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Biomedical subjects

S Panzer

Publications and source records attributed to S Panzer.

At least 145 records · Page 8Linked to original sources

Platelet-associated immunoglobulins IgG, IgM, IgA and complement C3c in chronic idiopathic autoimmune thrombocytopenia: relation to the sequestration pattern of 111indium labelled platelets.

Levels of platelet-associated immunoglobulins (PAIg) IgG, IgM, IgA and complement C3c were related to parameters of 111Indium-labelled platelet kinetics in 17 patients with chronic idiopathic autoimmune thrombocytopenia (cAITP). Elevated levels of PAIg/C3c were found in 14 patients (82%) (PAIgG n = 13, PAIgM n = 11, PAIgA n = 1, PAC3c n = 5). Only PAIgG correlated with platelet counts (RS = -0.71, p less than 0.01). Mean platelet life span (MLS) was shortened in all patients (median 12.0 h, range 0.3-45.6 h) and correlated with the platelet counts (RS = 0.49, p less than 0.05). MLS was correlated with PAIgG (RS = -0.52, p less than 0.05), but not with PAIgM, PAIgA, or PAC3c. The site of sequestration was splenic in 10 patients and splenic-hepatic in 7 patients. Although no significant correlation between either site of platelet sequestration and any of the investigated PAIg/C3c was demonstrable, platelets coated with higher PAIgG levels were more readily sequestrated in the spleen, while elevations of PAC3c were found in 4 out of 7 patients with hepatic involvement.

Adolescent↗

Acquired thrombasthenia due to GPIIb/IIIa-specific platelet autoantibodies.

An otherwise healthy woman developed a hemorrhagic diathesis with fluctuating clinical symptoms and laboratory findings, but without thrombocytopenia, over 8 years. In periods of bad clinical condition, a platelet defect, characteristic of thrombasthenia, was found. In contrast to classic thrombasthenia, electrophoresis of the patient's platelet membranes revealed normal amounts of glycoproteins IIb alpha, IIb beta, and IIIa in the normal positions. Monoclonal antibodies, specific for GPIIIa and GPIIb/IIIa, respectively, bound normally to the P1A1-positive platelets from the patient. Although no antibody and no platelet function inhibitor were evident in the autologous plasma, an IgG1 antibody that was bound to the patient's platelets and was directed against GPIIb/IIIa could be demonstrated. After elution from the patient's platelets, this antibody immunoprecipitated GPIIb (both subunits), IIIa, and a 200-kilodalton (kd) band (probably undissociated GPIIb/IIIa complex) from solubilized normal platelets, but did not react with thrombasthenic platelets. Adding the eluate from the patient's platelets to normal platelet-rich plasma immediately caused concentration-dependent inhibition of adenosine diphosphate (ADP)-induced and collagen-induced aggregation and also strong inhibition of ADP-stimulated fibrinogen binding. Because it was very unlikely from the patient's medical history that the antibody was caused by alloimmunization, the hemorrhagic diathesis must be interpreted as acquired thrombasthenia due to an anti-GPIIb/IIIa autoantibody.

Adult↗

Unexpected absence of a myeloid surface antigen (3-fucosyl-N-acetyllactosamine) in promyelocytic leukemia.

According to the criteria of the FAB classification we diagnosed acute promyelocytic leukemia in 19 out of 191 AML blast cell populations. The reaction pattern with the anti-myeloid monoclonal antibodies VIM2, MCS2 and MY9 and the MHC-class II antibody VID1 in all cases showed the characteristics which were expected from the normal granulopoiesis. The monoclonal antibody VIM-D5, which recognizes the myeloid cell surface structure 3-fucosyl-N-acetyllactosamine (3-FAL), was not reactive with the majority of promyelocytic blast cells, however. In 13 cases 3-FAL was not detectable and in 6 cases only low or moderate reactivity of VIM-D5 with blast cells was observed. The phenotype of leukemic promyelocytes thus differs from the majority of normal promyelocytes in this respect.

Antibodies, Monoclonal↗

High-dose intravenous immunoglobulin for post-transfusion purpura.

Five patients with post-transfusion purpura (four due to Zw(a), one presumably due to HLA antibodies) were treated with intravenous immunoglobulin (IgG) at doses of 0.4 g per kg body weight. IgG therapy was immediately effective as indicated by cessation of bleeding and rise of platelet counts in four out of five cases.

Adult↗

Treatment of severe chronic idiopathic thrombocytopenic purpura in adults with high-dose intravenous gammaglobulin.

12 patients with severe chronic idiopathic thrombocytopenic purpura (ITP) were treated with i.v. polyvalent intact immunoglobulin (0.14-0.4 g/kg body weight for 5 d) because of various bleeding episodes or prior to surgery. In 9 patients a significant rise in platelet counts was noted, starting on d 2 and reaching its maximum between d 4 and 11. Thereafter, platelet counts decreased slowly, approaching pre-treatment values after 20 d in most cases. Response to immunoglobulin was reproducible, when infusions were repeated. Response to high-dose immunoglobulin was independent of age of patients and duration of disease. Platelet-associated IgG decreased in all patients tested. A pepsin-treated immunoglobulin preparation was ineffective in 3 patients.

Adult↗

Quantitative evaluation of elution methods for red cell antibodies.

Two recent techniques using xylene and chloroform for antibody elution from red blood cells (RBC) were compared with the most widely used ether and heat elution by means of a quantitative 125I-antiglobulin test. Free serum alloantibodies and cell-bound alloantibodies from in vivo sensitization of delayed hemolytic transfusion reactions and of hemolytic disease of the newborn as well as autoantibodies in autoimmune hemolytic disease were studied. With alloantibodies, xylene proved more efficient than chloroform (p less than 0.025), while both methods were superior to heat or ether elution (p less than 0.005). Autoantibody elution was equally effective with xylene and chloroform (p less than 0.1) but again better than heat or ether elution (p less than 0.02). However, no single method produced the strongest eluate with all antibodies studied. We conclude that xylene and/or chloroform elution are valuable implementations in RBC serology, but, in selected instances, the classical elution methods will retain their importance.

Autoantibodies↗

Glycosylated hemoglobin as a long-term parameter in appraising the severity of hemolytic disease.

Reduced levels of glycosylated hemoglobins (GHb) have been found to be closely related to red cell survival. We therefore studied the relation of this parameter to the clinical applicability in patients with hemolytic disease (n = 20). During a 5-week period we repeatedly measured severity of anemia, i.e., hemoglobin (Hb), packed red cell volume (VPRC), and red blood cell count (RBC), as well as reticulocytosis and parameters of red cell destruction such as serum concentration of lactic dehydrogenase (LDH) and bilirubin together with GHb. There was a weak correlation between simultaneously measured GHb and RBC (r = 0.5, P = 0.02), but none was demonstrable between GHb and Hb, VPRC, reticulocyte counts, LDH, or bilirubin. A much closer correlation, however, was found between actual GHb levels and RBC determined 3-5 weeks previously (r = 0.72, P = 0.001), as well as Hb (r = 0.56, P = 0.015), VPRC (r = 0.57, P = 0.013), reticulocyte counts (r = -0.63, P = 0.006), LDH ( r = -0.53, P = 0.02), and serum bilirubin concentrations ( r = -0.55, P = 0.016). Ghb was also significantly decreased in patients with consistently low values of reticulocytes when red cell destruction was demonstrable. These results show that GHb is a measure of red cell destruction and restitution, and thus may be usefull for long-term monitoring of patients with hemolytic disease.

Adolescent↗

Impact of euglycaemia and hyperglycaemia on the release of growth hormone and prolactin in type II-diabetics.

The influence of different blood glucose concentrations on the arginine (30 g/30 min i.v.) and TRH (400 micrograms i.v.) induced release of growth hormone and prolactin was studied in six male type II-diabetic patients. Blood glucose concentrations were clamped at euglycaemic (4-5 mmol/l) or hyperglycaemic (12-18 mmol/l) levels by means of an automated glucose-controlled insulin infusion system. The response of growth hormone to arginine, and irregular spikes in growth hormone concentrations following TRH seen in the euglycaemic state were suppressed during hyperglycaemia. The suppression of the arginine-induced release of growth hormone by hyperglycaemia was observed both with and without concomitant administration of exogenous insulin. The rise in serum prolactin concentrations in response to arginine was unaffected by hyperglycaemia, whereas the TRH-induced release of prolactin was suppressed. Since arginine induces the release of growth hormone and prolactin via the hypothalamus, while TRH acts at the pituitary level, the glycaemic state appears to exert a modulatory effect on the secretion of growth hormone and prolactin in type II-diabetics at both locations.

Arginine↗

Increased secretion of insulin but unchanged secretion of growth hormone in hyperglycaemic type II diabetics treated with acetyl-salicylic acid.

The effect of acetyl-salicylic acid (ASA, 3 g/d for three days) on basal and arginine-stimulated concentrations of insulin and growth hormone was studied in seven type II diabetics. From 120 min before until 120 min after the infusion of arginine-hydrochloride (30 g/30 min) blood glucose concentrations were clamped at hyperglycaemic levels both during treatment with ASA (blood glucose: 12.7 +/- 1.2 mmol/l) and during a control experiment without ASA (blood glucose: 12.9 +/- 1.3 mmol/l). Concentrations of serum insulin in the hyperglycaemic state prior to arginine infusion were increased during treatment with ASA, whereas increments of serum insulin induced by i.v. arginine were unaffected. No difference was seen in either basal or stimulated concentrations of growth hormone. Thus, ASA enhances glucose-induced secretion of insulin in type II diabetics but fails to potentiate the glucose-dependent suppression of arginine-stimulated growth hormone release. In contrast to the pancreatic beta-cell the glucose-sensitive regulatory mechanism of growth hormone release appears to be unaffected by the inhibition of endogenous prostaglandin synthesis.

Aged↗

[Clinical significance of bacterial contamination of enteral nutrition solutions].

Tube feeding with elemental and peptide diets is used as therapy for the acute phase of Crohn's disease. It should improve the nutritional status of the patients and reduce bacterial counts in the intestine. In this study we investigated the frequency of bacterial contamination of solutions of chemically defined diets and the clinical effects of the application of contaminated diets (stool frequency, body temperature, leucocyte counts). 15 patients with acute phase of Crohn's disease were treated with chemically defined diets over a total period of 323 days via a nasoduodenal tube. 7 patients received BSD, 8 patients Peptisorb. In all 36 BSD solutions examined in concentration procedures we found microbes, most frequently Streptococcus and Bacillus spp. Without concentration procedures it was possible to cultivate bacteria in 12% out of BSD solutions and in 81% out of Peptisorb solutions; in BSD mostly Streptococcus and in Peptisorb solution E. coli, Bacillus spp. and aerobic spore forming bacilli. Stool frequency, body temperature and leucocyte counts did not show significant differences after application of contaminated solutions in comparison to the others. Deterioration of the disease has not been observed in any case.

Adult↗

Adrenergic mechanisms and blood pressure regulation in diabetes mellitus.

Changes in blood pressure (BP) and plasma norepinephrine (NE) following various stimuli of the sympathetic, nervous system were studied in six healthy subjects and in 17 diabetic patients. The latter were subdivided in three groups: (1) six patients with neither peripheral neuropathy nor autonomic dysregulation, (2) six patients with severe peripheral neuropathy without autonomic dysregulation, and (3) five patients with autonomic dysregulation, three of whom suffered also from peripheral neuropathy. The following procedures were performed: (1) cold pressor test (2 min), (2) mechanical irritation of the skin by suction (0.75 kg/cm2, 10 min), (3) orthostasis (10 min), and (4) i.v. infusion of NE (50, 100, 200 ng kg-1 min-1 for 15 min each). Both the stimulated endogenous plasma NE levels and BP response to exogenous NE were the same in normal subjects, in diabetic controls and in diabetics with peripheral neuropathy without autonomic dysregulation. In contrast, diabetics with postural hypotension showed a less pronounced release of NE to standing (P less than 0.05), but not to cold pressor test and mechanical skin irritation. Furthermore, they showed increased vasoreactivity to the highest dose (P less than 0.05), but not to the lower doses of exogenous NE. Thus NE release and adrenergic BP regulation seem to be altered only in diabetics with clinical signs of autonomic dysregulation. These alterations can only be evaluated when patients are exposed to stimuli of higher intensity, such as orthostasis or infusion of a high NE dose.

Adult↗

The effect of histamine2 and muscarine receptor antagonists on plasma levels of parathyroid hormone and calcitonin.

Long-term administration of cimetidine, a histamine2 receptor antagonist, has been reported to normalize elevated parathyroid hormone (PTH) concentrations in patients with secondary [1] and primary hyperparathyroidism [2] and even to improve the clinical symptoms. We have compared the effect of cimetidine and pirenzepine on PTH and calcitonin (CT) plasma levels in a short-term trial on patients with secondary hyperparathyroidism. After cimetidine a significant effect on PTH was seen within 30 min lasting 30 min and after pirenzepine, within 60 min and lasting 60 min. The effect on CT was only significant after cimetidine.

Adult↗

Glycosylated hemoglobins (GHb): an index of red cell survival.

Levels of glycosylated hemoglobins (GHb) are significantly (p less than 0.0005) lower in patients with hemolytic anemia (n = 20; mean = 3.9% +/- 0.1% SD GHb of total Hb) compared to patients with nonhemolytic anemia (n = 20; mean = 7.0% +/- 0.7% GHb) and normal controls (n = 30; mean = 6.7% +/- 0.7% GHb). A curvilinear correlation between GHb and red cell survival is demonstrable (n = 20;r2 = 0.88; p less than 0.001). Determination of GHb may be useful as a screening test for hemolytic anemia and for the evaluation of the degree of hemolysis, provided that diabetes mellitus can be excluded.

Adolescent↗

The impact of euglycemia and hyperglycemia on stimulated pituitary hormone release in insulin-dependent diabetics.

To study the influence of different blood glucose (BG) concentrations on the release of pituitary hormones, the effect of the simultaneous iv administration of LRH (200 micrograms), TRH (400 micrograms), and arginine (30 g/30 min) upon the serum concentrations of LH, FSH, TSH, PRL, and GH was determined in six male insulin-dependent diabetics. BG concentration was clamped by feedback control and an automated glucose-controlled insulin infusion system at euglycemic (BG 4-5 mmol/liter) or hyperglycemic (BG, 14-18 mmol/liter) levels. Increments in serum concentrations of LH, FSH, TSH, and PRL were similar in the euglycemic and hyperglycemic steady states, whereas the GH response to arginine was suppressed during the hyperglycemic clamp (P less than 0.01). Omission of exogenous insulin during hyperglycemia did not modify the observed hormonal responses. Thus, the release of LH, FSH, TSH, and PRL in response to adequate acute stimuli at the pituitary level is not modulated by hyperglycemia in insulin-dependent diabetes, while arginine-induced GH release is suppressed. Since the effect of arginine on GH is most likely mediated by an action on the hypothalamus, the data suggest that elevated glucose concentrations may exert their modulatory influence on GH secretion at the hypothalamic rather than at the pituitary level.

Adult↗

[Acute self-poisoning with arsenic and treatment with BAL (author's transl)].

A case of attempted suicide by ingestion of 4.8 g As2O3 (more than 20 times the estimated lethal dose) is reported. Absorption of arsenic caused elevated urinary levels over 5 days BAL treatment was started within three hours after arsenic ingestion. The patient did not develop any signs of polyneuropathy or other clinical changes.

Arsenic Poisoning↗

The clinical significance of HLA antigens on red cells. Survival studies in HLA-sensitized individuals.

To investigate the clinical significance of HLA determinants expressed on red cells (RBCs), 51Cr survival studies were carried out in six women (four healthy individuals, two patients with solid carcinoma) immunized against HLA antigens by pregnancy or blood transfusions, respectively. Donors were selected who were compatible in typical RBC antigen systems assayed by conventional techniques but were mismatched for the HLA antigens in question. Crossmatches also were performed with RBC, as well as with lymphocytes, by means of a radioimmune anti-IgG test (RIAT). We found that RBC survival was shortened in all cases. The mean life-span of RBCs depended on antigen specificity rather than on the antibody strength. HLA incompatibility of RBCs could be monitored by the RIAT in all donor/recipient pairs. We conclude that a shortened mean life-span of RBC is to be expected by HLA antibodies, especially when HLA-B7 is involved, but the severity of an in vivo immune reaction in HLA incompatible transfusions cannot be predicted from the in vitro tests used.

Adult↗

Immune thrombocytopenia in severe hemophilia A treated with high-dose intravenous immunoglobulin.

Five patients with severe hemophilia A receiving long-term treatment with commercial factor VIII concentrates developed severe immune thrombocytopenia (ITP, platelet counts less than 20 X 10(9)/l). Concomitantly, they presented with a marked elevation of serum IgG concentrations (mean, 2364 mg/dl;range, 1712-2954 mg/dl). In four patients, the T helper to suppressor cell ratio was below 1. Treatment with high-dose intravenous immunoglobulin (IgG, 7s) at doses of 0.2g (n = 2) or 0.4g (n = 3) per kg of body weight on 5 consecutive days was effective immediately. The bleeding tendency ceased and platelet counts rose transiently. In three cases, treatment was repeatedly effective and patients underwent uneventful splenectomies. Thus, high-dose IgG therapy may serve as a life-saving agent in patients with severe hemophilia complicated by ITP.

Adolescent↗

Immunoglobulin administration to fetuses with anemia due to alloimmunization to D.

BACKGROUND: The purpose of this study was to examine fetal tolerance of high-dose intravenous immunoglobulin (IVIG), given directly at the time of intravascular transfusion, and its effects on fetal hemolysis and pregnancy outcome in the setting of alloimmunization to D. STUDY DESIGN AND METHODS: Thirteen consecutive D+ fetuses requiring transfusion for maternal alloimmunization received high-dose IVIG (1.0 g/kg) and red cell transfusions. Twenty-four previous, consecutive fetuses with maternal anti-D served as controls. The schedules for subsequent transfusions were the same in the two groups. RESULTS: High-dose IVIG was well tolerated by all fetuses. In the IVIG group, daily decreases in hematocrit were smaller than those in controls after the second administration of IVIG (mean hematocrit decrease, 0.72 percent/day vs. 1.45 percent/day; p = 0.007). No significant difference was found in the total number of fetal transfusions, the gestational age at delivery, the duration of neonatal intensive care, the number of neonates requiring postnatal transfusion therapy, and perinatal mortality. CONCLUSION: In this small pilot study, direct administration to fetuses of IVIG with red cell transfusions was well tolerated and appeared to have a beneficial effect on fetal hemolysis.

Female↗