Apoptosis and oxidative status in peripheral blood mononuclear cells of diabetic patients.

We have compared the concentrations of intracellular glutathione (GSH), glutathione-dependent antioxidative enzymes, the cell death rate and immunophenotype profile of peripheral blood mononuclear cells (PBMC) from healthy donors and from patients with insulin-dependent type II (NIDDM) diabetes mellitus. The IDDM and NIDDM patients had above-normal absolute lymphocyte counts, whereas the percentages of CD3, CD4 adn CD8 T lymphocytes were significantly reduced. In contrast, the absolute number and percentage of B lymphocytes was higher in diabetic patients than in healthy donors. The low intracellular reduced glutathione(GSH) and the unbalanced profile of key enzymes involved in GSH metabolism, gamma-glutamyltransferase (gamma-GT) and glutathione-S-transferase (GST), account for the increased oxidative status of PBMC from diabetic patients. The plasma membranes of PBMC for diabetic patients were less permeable to propidium iodide than those of PBMC from healthy donors, indicating that the apoptotic cell death rate was lower in the cells from diabetic patients. These differences are potentially useful markers of pathogenic metabolic changes which occur during clinical diabetes and if they are confirmed could be use dot identify the onset of diabetes.

[Insulin treatment of Type II diabetes]. / Insulinbehandlung des Typ-II-Diabetes.

Secondary failure to oral hypoglycemic agents occurs in some 5% of type II diabetic patients per year, such that treatment with insulin becomes warranted. In most of the cases only hyperglycemia is apparent, while signs of severe metabolic derangement such as thirst, polyuria and weight loss are lacking. However, the hyperglycemic state adversely affects endogenous insulin secretion and favors the development of microvascular complications and neuropathy. In addition, dyslipidemia is often present, and the patient's well-being may be impaired. To differentiate between real secondary drug failure and transient metabolic impairment due to insufficient compliance with the diet prescriptions, plasma C-peptide should be measured. Insulin therapy should be initiated with a dose of 6-8 IU of an intermediate-action preparation and subsequently adjusted based on blood glucose measurements. Frequently it will be necessary to employ twice daily a mixture of (rapid- and intermediate-action) insulin in order to achieve adequate control of postprandial hyperglycemia. In some cases insulin therapy can be discontinued since the endogenous insulin secretion may improve during insulin treatment. We do not recommend to use as initial therapy of patients with secondary failure to oral hypoglycemic agents a combination of sulfonylureas and insulin since the 'insulin-saving' effect is small and not cost-effective.

[Plasmapheresis therapy in Guillain-Barré polyneuroradiculitis]. / Plasmapheresetherapie bei Polyneuroradikulitis Guillain-Barré.

The outcome of Guillain-Barré polyneuritis is not always benign. Since no therapy of proven effectiveness is available and an immunologic etiology is presumed, plasma exchange treatment has been repeatedly used. We report on three patients with severe polyneuritis who were unable to walk. Two were also in acute respiratory failure. All the cases exhibited surprisingly good improvement correlating in time with plasma exchange. A review of the literature suggests that plasma exchange can at least be recommended in severe cases of Guillain-Barré acute polyneuritis with inability to walk. Treatment should be started within 1-2 weeks of onset of the disease.

[Interstitial pneumopathy and amiodarone]. / Pneumopathie interstitielle et amiodarone.

The case of a patient who developed interstitial pneumopathy after 4 1/2 years of treatment with a normal dose of amiodarone is reported. Drug interruption and additional steroid therapy normalized the pulmonary picture and lung function within 4 months. During this period serum iodine, amiodarone, its metabolite desethyl-amiodarone and urinary iodides were measured and the results compared with the improvement of the clinical and radiological situation. Possible interrelationships between the drug and the pneumopathy, and hypotheses regarding pathogenesis are discussed. During long-term amiodarone therapy radiological checks at regular intervals are important.

[Familial myeloproliferative syndrome]. / Syndrome myéloprolifératif familial.

The case histories of three patients with hematologic disorders are reviewed. The patients are members of the same family composed of three brothers and two sisters. Two have osteomyelofibrosis and one essential thrombocythemia. Hematologic, enzymatic, cytogenetic, immunocytologic and immunogenetic investigations allow the following conclusions: - all the 5 siblings have identical blood group and rhesus factor (0+); - there is an HLA identity in the 5 siblings characterized by the alleles: A2, A3, B5, B7 (w4, w6); - the white blood cell alkaline phosphatase is not increased; - no monoclonality can be shown; - the chromosome Ph 1 is absent. In the second (osteomyelofibrosis) and third (essential thrombocythemia) patient an additional chromosome has been found, while the caryotype of the other three siblings, including the first patient with osteomyelofibrosis, is normal.

[Prolymphocytic leukaemia: a new clinical entity (author's transl)]. / Die prolymphozytäre Leukämie: eine neue klinische Entität. Ein kasuistischer Bericht mit Ubersicht über die Literatur.

A 67-year-old woman, at first diagnosed to have acute lymphocytic leukaemia, developed all the characteristic signs of so-called prolymphocytic leukaemia, namely severe general symptoms of illness, marked hepatosplenomegaly in the absence of lymphadenopathy, extreme leukocytosis (at times more than 1000 x 10(9)/l). Prolymphocytic leukaemia is now considered to be an especially unfavourable form of chronic lymphocytic leukaemia.