Biomedical subjects

C Nissen-Druey

Publications and source records attributed to C Nissen-Druey.

12 recordsLinked to original sources

PubMed1990

Pathophysiology of aplastic anaemia.

It is the conventional opinion that acquired aplastic anaemia is a heterogenous disease including basically different conditions, such as idiopathic or virus induced pancytopenia, toxic-allergic marrow damage or autoimmunity. Here, an alternative concept is proposed, according to which aplastic anaemia is one disease, but multifactorial in all patients, apparent differences being due to the relative prevalence of one or the other pathophysiological component in individual patients. Bone marrow from patients in the severe phase of aplastic anaemia does not grow in culture and is therefore not suitable for experimentation. Alternatively, bone marrow from patients who have resumed some degree of autologous bone marrow function, but still have residual signs of the disease after non-invasive therapy, offers the possibility to study pathophysiological mechanisms in vitro. The majority of experiments presented in this chapter have been done in such patients, assuming that their status of disease in some way reflects the original, more serious pretreatment condition. Three major pathophysiological components will be discussed, and it will be proposed how these factors act in concert to cause or aggravate aplasia.

Anemia, Aplastic↗

PubMed1989

Pathophysiology of aplastic anaemia.

No single pathophysiological phenomenon--neither the intrinsic defect of haemopoiesis nor any of the described immune effects--explains aplastic anaemia. Since the intrinsic defect is compatible with near normal haemopoietic function, as seen in autologous bone marrow reconstitution, it cannot be the cause of severe pancytopenia. On the other hand, immune mechanisms cannot be the primary cause of the disease, otherwise haemopoietic function would recover to complete normality after immunosuppressive therapy. From these observations we deduce that the intrinsic defect, a premalignant haemopoietic disorder, can either be clinically quiescent by virtue of repair mechanisms, or induce auto-reactivity of the immune system against the abnormal haemopoietic tissue, drugs, chemicals and viruses acting as non-specific triggers or amplifiers. In this sense, aplastic anaemia could be interpreted as an attempt to 'self-cure' from a variant type of preleukaemia. This means that the original concept of aplastic anaemia being a hypoplastic variant of leukaemia may be true. The fact that aplastic anaemia can present either as acute severe bone marrow failure, as chronic mild pancytopenia or as a myelodysplasia-like syndrome does not imply that the underlying pathophysiological mechanisms are basically different. Variations of the clinical course and the response to immunosuppressive treatment could be explained by variations in the balance between the primary defect and the secondary immune reaction; the co-involvement of accessory cells in the primary disease; the relative time course of the two components and the efficiency of repair mechanisms. From repeated in vitro studies in a large group of aplastic anaemia patients at various stages of disease this concept can be applied to the majority of cases, including chloramphenicol- and virus-induced aplastic anaemia. In a small proportion of patients with pancytopenia occurring after exposure to certain drugs other than chloramphenicol, aplastic anaemia is rapidly and completely reversible after withdrawal of the drug. These patients probably have truly benign aplastic anaemia and thus differ from the majority of patients who are left with a permanently fragile bone marrow once they have acquired aplastic anaemia.

Anemia, Aplastic↗

PubMed1989

Human recombinant hemopoietic growth factors G-CSF and GM-CSF: first results of clinical trials.

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Agranulocytosis↗

PubMed1979

Myeloid differentiation in cultures of human hemopoietic precursor cells.

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Blood Cells↗

PubMed1978

Differential counts of neutrophil, eosinophil, and macrophage colonies in cultures from human bone marrow and peripheral blood.

Differential counts for neutrophil, eosinophil, and macrophage colonies were performed in 364 methylcellulose cultures of myeloid precursor cells. 2n bone marrow cultures from normals we found a mean total colony count of 56 +/- 17/10(5), of which 65% were neutrophil, 12% eosinophil, and 23% macrophages. In cultures from normal peripheral blood, the mean total colony count was 26 +/- 16/10(6) with 49% neutrophils, 44% eosinophils and 7% macrophages. There was an increase of eosinophil and macrophage colonies in cultures from patients with malignant hematological diseases, solid tumors and Graft-versus-Host disease. Highest eosinophil colony counts were found in Graft-versus-Host disease, highest macrophage colony counts in untreated Hodgkin's disease. Only 1 patient with extremely high eosinophil colony counts had eosinophilia in the peripheral blood. We conclude that in vitro conditions favor eosinophil "commitment". Its increase as nonspecific sign of disease is thus more likely to be recognized in vitro than in vivo.

Blood↗

PubMed1975

[T-infarct in exercise electrocardiography].

In a study of 60 patients with negative T-waves in the ECG following a first myocardial infarction it was found that during milk to moderate exercise the T-wave vector turned towards normal in 36. It is assumed that during exercise the T-vector points towards the region of maximum ischemia, i.e. the border of the recent infarction. The conclusion is drawn that unexpected transitory normalization of the T-wave after myocardial infarction means "worse" not "better". It is recommended that follow-up ECGs after myocardial infarction should always be taken at complete rest.

Electrocardiography↗

PubMed1974