Biomedical subjects

K Geissler

Publications and source records attributed to K Geissler.

At least 73 records · Page 4Linked to original sources

PubMed1999

Tissue distribution of virus replication in cats experimentally infected with distinct feline calicivirus isolates.

Four specific pathogen-free (SPF) cats were each inoculated with one of two genetically and antigenically well characterized feline caliciviruses originally isolated from cats with acute respiratory disease (FCV-KS100/2), or with chronic stomatitis (FCV-KS20). Two cats of each group were euthanized at day 10 post infection and two cats at day 28. No clear differences between the clinical disease induced by the two isolates could be observed, and no apparent differences in the tissue spectrum were seen between day 10 and 28. No persistent virus shedding was observed over the 4-week period of this experiment.

Animals↗

PubMed1999

Treatment of acute leukemia.

Leukemic cells are highly sensitive to chemotherapeutic agents. A reduction of the leukemic burden is easily achieved by chemotherapy in most cases. However, it is difficult to reduce the number of leukemic cells to such an extent that a regrowth does not occur and the patient is cured. Traditionally the therapy of acute leukemia is divided into induction and post remission therapy. The aim of the induction therapy is to reduce the number of leukemic cells to a morphologically undetectable level allowing normal hemopoiesis to recover. The goal of the post remission treatment is a further reduction of leukemic cells to zero or to very low levels which can be controlled by (still unknown) endogenous mechanisms. In some recent treatment protocols induction and the early part of post remission treatment are not strictly separated.

Acute Disease↗

PubMed1998

[Advances in the treatment of chronic lymphocytic leukemia (CLL)].

CLL is a chronic lymphoproliferative disorder which is characterized by the proliferation of a CD5 positive B cell clone. At diagnosis most patients are in early stage of the disease (stage A). It is well established that an early treatment in stage A is not associated with a survival advantage. Therefore, the disease should be treated only when signs of progression are present. The standard initial therapy is chlorambucil +/- prednisone. By this treatment remissions (mostly partial remissions) are achieved in about half of the patients. Fludarabine, a purine analogue, is more effective than chlorambucil as initial treatment (75% remissions, 27% complete remissions, 33 months progression free survival). However, the overall survival is not prolonged when compared to chlorambucil treatment. Fludarabine has a high efficacy in patients with recurrent disease, in particular in those who are resistant to alkylating agents. The allogeneic and autologous stem cell transplantation is an experimental treatment which may be indicated in younger patients who show a response to conventional treatment. With both procedures hematological remissions are frequently achieved and in some of the patients long lasting molecular remissions were obtained. Currently, it is unknown whether patients can be cured by stem cell transplantation and longer follow-up will be necessary to clarify this question. Monoclonal B-cell antibodies are effective in vivo and partial remissions can be obtained in chemotherapy refractory patients. Antibodies have a high efficacy in clearing lymphoma cells from peripheral blood and bone marrow but are less effective on the organomegaly.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1998

Interleukin-10 inhibits erythropoietin-independent growth of erythroid bursts in patients with polycythemia vera.

In polycythemia vera (PV) erythroid colonies that grow in vitro in the absence of exogenous erythropoietin (EPO) arise from the abnormal clone that is responsible for overproduction of red blood cells. Although the mechanism of autonomous formation of burst-forming units-erythroid (BFU-E) is not fully understood, a spontaneous release of growth regulatory molecules by PV cells and/or by accessory cells is likely to be involved. Because of its cytokine synthesis inhibiting action, interleukin-10 (IL-10) could be a potentially useful molecule to modulate abnormal erythropoiesis in PV. We studied the effect of recombinant human IL-10 on the EPO-independent growth of erythroid bursts derived from peripheral blood mononuclear cells (PBMNCs) of patients with PV. IL-10 showed a profound, dose-dependent, and specific inhibitory effect on autonomous BFU-E formation. Ten nanograms per milliliter of IL-10 significantly suppressed spontaneous growth of erythroid colonies in methylcellulose in five of five PV patients tested with a mean inhibition by 81% (range, 72-94). To elucidate the possible mechanism of the inhibitory action of IL-10 we further studied the effect of anticytokine antibodies on autonomous BFU-E growth and the ability of exogenous cytokines to restore IL-10-induced suppression of erythroid colony growth. Among a panel of growth regulatory factors tested (granulocyte-macrophage colony-stimulating factor [GM-CSF], IL-3, granulocyte colony-stimulating factor, stem cell factor, and insulin-like growth factor-1) GM-CSF was the only molecule for which both an inhibition of spontaneous BFU-E formation by its respective antibody as well as a significant restimulation of erythroid colonies in IL-10-treated cultures by exogenous addition was found. Moreover, inhibition of GM-CSF production by IL-10 was shown in PV PBMNCs at the mRNA level. Our data indicate that autonomous BFU-E growth in PV can be profoundly inhibited by IL-10 and that this inhibitory effect seems to be at least in part secondary to suppression of endogenous GM-CSF production.

Adult↗

PubMed1998

Neutrophil granulocyte-committed cells can be driven to acquire dendritic cell characteristics.

Polymorphonuclear granulocytes (PMNs) are thought to fulfill their role in host defense primarily via phagocytosis and release of cytotoxic compounds and to be inefficient in antigen presentation and stimulation of specific T cells. Dendritic cells (DCs), in contrast, are potent antigen-presenting cells with the unique capacity to initiate primary immune responses. We demonstrate here that highly purified lactoferrin-positive immediate precursors of end-stage neutrophilic PMN (PMNp) can be reverted in their functional maturation program and driven to acquire characteristic DC features. Upon culture with the cytokine combination granulocyte/macrophage colony-stimulating factor plus interleukin 4 plus tumor necrosis factor alpha, they develop DC morphology and acquire molecular features characteristic for DCs. These molecular changes include neo-expression of the DC-associated surface molecules cluster of differentiation (CD)1a, CD1b, CD1c, human leukocyte antigen (HLA)-DR, HLA-DQ, CD80, CD86, CD40, CD54, and CD5, and downregulation of CD15 and CD65s. Additional stimulation with CD40 ligand induces also expression of CD83 and upregulates CD80, CD86, and HLA-DR. The neutrophil-derived DCs are potent T cell stimulators in allogeneic, as well as autologous, mixed lymphocyte reactions (MLRs), whereas freshly isolated neutrophils are completely unable to do so. In addition, neutrophil-derived DCs are at least 10,000 times more efficient in presenting soluble antigen to autologous T cells when compared to freshly isolated monocytes. Also, in functional terms, these neutrophil-derived DCs thus closely resemble "classical" DC populations.

Antigen Presentation↗

PubMed1998

Expression of the lung resistance protein predicts poor outcome in de novo acute myeloid leukemia.

The 110-kD lung resistance protein (LRP) is overexpressed in P-glycoprotein-negative multidrug-resistant cell lines and most likely involved in the multidrug resistance (MDR) of these cell lines. To determine the clinical significance of LRP, we have studied LRP expression of leukemic blasts and its association with clinical outcome in patients with de novo acute myeloid leukemia (AML). LRP expression of leukemic blasts obtained from peripheral blood or bone marrow of previously untreated patients (n = 86) was determined by immunocytochemistry by means of monoclonal antibody LRP-56. LRP expression at diagnosis was detected in 31 (36%) patients. LRP expression was independent of age and sex of the patients, French-American-British subtype, cytogenetic abnormalities, and lactate dehydrogenase levels, but correlated with white blood cell count (P = .01). Eighty-two patients received standard induction chemotherapy that included cytarabine and MDR drugs (daunorubicin in most patients, additional etoposide in the majority of patients). The complete remission rate of induction chemotherapy was 72% (95% confidence interval [CI] = 61% to 82%) for the total study population. The complete remission rate was 81% (95% CI = 67% to 91%) for patients without LRP expression but only 55% (95% CI = 36% to 74%) for patients with LRP expression (P = .01). Overall survival and disease-free survival were estimated according to Kaplan-Meier in 82 and 59 patients, respectively. Overall survival was significantly longer in patients without LRP expression than in patients with LRP expression. At a median follow-up of 16 months, median overall survival was 17 months (95% CI = 12 to 38 months) for LRP-negative patients but only 8 months (95% CI = 4 to 12 months) for -positive patients (P = .006). Disease-free survival was 9 months (95% CI = 7 to 11 months) for LRP-negative patients and 6 months (95% CI = 5 to 8 months) for -positive patients (P = .078). Outcome was best in patients lacking both LRP and P-glycoprotein expression. In conclusion, LRP predicts for poor outcome and thus the LRP gene appears to be another clinically relevant drug resistance gene in AML.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1998

Gene transfer with IL-4 and IL-13 improves survival in lethal endotoxemia in the mouse and ameliorates peritoneal macrophages immune competence.

Systemic anti-cytokine therapies have been unsuccessful in preventing mortality from gram-negative bacteremia in humans partly because of the failure to neutralize pro-inflammatory cytokines at sites of exaggerated production. In an attempt to deliver anti-inflammatory cytokines to organs directly, gene transfer was employed. Thirty-six BALB/c mice were injected intraperitoneally with cationic liposomes containing plasmids encoding the human interleukin-4 (hIL-4) or IL-13 gene. Both, hIL-4 and hIL-13 mRNA were detected by reverse transcription-polymerase chain reaction analysis in the liver and the spleen of the animals. Fourty-eight hours after the in vivo gene transfer, these 36 mice and 18 mock-transfected mice, were challenged with a lethal dose of E. coli lipopolysaccharide with D-galactosamine (D-GalN). Gene transfer with hIL-4 reduced the serum tumor necrosis factor (TNF)-alpha production in response to endotoxin/D-GalN by 80% from 113.1 pg/ml in mock-transfected animals to 22.2 pg/ml (p < 0.05); human IL-13 gene transfer reduced serum TNF-alpha levels by 90% (113.1 pg/ml to 11.6 pg/ml; p < 0.05). Survival was improved from 20% to over 83% in both treatment groups (p < 0.001). Our data demonstrate a potent in vivo anti-inflammatory action of both IL-4 and IL-13. In addition, the immune functions of peritoneal macrophages are significantly ameliorated in both treatment groups, with IL-13 demonstrating better macrophage immune modulation than IL-4 (p < 0.05).

Animals↗

PubMed1998

Hypofibrinogenemia in non-M3 acute myeloid leukemia. Incidence, clinical and laboratory characteristics and prognosis.

Among 379 patients with AML with FAB type M1, 2 and M4-7 diagnosed between 1978 and 1997 in our institution, 19 (5%) had hypofibrinogenemia (HF), ie a fibrinogen level <180 mg/dl. Compared to patients with normal fibrinogen (n = 360) patients with HF had significantly elevated markers of activation of coagulation (TAT, F1.2, FPA) and fibrinolysis (D-dimer, FDP) indicating that disseminated intravascular coagulation/hyperfibrinolysis was the cause of hypofibrinogenemia. Patients with HF had significantly longer prothrombin times, thrombin clotting and reptilase times. Factor X and VIII were significantly lower than in patients without HF. With the exception of M7, HF occurred in all FAB subtypes, but was most common in M5 (12.1%). Patients with HF did not differ from those with normal fibrinogen with regard to age, sex, leukocyte count and other hematological parameters. During induction chemotherapy fibrinogen normalized rapidly (median 5 days) and there was no increased incidence of early hemorrhagic death. The overall and disease-free survival was similar to that of patients without HF.

Adult↗

PubMed1998

Recombinant human megakaryocyte growth and development factor increases levels of circulating haemopoietic progenitor cells post chemotherapy in patients with acute myeloid leukaemia.

By participating in a randomized safety and efficacy study of pegylated-recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) post induction and consolidation chemotherapy for de novo acute myeloid leukaemia, serial determinations of circulating haemopoietic progenitor cells were performed during 18 chemotherapy courses in eight patients (three receiving placebo; one, 2.5; and four, 5.0 microg/kg/d MGDF, respectively). Whereas failure to achieve complete remission (CR) was generally associated with poor progenitor cell increments following chemotherapy, substantial progenitor cell mobilization consistently occurred during haemopoietic recovery in patients entering, or in CR, with significantly higher peak values in patients receiving 5 microg/kg/d of MGDF as compared to controls. The median increases of progenitor cell numbers by chemotherapy alone and chemotherapy plus 5.0 microg/kg/d MGDF over that in normal individuals with steady-state haemopoiesis were 10- and 45-fold for CFU-GM, 3- and 17-fold for BFU-E, and 2- and 18-fold for CFU-mix. CFU-Mk levels were not increased above normal by chemotherapy alone but were 15-fold enhanced by chemotherapy plus MGDF. Recruitment of CD34+ cells post chemotherapy was also potentiated by MGDF. Our results suggest MGDF as a potent agent to augment progenitor cell mobilization after successful induction or consolidation chemotherapy in patients with AML.

Acute Disease↗

PubMed1998

Systemic mastocytosis associated with acute myeloid leukaemia: report of two cases and detection of the c-kit mutation Asp-816 to Val.

A subset of patients with systemic mastocytosis (SM) develop acute myeloid leukaemia (AML). However, little is known about the biology of such leukaemias and their relationship to the mast cell (MC) lineage. We report on two female patients who suffered from SM and AML. According to FAB criteria, the leukaemias were classified as AML-M4 (patient 1) and AML-MO (patient 2). The coexistence of the two distinct neoplasms (AML and SM) was demonstrable by immunostaining of serial bone marrow (BM) sections with monoclonal antibodies (mAb). In particular, the MC infiltrates were found to react with mAb against MC-tryptase and MC growth factor receptor c-kit (CD117), but not with mAb to CD15 or CD34. In contrast, the AML blasts were immunoreactive for CD15 (patient 1) or CD34 (patient 2), but did not express tryptase. The c-kit point mutation Asp-->Val at codon 816, considered to play a role in the transformation of MC progenitors, was detected in patient 1 in a BM cell fraction containing 4% MC. However, no c-kit mutation was found in pure AML blasts (<1% MC). These findings argue against an evolution of the AML clone from neoplastic MC or MC-committed progenitors.

Acute Disease↗

PubMed1998

High-dose recombinant human erythropoietin stimulates reticulocyte production in patients with multiple organ dysfunction syndrome.

OBJECTIVE: To investigate erythropoietin (EPO) production and the erythropoietic potency of recombinant human EPO in the multiple organ dysfunction syndrome. DESIGN: Randomized, prospective, controlled clinical trial. MATERIALS AND METHODS: Patients received either 600 IU/kg intravenous EPO three times weekly (n = 9) or saline (control, n = 10). MEASUREMENTS: EPO levels, circulating soluble receptors for tumor necrosis factor and interleukin-2, levels of interleukin-6 and intercellular adhesion molecule, and early peripheral blood cell progenitors. RESULTS: EPO production in the control group remained low. Pharmacologic EPO blood levels were associated with increased reticulocyte counts compared with both controls (p < 0.04) and baseline (p < 0.006). Increased levels of soluble receptors for tumor necrosis factor in the treatment group compared with the controls did not prevent this effect. Interleukin 6 inhibited reticulocyte production. CONCLUSION: Despite increased cytokine levels, pharmacologic EPO blood levels were associated with increased reticulocyte counts in patients with multiple organ dysfunction syndrome.

Cytokines↗

PubMed1998

No evidence for a role of modified live virus vaccines in the emergence of canine parvovirus.

In this study the early evolution and potential origins of canine parvovirus (CPV) were examined. We cloned and sequenced the VP2 capsid protein genes of three German CPV strains isolated in 1979-1980, as well as two feline panleukopenia virus (FPV) vaccine viruses that were previously shown to have some restriction enzyme cleavage sites in common with CPV. Other partial VP2 gene sequences were obtained by amplifying CPV DNA from paraffin-embedded tissues of dogs which were early parvovirus disease cases in Germany in 1978-1979. Sequences were analysed with respect to their evolutionary relationships to other CPV and FPV isolates. Those analyses did not support the hypothesis that CPV emerged as a variant of an FPV vaccine virus. Neither did they reveal ancestral sequences among the very early CPV isolates examined. Other possible sources for the origin of CPV are examined, including the involvement of viruses from wild carnivores.

Animals↗

PubMed1998

Endocarditis and aortal embolization caused by Aspergillus terreus in a patient with acute lymphoblastic leukemia in remission: diagnosis by peripheral-blood culture.

Disseminated infection with Aspergillus terreus is a rare disease that affects only the immunocompromised host. We report a case of systemic infection with A. terreus resulting in endocarditis, aortic embolization, and splenic infarction in a patient with acute lymphoblastic leukemia. Diagnosis through peripheral blood culture, lack of pulmonary involvement, and onset of disease during complete remission from leukemia constitute uncommon features of this case.

Aorta, Abdominal↗

PubMed1997

Granulocyte colony-stimulating factor as an adjunct to induction chemotherapy for adult acute lymphoblastic leukemia--a randomized phase-III study.

Because of the recommendation to avoid the concomitant administration of growth factors and chemotherapy, there is only limited information on colony-stimulating factor (CSF) therapy in acute lymphoblastic leukemia (ALL) induction protocols, in which cytotoxic drugs are administered in divided doses over a prolonged period of time, thus requiring a simultaneous administration of growth factors and chemotherapy. We conducted a prospective, randomized, controlled study to determine the safety and efficacy of granulocyte colony-stimulating factor (G-CSF; filgrastim) as an adjunct to phase I of induction chemotherapy for adult ALL. Patients (n = 53) were randomized to receive no growth factor or G-CSF (5 microg/kg/d subcutaneously) starting on day 2 of chemotherapy consisting of daunorubicin (45 mg/m2) and vincristine (1.5 mg/m2) on days 1, 8, 15, and 22; L-asparaginase (2500 U/m2) on days 1 through 14; and prednisone (60 mg/m2) on days 1 through 28. A total of 25 patients in the G-CSF group and 26 patients in the control arm fulfilled the inclusion criteria of the study. G-CSF markedly ameliorated neutropenia because the median proportion of days with neutropenia less than 1,000/microL was 29% in the G-CSF group as compared with 84% in the control arm (P < .00005). The median time to reach absolute neutrophil counts (ANC) > or = 1,000/microL was 16 days in G-CSF patients and 26 days in controls (P < .001). More importantly, G-CSF significantly reduced the incidence of febrile neutropenia (12% v 42% in controls, P < .05) and documented infections (40% v 77%, P < .05). No significant differences were found with regard to requirements for red blood cell transfusions and platelet concentrates. A total of 24 of 25 (96%) patients in the G-CSF group and 20 of 25 (80%) evaluable control patients had complete remission after phase I of induction therapy. We conclude that G-CSF can be safely administered as an adjunct to induction therapy of ALL and is clinically beneficial by ameliorating neutropenia and reducing infectious complications.

Adolescent↗

PubMed1997

Interleukin-10 inhibits spontaneous colony-forming unit-granulocyte-macrophage growth from human peripheral blood mononuclear cells by suppression of endogenous granulocyte-macrophage colony-stimulating factor release.

Spontaneous growth of myeloid colonies (colony-forming unit-granulocyte-macrophage [CFU-GM]) can be observed in methylcellulose cultures containing peripheral blood mononuclear cells (PB-MNCs) and is supposedly caused by the release of colony-stimulating factors (CSF) by accessory cells. Because of its cytokine synthesis-inhibiting effects on T lymphocytes and monocytes, interleukin-10 (IL-10) may be a potential candidate for indirect modulation of hematopoiesis. We studied the effect of recombinant human IL-10 (rhIL-10) on spontaneous growth of myeloid colonies derived from human PB-MNCs. A total of 10 ng/mL of IL-10 almost completely inhibited spontaneous CFU-GM proliferation (by 95.1%; P < .001, n = 7) in unseparated PB-MNCs. This effect was dose-dependent and specific, because a neutralizing anti-IL-10 antibody was able to prevent IL-10-induced suppression of CFU-GM growth. Spontaneous CFU-GM growth, which required the presence of both monocytes (CD14+ cells) and T lymphocytes (CD3+ cells), was also greatly suppressed by a neutralizing anti-granulocyte-macrophage CSF (GM-CSF) antibody but was only slightly or not at all inhibited by antibodies against G-CSF or IL-3. Moreover, IL-10-suppressed colony growth could be completely restored by the addition of exogenous GM-CSF. Using semiquantitative polymerase chain reaction, we were able to show that GM-CSF transcripts that spontaneously increased in PB-MNCs within 48 hours of culture were markedly reduced by the addition of IL-10. Inhibiton of GM-CSF production in PB-MNCs by IL-10 was also confirmed at the protein level by measuring GM-CSF levels in suspension cultures. Our findings suggest that autonomous CFU-GM growth, resulting from an interaction of monocytes and T lymphocytes, is mainly caused by endogenous GM-CSF release and can be profoundly suppressed by the addition of exogenous IL-10. Considering the strong inhibitory action of IL-10 on GM-CSF production and spontaneous cell growth in vitro, this cytokine may be useful in myeloid malignancies in which autocrine and/or paracrine mechanisms involving GM-CSF are likely to play a pathogenetic role.

Cell Differentiation↗

PubMed1997

Genetic and antigenic heterogeneity among feline calicivirus isolates from distinct disease manifestations.

The capsid protein genes of five feline calicivirus (FCV) isolates associated with different disease manifestations were cloned and sequenced. The viruses represented two recent isolates from cats with chronic stomatitis, one recent isolate from a cat with acute stomatitis, one recent isolate each from a cat with acute respiratory symptoms and the classical limping syndrome strain FCV-2280. The amino acid sequences were compared with eight other published sequences and analyzed for their relationships. Phylogenetic analysis of the complete capsid protein sequences or of known antigenic regions of that protein (hypervariable regions A and E) did not group the isolates of different disease manifestations in distinct subclusters. Monoclonal antibodies (MAbs) generated against either a chronic stomatitis isolate or a recent isolate associated with respiratory symptoms were tested against a panel of 11 recent isolates and four "classical' FCV strains, covering all known disease associations. With those MAbs no obvious clustering with respect to disease manifestation could be seen. Four specific sera prepared in rabbits against our prototype isolates also failed to cluster those isolates according to the disease manifestations when examined in neutralization tests. From these antigenic and genetic analyses of the capsid protein the hypothesis of the existence of biotypes of FCV responsible for distinct disease manifestations could not be confirmed.

Acute Disease↗

PubMed1997

Prognostic significance of WT1 gene expression at diagnosis in adult de novo acute myeloid leukemia.

We examined the presence of WT1-specific mRNA in bone marrow samples of 125 patients with de novo acute myeloid leukemia at diagnosis by two-step RT-PCR. The sensitivity of the assay was 1:100 (first step) and 1:10000 (second step), respectively. WT1-specific mRNA was detected in 73% of patients. No correlation was found between WT1 gene expression and age, FAB type, LDH and karyotype at diagnosis. All patients were treated with standard induction chemotherapy. There was no difference in the CR rate between WT1-positive and -negative patients. Using Kaplan and Meier plot analysis we found no difference in disease-free survival (DFS) and overall survival (OS) between patients displaying the WT1 transcript and WT1-negative patients. Furthermore, no significant interactions between WT1 PCR results and age, FAB type, LDH and karyotype on DFS and OS were demonstrable using Cox regression analysis. Eight patients who were WT1 PCR positive at diagnosis and achieved complete hematological remission following chemotherapy were monitored during the course of the disease. Based on our limited data demonstrating a heterogeneity of WT1 PCR results in CR we cannot draw any conclusions regarding the usefulness of WT1 PCR analysis for the early detection of relapse. We conclude that WT1 gene expression at diagnosis is not associated with specific characteristics of AML blast cells and is not a prognostic factor for CR, remission duration and overall survival in acute myeloid leukemia.

Acute Disease↗

PubMed1997

Effect of successful parathyroidectomy on hematopoietic progenitor cells and parameters of red blood cells in patients with primary hyperparathyroidism.

Elevated levels of parathyroid hormone (PTH) in primary and secondary hyperparathyroidism inhibit hematopoiesis at the level of hematopoietic progenitor cells, mainly the burst forming units-erythroid (BFUe). Removal of parathyroid adenomas is associated with an increase in hematopoietic progenitor cells. In contrast, a certain amount of PTH and calcium is needed to correct anemia after bleeding demonstrating that PTH has also a stimulatory effect on the bone marrow. We examined the effect of parathyroidectomy (PTX) in 10 patients with histologically proven primary hyperparathyroidism on hematopoietic progenitor cells and several parameters of red blood cells before and at 5, 30 and 90 days after PTX. After successful surgery serum levels of iPTH (p < 0.01) and calcium (p < 0.001) decreased significantly. Subsequently a steady increase in all hematopoietic progenitor cell classes was observed reaching significance for BFUe only (p < 0.05). Red blood cells and hemoglobin reached nearly pretreatment values within 90 days after PTX after they had decreased due to surgery associated blood loss. 8 patients undergoing hemithyroidectomy without PTX showed a similar decrease in red blood cells and hemoglobin followed by a rise after the operation. The changes of these parameters did not differ significantly from the patients with pHPT. In contrast to the patients with pHPT, no changes in hematopoietic progenitor cells during the 90 days were observed. The presented data provide further evidence that increased PTH concentrations might inhibit hematopoiesis in humans in vivo. The inhibition can be reversed following PTX by normalisation of PTH concentrations.

Aged↗