OSA is associated with a high prevalence of PAD. This implies substantial diseasés under-recognition and a presumable atherogenic role of OSA in the pathogenesis of PAD. However, vasoprotective impact of OSA treatment remains to be determined.
In acute liver failure (alf) there is a defect in synthesis of coagulation factors in addition there is a disseminated intravascular coagulation which is followed by an impairment of the microcirculation. With an early substitution of Antithrombin III (AT III) we tried to stop this situation. In 22 patients (10 female, 12 male, age 10-68) with alf presenting with hepatic coma (grade I-IV) we studied the time course of AT III plasma activity (the study started in December 1978 and is continued until now). AT III was measured with the chromogenic substrate method. When AT III activity fell below the level of 80% of normal, we started to substitute AT III and to give low dose heparin (125-500 U/hrs). In addition in case of bleeding or a decrease of coagulation factors or fibrinogen under the hemostatic active concentration, complexes of prothrombin and fibrinogen were administered. Besides the usual conservative treatment for alf, patients in coma (grade IV) were undergoing baboon liver perfusion. The rapid fall of the hepatic coagulation factors stopped. In patients, who still were able to synthesize coagulation factors a reincrease of these factors after administration of AT III was seen and there was a further fall in fibrinogen. The dosage of AT III in alf required to bring AT III to normal values depended on the degree of intravascular coagulation. The average dose in our study was 250 U/3 hrs. The clinical course of alf was prolonged in all patients and 7 patients with the prognostic deleterious colombindex (sum of factors II + V + VIII) < 75% eventually survived the alf. The coagulation disorders in alf can be treated with an early substitution of AT III; thus, there is more time for liver regeneration. Our results suggest an improved prognosis of the acute liver failure.
The neuraminidase inhibitors signifies a breakthrough in the treatment of influenza. We compared the outcomes of influenza in 56 patients treated with zanamivir or oseltamivir to a group of 52 influenza patients from the time before these drugs were available. The duration of illness was reduced by 45%, the severity of symptoms by 40% and the administration of antibiotics by 32%. The data from this small group of patients of our ambulatory practice correspond to the results of large randomized placebo-controlled double-blind studies on zanamivir and oseltamivir. Our clinical observations and painful experiences have taught us to take every case of suspected influenza seriously. Since considerable influenza-related complications are common even in otherwise healthy individuals, patients should immediately consult their doctor when an illness with sudden onset of fever and cough or another respiratory symptom occur.
Influenza viruses type A and B can cause a wide spectrum of illness, and they are responsible for considerable mortality and morbidity. With the new neuraminidase inhibitors, of which zanamivir was the first drug to be licensed, the physician has antivirals at his disposal which are safe and effective against both influenza virus type A and type B. Available data from clinical Phase III studies indicate benefits in terms of a reduction in the median time to alleviation of major symptoms by 1.5 to 3 days when treatment is started within 36 to 48 h after onset of influenza. Similar results have been obtained with oseltamivir. Neuraminidase inhibitors provide a valuable treatment option, particularly for individuals not protected by vaccination, and those at high risk of influenza-related complications. The study results obtained so far indicate that patients with pre-existing diseases and those with severe influenza symptoms profit most from the treatment. This is confimed by our own experience in treating severe influenza conditions.
The clinical manifestations of primary or idiopathic hemochromatosis include mainly hepatomegaly, diabetes mellitus, and hypogonadism. Most investigators postulated that the hypogonadism is caused by pituitary dysfunction and that the deposition of iron in the testes is of little importance. We found not only pituitary failure in a 45-year-old man with idiopathic hemochromatosis (low LH and FSH levels, no response to GnRH) but could also detect by light microscopy deposition of iron in capillary endothelial cells and in the perivascular space of the testicular tissue. Electron microscopic study of tissue from the testes showed intracytoplasmic hemosiderin deposits in capillary endothelial cells. Abundant lipofuscin granules were present in Sertoli cells and Leydig cells. The serum testosterone levels were low and there was no response in the HCG test. The intratesticular testosterone levels were also lowered. In our opinion, the androgenic deficiency in idiopathic hemochromatosis is not only caused by pituitary failure but also by testicular dysfunction due to deposits of hemosiderin and lipofuscin in the testes.
ldiopathische Harnochromatose bei einem 45jahrigen unfruchtbaren MannZusammenfassung: Die klinischen Manifestationen der primaren oder idiopathischen Hamochromatose sind hauptsachlich Hepatomegalie, Diabetes mellitus und Hypogonadismus. Die meisten Untersucher nehmen an, dai3 der Hypogonadismus durch eine Storung der Hypophysenfunktion bedingt ist , und daB Eisenablagerungen in den Hoden von untergeordneter Bedeutung sind. Wir fiiden bei einem 45 Jahre alten Mann mit idiopathischer Hamochromatose nicht nur eine Hypophysenfehlfunktion (niedrige LH-und FSH-Werte, kein Ansprechen auf GnRH), sondern konnen auch lichtmikroskopisch Eisenablagerungen in Kapillarendothelzellen und im Perivaskularraum des Hodengewebes nachweisen. Die elektronenmikroskopische Untersuchung von Hodengewebsproben zeigt intrazytoplasmatische Hamosiderinablagerungen in Kapillarendothelzellen. In Sertoli-und in Leydigzellen sind massenhaft Lipofuszingranula vorhanden. Die Serum-Testosteronwerte sind erniedrigt und zeigen keinen Anstieg im HCG-Test. Auch die intratestikularen Testosteronwerte sind erniedrigt. Nach unserer Meinung ist das Androgendefiiit bei der idiopathischen Hamochromatose nicht nur auf eine Hypophysenfehlfunktion, sondem auch auf eine Funktionsstorung der Hoden durch dort abgelagertes Hamosiderin und Lipofuszin zuriickzufiihren.
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