Chloroquine and hydroxychloroquine are still used for the prevention and treatment of malaria. Moreover, they are experiencing a renaissance in the long-term therapy of connective tissue diseases (particularly in systemic lupus erythematosus). They induce a lysosomal dysfunction with an accumulation of pathologic metabolic products, which can be seen in ultrastructural histology as pathognomonic cytoplasmic inclusion bodies. Due to its lower toxicity, hydroxychloroquine is the form used predominantly today. Retinopathy as a toxic result of this medication is well known. Cardiac side effects are rarely reported, but in some cases can be severe and irreversible - two cases of organ transplantation have been described in the literature. They comprise conduction disturbances (bundle-branch block, atrioventricular block) and cardiomyopathy - often with hypertrophy, restrictive physiology and congestive heart failure. As the clinical features of cardiotoxicity are unspecific, the identification and follow-up of potentially affected patients is of utmost importance. Confirming the diagnosis of this toxic storage disease requires histological examination of the myocardium in conjunction with electron microscopy. The primary clinical parameters (diagnostic criteria for this cardiomyopathy, differential diagnostics, incidence, risk factors, prognosis) as well as the diagnostic procedures are discussed against the background of the available literature.
The cell-mediated and humoral immune responses were assessed in 15 patients with Crohn's disease and in 28 age-matched control subjects by means of several in vivo and in vitro methods. The disease activity in most patients was absent or moderate. Studying cellular immunocompetence we investigated the skin reactivity to various recall antigens (Candida, Trichophytin, Mumpsantigen, Streptokinase-Streptodornase, PPD), the primary immune response to Dinitrochlorobenzene (DNCB) and Keyhole Limpet Hemocyanin (KLH), and the lymphocyte transformation induced by mitogens (Phytohemagglutinin, Concanavaline A, Pokeweed Mitogen) and specific antigens. Humoral immunity was studied by measuring immunoglobulins, isohemagglutinins, and the antibody response to KLH. In addition, complement components and (in 10 patients) the proportions of T- and B-lymphocytes in the peripheral blood were evaluated. Cutaneous responsiveness to Candida, Mumps-antigen, SK-SD, and DNCB as well as the cellular immune response to KLH were impaired in patients with Crohn's disease (significance was reached for SK-SD, DNCB, and the mean area of induration). The lymphocyte transformation test with PHA, ConA, and PWM revealed normal results. For specific antigens (PPD, SK-SD, KLH) a good correlation could be demonstrated between delayed hypersensitivity and the in vitro lymphocyte responsiveness. Humoral immunity was not unequivocally impaired in Crohn's disease. Five patients with Crohn's disease proved constantly decreased total absolute lymphocyte counts in peripheral blood. The proportions of T- and B-lymphocytes and the complement-levels were corresponding to those in normal controls. No correlation was found between immunological and clinical parameters. In conclusion, patients with Crohn's disease exhibited a partial impairment of the cellular immune response, whereas humoral immunity was not affected. However, it remains to be elucidated whether this immune defect represents a basic pathogenetic factor in the onset of the disease.
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