an important role.
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PMID:Rhabdomyolysis as a complication of canine babesiosis. 896 83


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