[Therapy of coronary disease].
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Biomedical subjects
Publications and source records attributed to H Lydtin.
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A 77-year-old man with chronic obstructive pulmonary disease was treated with low-dose methotrexate (7.5-15 mg per week). After 15 months a diagnosis of urothelial carcinoma of the bladder was made; after a further 6 months pneumonitis and pancytopenia developed. The patient died due to massive pulmonary hemorrhage. A malignant teratoma was diagnosed in a 65-year-old asthmatic man 16 months after initiation of methotrexate therapy (15 mg per week). The patient died 4 months later due to fulminant progression of the neoplasm. A third malignant neoplasm (dermal squamous cell carcinoma) was seen in a 64-year-old woman with rheumatoid arthritis after 13 months treatment with 7.5 mg methotrexate per week. These three cases, while obviously not proving a causal relationship between long-term treatment with low-dose methotrexate and development of malignant neoplasm, do call for stringent treatment criteria, close surveillance, and prospective studies.
Cerebral hemorrhage is a rare complication of the acquired immunodeficiency syndrome. We report a case of multifocal hemorrhage in a 37-year-old homosexual man with cerebral toxoplasmosis. Histopathologic examination, performed at cerebral autopsy, confirmed the findings on CT and MRI.
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The current literature contains reports of sarcoidosis with polyclonal increases in immunoglobulins. There are also reports of lymphoma in patients with pre-existing sarcoidosis. This is believed to be the first report of a patient in whom a monoclonal IgM kappa paraproteinemia developed after the diagnosis of sarcoidosis. This paraproteinemia was linked with a histologically proved non-Hodgkin's lymphoma. The possible relationships between the two disease entities are discussed.
In a 42-year-old man with abdominal symptoms, loss of hair and increasing distal polyneuropathy in both legs, the clinical suspicion of thallium poisoning was confirmed by urinary and blood analysis. Hair analysis provided a pointer to the time of poisoning. In addition to symptomatic measures, treatment consisted of administration of potassium-iron (III) hexacyanoferrate (II) (Berlin blue), combined with forced diuresis. Despite the overall favourable course, residual symptoms of distal polyneuropathy were still present 6 months after discharge from hospital.
In an open study in patients with tumour-induced pain the analgetic effects of the prostaglandin-inhibiting compound diflunisal and the centrally-acting analgetic tilidine N were compared. A dosage of 1 g diflunisal was found to be equivalent to 50 drops of tilidine N and to be subjectively well-tolerated. In the pain-relieving therapy of tumour patients diflunisal appears to offer a genuine alternative to centrally-acting analgetics.
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Unwanted effects of beta-receptor blocking agents can be divided into three categories: 1. Those arising specifically from the pharmacologic, i.e., beta-blocking action. 2. Side effects not directly (or not with certainty) related to beta-blockade. 3. Adverse and potentially specific reactions to individual beta-blocking agents. Category 1 covers the majority of adverse effects (heart failure, severe bradycardia and hypotension, arterial insufficiency, increased airways resistance, gastrointestinal symptoms, hypoglycemia). These can largely be avoided by proper selection and preparation of patients. Category 2 covers cutaneous reactions (rashes, alopecia, pruritus), purpura (thrombocytopenic and nonthrombocytopenic) etc. as well as side effects attributable to the central nervous system (antianxiety effects, nightmares etc.). In the third category the "oculo-cutaneous syndrome" associated with practolol is discussed.
A double blind trial was undertaken to determine whether the addition of the beta-receptor blocker Betadrenol in two different doses to a lidocaine solution containing adrenaline could influence the exogenous and endogenous beta-adrenergic effects in the field of dental interventions under local anesthesia. It could be shown that already very small amounts of the beta-receptor blocker Betadrenol could suspend beta-adrenergic stimulation of the heart and so prevent unwanted circulatory reactions without side effects on the central nervous system.
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