Renal transplant artery thrombosis following treatment of allograft rejection with monoclonal anti-CD3 antibodies (OKT3).
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Biomedical subjects
Publications and source records attributed to F R Pruvot.
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Allograft recipients undergoing cytomegalovirus infection present increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction revealed selective imbalances of peripheral blood CD8+ T cell subsets. Initially, CMV viraemia is associated with elevated CD8+bright T cell numbers and T cell activation. Activation markers fall to normal when viral cultures become negative (before the end of the first month). During the second to sixth month, most (12/16) patients keep up high CD8+ T cell counts (1050-2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCR alpha beta+, but were not stained by anti-CD28, CD11b, CD16, CD56, and CD57 antibody. Unexpectedly, CD8+CD57+ T cells, a hallmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively thereafter. They become the predominant CD8+ T cell subset after 6 months of infection and their persistence for several (up to 4) years is strongly correlated (r = 0.87) with expansion of CD8+ cells. By analysis with MoAbs, there was no bias towards the use of particular TCR-V beta gene families at any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8+CD57- subset and its progressive replacement by CD8+CD57+ T cells that are chronically elicited by CMV.
Allograft recipients with cytomegalovirus (CMV) infection develop increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and 5 liver allograft recipients with primary CMV infection but no other aetiological factor to explain graft dysfunction revealed selective imbalances in peripheral blood CD8+ T cell subsets. Initially, CMV viraemia was associated with elevated CD8+bright T cell numbers and T cell activation. Activation markers fell to normal when viral cultures became negative (before the end of the 1st month). During the 2nd-6th months, most (12/16) patients continued to have high CD8+ T cell counts (1050-2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCRalphabeta+ but were not stained by anti-CD28, CD11b, CD16, CD56 and CD57 antibody. Unexpectedly, CD8+ CD57+ T cells, a hallmark of CMV infection, did not appear until the 2nd-6th months of primary CMV infection, and their numbers increased progressively thereafter. They became the predominant CD8+ T cell subset after about 6 months of infection and their persistence for several (up to 4) years was strongly correlated (r = 0.87) with expansion of CD8+ cells. Persistence of CD8 lymphocytosis was, thus, directly related to the rate of expansion of an uncommon CD8+ CD57- subset and its progressive replacement by CD8+ CD57+ T cells that were chronically elicited by CMV.
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Acute adrenal insufficiency is an uncommon complication of lung cancer and adrenal metastasis resection. Diagnosis is difficult to establish but an early recognition and treatment may be life-saving. A 55-year-old man underwent right upper lobectomy and adrenalectomy for lung carcinoma with right adrenal metastasis. Anaesthesia was obtained with propofol, alfentanil, atracurium and isoflurane. Blood pressure remained stable throughout surgical procedure and blood loss was about 3,000 ml. Several hours after the end of the procedure which was uneventful the circulator status worsened. The blood pressure was initially controlled with 500 ml of gelatin. External blood loss was about 200 ml. Clinical examination, chest X-ray and ECG were normal. Postoperative laboratory data showed a serum sodium at 134 mmol-1.l-1 and a serum potassium 5.1 mmol.l-1; haemoglobin concentration was 93 g.l-1. Arterial blood gas analysis, with a 5.1.min-1 nasal O2 flow showed a PaO2 at 108 mmHg, a PaCO2 at 30 mmHg and a pH at 7.44. Twelve hours later, a transient cardiac arrest occurred which responded to fluid load, dopamine and dobutamine. Six hours later, the patient went in ventricular fibrillation responding to an external electric countershock. No change in clinical status was noticed, except hyperthermia at 39.5% degrees C. Serum potassium concentration before cardiac arrest was 4.7 mmol-l-1. Main considered diagnoses were septic shock and acute adrenal insufficiency. Antibiotics (imipenem, amikacin and vancomycin) and hormonal treatment (hydrocortisone 200 mg.day-1), after blood samples had been obtained for bacteriological and hormonal examinations. The patient's condition improved dramatically within 48 hours. Shock was under control, dopamine and dobutamine were rapidly discontinued.(ABSTRACT TRUNCATED AT 250 WORDS)
This report concerns a case of hepatic epithelioid hemangioendothelioma presenting with liver enlargement, multiple hepatic calcifications on the plain abdominal film and bilateral interstitial pneumonia. Epithelioid hemangioendothelioma is an unusual soft tissue tumor of "intermediate malignancy" characterized by a multicentric involvement of the liver and originating from endothelial cells. Histopathologic diagnosis may be difficult because of possible confusion with sclerosing epithelial tumors.
Late portal vein thrombosis of liver grafts is uncommon and is usually revealed by variceal bleeding. We herein report a case of thrombosis discovered in an adult 10 months after liver transplantation, due to stenosis of the portal vein by extrinsic compression, probably secondary to a biopsy-induced hematoma. Development of venous collateral circulation allowed for normal function of the liver graft.
We analyzed the records of 3 patients transplanted for end-stage renal failure due to primary hyperoxaluria and evaluated on repeat biopsies the role played by oxalate deposits in the constitution of renal failure after isolated kidney graft, or combined liver and kidney transplantation. Early failure of the renal graft is frequent and often interpreted as the consequence of recurrence because of the presence of oxalate deposits on the graft biopsy. In fact, the decrease in oxalate deposits observed in our 2 cases of combined liver and kidney transplantation despite the progressive renal failure, indicates that crystal deposition is not responsible for the renal lesions. However, we cannot exclude that the oxalate molecule toxicity plays a role in the constitution of the diffuse sclerosis which occurred in these two cases after a primary renal non function, aggravating a hemodynamic process by using cyclosporin. On the other hand, as observed in our isolated kidney graft, renal crystal deposition occurring before the onset of renal failure suggests the true mechanism explaining the slow recurrence of renal oxalosis.
Reported cases of HUS/TTP (hemolytic uremic syndrome/thrombotic thrombopenic purpura) with cyclosporin (CsA) are more and more frequent, which led us to evaluate the incidence of microangiopathic process in kidney graft patients. In our first retrospective study we noted 9.4 percent of HUS/TTP among 117 patients. We tried to detect infraclinical hemolytic events prospectively in 40 new patients by systematic measurement of haptoglobin levels after introduction of CsA. The incidence of falls in haptoglobin levels was 25 percent. The immunological context was always noted: rejection crisis in 5 cases, cytomegalovirus infection in 3 cases, isolated markers of lymphocyte-activity in 2 cases. We never found a clinical or infraclinical form of microangiopathic process without a symptomatic or asymptomatic immunological complication. Monitoring haptoglobin levels make it possible to detect early endothelial injuries which could be linked to the future arteriolopathy described with CsA therapy.
1. Using crossed immunoaffinity electrophoresis with free concanavalin A in the first dimension, we studied the microheterogeneity of alpha 1-antichymotrypsin due to various glycoforms in sera from patients with various liver diseases and after liver transplantation. 2. Studies by isoelectric focusing and immunoblotting and by crossed immunoelectrophoresis without concanavalin A in the first dimension allowed us to show that there is no dramatic variation in electrophoretic heterogeneity of alpha 1-antichymotrypsin in the serum of patients with liver diseases or after liver transplantation when compared with that of normal subjects. Therefore the heterogeneity observed in crossed immunoaffinity electrophoresis is due to various interactions with concanavalin A. 3. The results were expressed as the ratio of concanavalin A non-reactive glycoforms plus concanavalin A weakly reactive glycoforms to concanavalin A reactive glycoforms, called R alpha 1-ACT. R alpha 1-ACT was significantly higher in patients with cirrhosis (n = 53) when compared with normal subjects (n = 30). The median R alpha 1-ACT was 1 (range 0.72-1.25) in normal subjects. It was 1.6 (range 1.18-3.02), 1.45 (range 0.65-4.12) and 2.24 (range 1.03-19) in cirrhosis of Child's grade A, B and C, respectively. There was a dramatic decrease in glycoforms with mostly biantennary glycans in some patients with Child's grade C cirrhosis. Serum levels of alpha 1-antichymotrypsin were lower than normal only in some patients with Child's grade C cirrhosis. 4. Among the patients with acute viral hepatitis studied (n = 17), five were studied longitudinally.(ABSTRACT TRUNCATED AT 250 WORDS)
The incidence of cyclosporine (CsA) vascular toxicity is open to debate. We attempted to evaluate the incidence of hemolytic accidents in our series of patients taking all clinical forms into consideration. From January, 1989, to December, 1990, 117 patients received kidneys from cadaver donors and were treated with CsA. Five patients presented hemolytic uremic syndrome (HUS) accompanied by a rejection crisis; 6 patients presented hemolytic anemia associated in 2 cases with marked thrombocytopenia without any evidence of rejection. Cytomegalovirus (CMV) infection was diagnosed in 2 patients and bacterial infection preceded hemolysis in 2 other cases, suggesting a triggering factor. In addition, when we systematically determined haptoglobin levels after introduction of CsA treatment, we found asymptomatic hemolytic episodes more frequently. Our incidence of hemolytic accidents was approximately 10%. Hemolysis could indicate ischemic vascular damage leading to arteriolar medial hyalinosis preceding fibrosis in CsA nephrotoxicity. Thus, it would be interesting to detect asymptomatic forms of hemolysis by monitoring haptoglobin levels. This approach could lead to a reduction of the CsA dose in patients presenting low haptoglobin levels, even in the absence of evidence of nephrotoxicity.
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Twenty total gastric resections were performed on 80 patients admitted to surgery for severe oesophagogastric corrosive injuries, with immediate or delayed full-thickness necrosis or perforation of the stomach. The duodenum, cardia and cervicothoracic oesophagus were sutured. A cervical oesophagostomy and a feeding jejunostomy were done. The oesophagus was thus excluded. All the corrosive agents were liquid. The ingested quantities were higher than 150 ml in 11 cases. Oesophagoscopy was performed in 12 patients: 4 lesions were stage III, 5 stage II, 2 stage I, while in 1 the mucosa appeared normal. Five patients died, but only 1 from an oesophageal complication, an oesophago-tracheal fistula on the 33rd post-operative day. The survivors had a secondary colon bypass and 5 patients developed a secondary mucocele. We suggest that the low incidence of tracheo-oesophageal fistula in our series and the possible formation of a mucocele in the excluded oesophagus are two arguments for a conservative attitude towards the oesophagus in most cases of emergency gastric surgery for corrosive lesions. Immediate oesophagectomy adds another traumatic factor to the effects of the burns. A subsequent oesophagectomy should be contemplated during coloplasty to prevent the formation of a mucocele.
Twenty cases of cystic adenomatoid malformation of the lung were observed: 2 had died in utero; the diagnosis was made at birth in 13 infants of which 3 were premature. A Bochdalek's hernia had been diagnosed before birth in 2 cases by echo-tomography. The correct antenatal diagnosis had been made in 2 cases. Two infants had no symptoms, 3 were dyspneic, 8 were in respiratory distress and had to be intubated and ventilated. Two had a prune belly syndrome. Eight infants had a thoracotomy during their first week of life. Pulmonary resections concerning those 13 patients comprised 10 lower lobectomies, 1 of which was associated with a lingulectomy, and 2 upper lobectomies, 1 of which was associated with a middle lobe resection. Five patients were diagnosed and operated upon between 10 months and 8 years of age; 4 had recurrent bronchitis and 1 was diagnosed during the treatment of a gastroenteritis. They had 3 lower and 2 upper lobectomies. Recovery was uneventful in all patients except for 1 who was reoperated upon for intestinal obstruction. Antenatal diagnosis of cystic adenomatoid malformation should become standard. The malformation may be mistaken for a pulmonary sequestration or bronchogenic cyst. Differential diagnosis of a congenital hernia is important.