Efficacy of low-dose OKT3 as cytolytic induction therapy in heart transplantation.

BACKGROUND: The need for prophylactic cytolytic treatment in heart transplantation is a controversial issue. Its use, however, might prevent the onset of cellular rejection in the immediate postoperative period, facilitating patient management. It has recently been suggested that the administration of these products at low doses might have the same immunologic impact and would reduce secondary effects and the cost of treatment. METHODS: In a nonrandomized retrospective study, we assessed 45 consecutive patients who underwent orthotopic heart transplantation in 1992 and 1993. Six patients who died before receiving the complete OKT3 dose were excluded. Twenty-three patients were treated with 5mg/day doses of OKT3 for 7 consecutive days. Another 16 patients received 2.5 mg of OKT3 for 7 consecutive days. RESULTS: There were no significant differences between the two groups with respect to CD3 counts on days 2 (0.1% +/- 0.3% versus 0.04% +/- 0.25%; p > 0.05) and 6 (0.2% +/- 0.45% versus 0.1% +/- 0.3%; p > 0.05), number of rejection episodes (1.45% +/- 0.8% per year of follow-up versus 1.7% +/- 1.2%, p = 0.66), number of infectious complications (8 versus 3, p > 0.05), total methylprednisolone dose used to treat rejection crises (3900 +/- 2765 versus 3600 +/- 1963 mg; p = 0.71), adverse effects attributed to OKT3 (two versus none), or length of the postoperative hospital stay (36.8 +/- 19 versus 30.2 +/- 20.9 days). CONCLUSIONS: As cytolytic induction therapy in heart transplantation, a daily regimen of 2.5 mg of OKT3 for 7 days achieves the same clinical and immunologic effect as the conventional 5 mg/day dose. In addition, it results in a considerable reduction in the cost of treatment.

[Pathology of the heart transplant]. / Patología del trasplante cardíaco.

The endomyocardial biopsy is the best diagnostic procedure of the rejection in the cardiac transplant. In this paper we analize the more frequent findings observed in the biopsies and in the dead patient's hearts after a transplant. Due to the fact that the rejection' lesions have a focal distribution the biopsy has to contain at least four fragments. The diagnostic criteria for rejection was stablished since 1990. There are other lesions that can suppose a problem being the most frequent the ischemia, the infectious miocarditis and the Quilty effect. The post mortem studies permit the diagnostic of vascular lesions that are not identified in the routine biopsies.

[Giant-cell myocarditis: a systemic disease? Apropos a case]. / Miocarditis de células gigantes: una enfermedad sistémica? A propósito de un caso.

Giant cell myocarditis is a rare disease of unknown etiology, which develops as a myocardial isolated affection or associated to different diseases. Its characteristics are such as necrosis, inflammation and giant cell presence in the myocardium. We present the case of a woman who suffered of giant cell myocarditis, thymoma, myasthenia gravis, chronic lymphocytic thyroiditis, giant cell myositis, granulomatous infiltration in the lymph nodes of the hilus of the lung and hypogammaglobulinemia; multiple association that we have not found in any published medical paper and that suggest the autoimmune origin of this illness. The cardiovascular symptoms and the associated diseases are revised, and we discussed the diagnostic and therapeutic topics, pointing out the necessity to take it into account for any patient with thymoma or myasthenia gravis developing to heart failure or arrhythmias.

Microsomal sphingomyelin accumulation in thioacetamide-injured regenerating rat liver: involvement of sphingomyelin synthase activity.

The purpose of this work was to determine whether alterations in the lipid composition of rat liver microsomal membranes existed during thioacetamide-induced injury prior to the development of hepatic cancer and biochemical mechanisms involved. Rats were injected intraperitoneally with (50 mg/kg body wt per day) thioacetamide or diluent for 8 days. Liver homogenates and microsomal membranes from liver homogenates were obtained. Incorporation of [32P]orthophosphate into whole liver lipids and hepatic microsomal lipids was evaluated 75 min after isotope administration. These determinations were made after two separate periods of treatment (3 and 8 days). Activity of sphingomyelin synthase was assayed in rat liver homogenates as well as in the purified microsomal fractions. Results demonstrated a maintenance of liver and hepatic microsomal contents of phosphatidylcholine during thioacetamide-induced injury even when the biosynthesis of this glycerophospholipid in both liver and their microsomal fractions appeared decreased. Also observed was a considerable increase of microsomal sphingomyelin, as well as an increased hepatic biosynthesis of sphingomyelin caused by thioacetamide treatment. The microsomal sphingomyelin/phosphatidylcholine radioactivity ratio significantly increased. Sphingomyelin synthase activity in liver homogenate appeared stimulated. In conclusion, our data are consistent with a thioacetamide-induced increase in microsomal sphingomyelin by a stimulation of sphingomyelin synthase. Based on this and previous studies, accumulation of sphingomyelin in the microsomal purified fraction is associated with the number of thioacetamide doses and is an early event clearly detected prior to tumoral characteristics of hepatocytes.

Acute pancreatitis and systemic lupus erythematosus: necropsy of a case and review of the pancreatic vascular lesions.

The role of systemic lupus erythematosus (SLE) in the development of acute pancreatitis is a matter of controversy since, in many cases, this complication has been attributed to the drugs administered. In this study, we present a patient diagnosed as having SLE who developed acute pancreatitis with no apparent cause aside from her basic disease, and in whose necropsy was observed vascular damage consisting of severe intimal proliferation. Pancreatic vascular lesions in previously reported patients with lupus are reviewed.

Isolation of rat liver lysosomes by a single two-phase partition on dextran/polyethylene glycol.

Crude mitochondria from liver rats were added to a two-phase system containing dextran and polyethylene glycol. The polymer and ionic concentration values of the two-phase system were changed in order to separate lysosomes from mitochondria. The best separation of lysosomes and mitochondria was obtained at 6.6-6.6% (w/w) dextran-polyethylene glycol and 5 mmol/kg ammonium chloride as shown by enzyme assays. This procedure showed good reproducibility, and lysosomes were never contaminated with more than 16% mitochondria, as determined by succinate dehydrogenase activity, and beta-D-galactosidase and acid phosphatase activities were enriched five- to sixfold. The lipid composition profile of lysosomes was quite similar to that obtained by means of free carrier electrophoresis, considered a reference method.

[Lymphoma of the rectum associated with lymphoid nodular hyperplasia in a common variable immunodeficiency]. / Linfoma rectal asociado a hiperplasia nodular linfoide en el seno de una inmunodeficiencia variable común.

A patient with common variable immunodeficiency developed lymphoid nodular hyperplasia and, subsequently, a follicular non-Hodgkin lymphoma with excellent response to chemotherapy. The patient remained in remission after 4 years. The very unusual type of this lymphoma and its localization are discussed, and the possible relations between these different conditions as a single spectrum of B lymphocyte are analyzed.

Effect of S-adenosyl-L-methionine on thioacetamide-induced liver damage in rats.

S-Adenosyl-L-methionine (Ado-met) administration to rats significantly improved liver necrosis induced by thioacetamide (TAA) as evidenced by reduction of TAA-elevated catalytic activity of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALAT). Ado-met, however, was not effective in reduction of catalytic activity of serum alkaline phosphatase (ALP) which increased as a consequence of TAA administration. Histologic analysis of the livers supported the biochemical data. Hepatocellular damage was evident from the first day of TAA treatment at daily (i.p.) doses of 50 mg/kg body wt. Maximal necrosis was apparent after 3 days of TAA administration. When rats were treated once a day, for 3 days with Ado-met (2 mg/kg body wt) as well as with TAA, significant reduction of hepatic necrotic area was observed. A similar effect was obtained when doses of 200 mg/kg body wt. of Ado-met were utilized.