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Biomedical subjects

D Geltner

Publications and source records attributed to D Geltner.

At least 37 records · Page 2Linked to original sources
PubMed1993

Mechanism of autoimmune hemolytic anemia in chronic lymphocytic leukemia.

Chronic lymphocytic leukemia (CLL) is a malignant clonal expansion of CD5+B lymphocytes. The CD5+B lymphocytes have been postulated to produce autoantibodies. CLL patients may demonstrate features of autoimmunity including autoimmune hemolytic anemia. However, the origin of the autoantibodies causing the hemolysis is not clear. The present studies were performed to determine whether these autoantibodies are the products of the neoplastic B-CLL clones. Immunoglobulins (Ig) were eluted from washed red blood cells (RBC) obtained from two CLL patients at the time they had autoimmune (DAT-direct antiglobulin test-positive) hemolytic anemia. The light chain phenotypes of these eluted autoantibodies were determined and found to be monotypic with exact correlation to the light chain expressed on the surface of the B-CLL clones. Elutions from RBC of DAT negative patients or normal volunteers failed to demonstrate measurable amounts of Ig. In contrast, Ig eluted from RBC obtained from SLE patients with DAT positive hemolytic anemia found to be polyclonal autoantibodies exhibiting both light chain types. Furthermore, CD5+B lymphocytes obtained from the same two CLL patients (DAT+) produce, in vitro understimulation with phorbal myristate acetate (PMA), monoclonal antibodies which react and bind to RBC. Thus these studies provide direct evidence demonstrating that the antibodies causing the autoimmune hemolytic anemia in our two CLL patients are the products of the B-CLL neoplastic clones.

Aged↗
PubMed1993

The role of anticardiolipin autoantibodies in the pathogenesis of autoimmune hemolytic anemia in systemic lupus erythematosus.

OBJECTIVE: To elucidate the role of anticardiolipin antibodies (aCL) in the pathogenesis of hemolytic anemia in patients with systemic lupus erythematosus (SLE). METHODS: Immunoglobulins (Ig) and cardiolipin reactivity were evaluated in red blood cell (RBC) eluates and in the sera of patients with SLE and controls by a solid phase enzyme linked immunosorbent assay. RESULTS: aCL were detected in sera of 2 patients with SLE with active hemolytic anemia. The RBC eluates of these patients contained Ig (mainly IgG) with significant cardiolipin reactivity. RBC eluates from healthy volunteers failed to demonstrate measurable amounts of Ig whereas Ig eluted from RBC of chronic lymphocytic leukemia patients with active hemolysis but no aCL did not react with cardiolipin. Furthermore, under treatment, one patient went into complete remission with resolution of the hemolysis, negative Coombs' tests and lower serum aCL. The other patient, however, continued to demonstrate both high sera aCL and positive Coombs' tests. CONCLUSION: aCL may play a direct role in the pathogenesis of hemolytic anemia in some patients with SLE by acting as anti-RBC autoantibodies.

Adult↗
PubMed1992

Case report: fatal seronegative rickettsial infection diagnosed by the polymerase chain reaction.

A previously healthy man presented with a five day history of high fever and headache, later followed by rash and the appearance of jaundice. On the second hospital day, he suddenly developed seizures, lapsed into a coma, and died. Polymerase chain reaction (PCR) amplification revealed a 434 base pairs DNA fragment common to the genome of typhus and spotted fever group rickettsiae in the patient's blood (estimated at about 1 x 10(2) organisms/ml), and to a lesser degree in the cerebrospinal fluid. However, serological tests for rickettsiae remained negative. PCR techniques may confirm the diagnosis at an early stage, even though the rickettsemia may be minimal and the patient seronegative.

DNA, Bacterial↗
PubMed1992

Acute oliguric renal failure complicating type A nonfulminant viral hepatitis. A case presentation and review of the literature.

Nonfulminant acute renal failure very rarely complicates type A viral hepatitis. So far only eight patients have been described in the English language, Japanese, or Israeli literature who had type A viral hepatitis with renal failure without any association with "hepatorenal syndrome," pregnancy, or other types of viral hepatitis. We describe a 52-year-old man with type A viral hepatitis, proven by IgM anti-A virus antibodies complicated by oliguric renal failure, which required hemodialysis. The patient recovered completely after a few weeks. Kidney biopsy demonstrated interstitial nephritis with no glomerular involvement. Review of the literature in relation to the causes and the rarity of the renal failure is included.

Acute Kidney Injury↗
PubMed1992

[Subclinical renal involvement in rheumatoid arthritis].

No evidence of renal involvement was found in 104 patients with rheumatoid arthritis in routine laboratory tests, including serum creatinine, urea, uric acid, sodium, potassium, calcium, phosphorus, and urinalysis. In view of recent publications (1-9) which report renal involvement in rheumatoid arthritis, we studied 16 patients of our group (nonrandomized, 3 men and 16 women, average age 55.4 years, average duration of disease 11.9 years). We examined creatinine clearance, urinary excretion of alpha-2 microalbumin, beta-2 microglobulin, cystine, and urine concentration and acidity after a 10-hour fast. 10 patients had disturbances in 1 or more of the functions examined, in 9 of whom tubular functions were involved. In 6 there was no evidence of renal involvement. There was no correlation between renal involvement and past or present therapy, but there were direct correlations between renal involvement, duration of disease and age. Thus we found evidence for subclinical renal damage not revealed by routine laboratory tests in patients with rheumatoid arthritis. This damage should be taken into consideration when operation, examination with contrast material, or treatment with other nephrotoxic agents are being considered in these patients.

Age Factors↗
PubMed1991

Mitral valve prolapse in young Israelis with thromboembolic brain disease.

In order to establish the association between mitral valve prolapse (MVP) and the incidence of thromboembolic disease of the brain we reassessed 36 patients (less than or equal to 50 years old) who were hospitalized during 1983-85 because of cerebrovascular accidents. The patients underwent complete physical and neurological examinations, blood tests including coagulogram and two-dimensional echocardiogram. The control group comprised 117 patients without cerebrovascular events. In the study group, 4 patients (11.1%) had MVP compared with 10 (8.5%) in the control group. Of these four, only one male did not have any risk factor for thromboembolic event; among the other three the risk factors were systemic lupus erythematosus, hyperlipidemia, diabetes, hypertension and pregnancy. We conclude that our results are in accordance with most of the literature that MVP is not a risk factor for thromboembolic disease except in Greek and Italian populations, which are ethnically more homogeneous than other Western societies studied.

Adult↗
PubMed1989

Stroke in Icelandic patients with hereditary amyloid angiopathy is related to a mutation in the cystatin C gene, an inhibitor of cysteine proteases.

Cystatin C is an inhibitor of lysosomal cysteine proteases and consists of 120 amino acids. A variant of cystatin C lacking the first NH2-terminal residues and having one amino acid substitution at position 68 forms amyloid deposits mainly in the walls of brain arteries, causing fatal strokes in Icelandic patients with familial cerebral hemorrhage secondary to a form of an autosomal dominant amyloidosis. To understand the molecular basis of the genetic defect, the gene encoding cystatin C was isolated from genomic DNA libraries made from normal tissue and the brain of an Icelandic patient with hereditary cerebral hemorrhage with amyloidosis (HCHWA-I). The data indicate that the cystatin C gene encodes a polypeptide of 146 amino acids, of which the first 26 correspond to a secretory peptide signal sequence. The gene contains two intervening sequences that interrupt the coding region at amino acids 55 and 93. Comparison with genes encoding salivary cystatins and kininogen proteins show sequence homology and conservation of exon-intron structure. Except for a mutation in the second exon (CAG instead of CTG in the normal gene, resulting in the substitution of glutamine for a leucine residue), the gene cloned from the brain of the Icelandic patient is identical to the normal cystatin C gene. Thus, HCHWA-I is the first familial type of amyloidosis related to a point mutation in a gene encoding for an inhibitor. The mutation in the structural gene encoding cystatin C appears to be the primary defect in this inherited disorder causing amyloid fibril formation and accumulation followed by cerebral hemorrhage.

Amino Acid Sequence↗
PubMed1988

Therapeutic approaches in mixed cryoglobulinemia.

In summary, one can say that, although EMCG is a perplexing and puzzling disease, and although there are more enigmas than solutions, we can establish a way of handling the disease, knowing how to divide it into benign or acute forms, and establishing a treatment attitude according to that knowledge. PP and its modifications, in combination with immunosuppressive agents, are the corner-stones to the acute form of the disease complicated by vasculitis, nephritis, chronic hepatitis and CNS involvement. Looking ahead, a new and more specific mode of treatment could emerge from our and others observations that the IgMs in the mixed cryoproteins are antiidiotypes to the IgGs. By producing autoantiidiotypes it might be possible to block some of the immune complex formation and to interfere with the cold precipitation, which is the basic pathophysiological process of essential mixed cryoglobulinemia.

Cryoglobulinemia↗