Vitamin C and iron overload in a chronic hemodialysis patient.
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Biomedical subjects
Publications and source records attributed to A Haubenstock.
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In nine patients with nephrotic syndrome the behaviour of plasma fibronectin was studied. Of nine patients seven showed elevated plasma fibronectin levels while the plasma fibrinogen level was increased in eight of the nine investigated patients. A positive correlation was found between plasma fibronectin levels and fibrinogen (P less than 0.01), cholesterol (P less than 0.01) and proteinuria (P less than 0.05). The results indicate that elevated plasma fibronectin levels could be an additional factor responsible for hypercoagulability in nephrotic syndrome.
The case of a 25-year-old man with the characteristic features of malignant histiocytosis (proliferation of abnormal histiocytic cells with erythrophagocytosis, hepatosplenomegaly, increased serum acid phosphatase, hypercalcemia, and bone pain) is reported. Chromosome studies revealed a near tetraploid karyotype with a pair of marker chromosomes. A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis. Cerebrospinal fluid (CSF) findings were consistent with a diagnosis of Guillain-Barré Syndrome. On the next day, disseminated intravascular coagulation (DIC) with severe hyperfibrinolysis occurred. After intensive chemotherapy, complete remission could be achieved.
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Plasma oxalic acid concentrations were measured in 13 chronic haemodialysis patients. The mean plasma oxalic acid concentration was 128.0 +/- 48.6 mumol/l, being approximately 8 times higher than the plasma concentration of 14 volunteers (mean = 16.8 +/- 5.2 mumol/l). Ultrafiltrates obtained in vivo from these patients showed a mean oxalic acid concentration of 138.2 +/- 56.5 mumol/l. Since in vivo ultrafiltrates are free of erythrocytes and plasma enzymes, an in vitro synthesis of oxalic acid from precursors by erythrocytes and plasma enzymes can be excluded. As the oxalic acid concentration of plasma corresponded to that of in vivo ultrafiltrates, it is concluded that any in vitro formation of oxalic acid in haemodialysis patients must be negligibly small, and is irrelevant for the measurement of plasma oxalic acid levels in patients receiving regular haemodialysis.
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Six cases of oral intoxication with lindane-solvent mixtures are reviewed. The ingested doses of lindane (mean dosage 120 mg/kg +/- 86 mg/kg) and benzene (mean dosage 366 mg/kg +/- 93 mg/kg) exceeded the toxic level. Symptoms (vomiting, dizziness and hyperreflexia) occurred within 30 min and all patients had epileptiform seizures. Two patients suffered from pulmonary edema and one of them had a severe rhabdomyolysis. Diazepam was sufficient to control convulsions in five cases. Gastric lavage was performed in five patients and activated charcoal, liquid paraffin with saline cathartic, and cholestyramine were used as adsorbents. Recovery was complete in all patients.
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Plasma glycollate and oxalate concentrations were measured in 20 patients undergoing chronic haemodialysis treatment. The mean plasma glycollate level was 173.7 +/- 52.9 mumol/l, which was not significantly different from the normal value (means = 145.8 +/- 37.8 mumol/l). The mean plasma oxalate concentration (means = 128.7 +/- 25.6 mumol/l) was about 8 times higher than the value found in normal volunteers (means = 16.8 +/- 6.0 mumol/l). During haemodialysis lasting for 6 hours the plasma oxalate concentration decreased by 53.5%. However, no decline in plasma glycollate levels was noted. Since glycollate was not found in ultrafiltrates obtained in vivo, it is concluded that glycollate is not eliminated during haemodialysis treatment.
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In this study clinical findings are presented of 31 patients with clonidinee intoxication and the therapeutic measures taken in these cases are discussed. In toddlers poisoning is seen after ingestion of a single tablet of 150 micrograms clonidine, whilst in adults poisoning may occur already at a dosage just exceeding the therapeutic limit, which is subject to wide individual variation (1 to 3 tablets). Primary elimination procedures must be instituted at these dosages, but, because of the rapid absorption of clonidine, gastric lavage and induced emesis provide no benefit to patients with complete symptomatology or those who took the overdose several hours before. Chlorpromazine-like effects, hypotension and bradycardia proved to be the outstanding features. Respiratory depression, disturbances of myocardial conduction or hypertension were less frequent. Symptoms lasted for a mean of 15.5 +/- 8.6 hours, with a range of 4 to 36 hours. Fluid therapy and, as necessary, dopamine for hypotension, phentolamine for hypertension and atropine for bradycardia caused prompt improvement in addition to essential measures such as meticulous control of respiratory function, body temperature and of ECG changes. There was no need to implement the central clonidine antagonist, tolazoline in any of these cases.
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4 cases of baclofen intoxication were reported to the Vienna Poison Information Center during the years 1974-1982. These cases are presented and are discussed along with previously published cases of baclofen intoxication. A review of symptomatology and therapy is given.
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The case report is presented of a patient with gluten sensitive enteropathy who subsequently developed an intestinal non-Hodgkin lymphoma. When steatorrhoea or diarrhoea develops in a patient with abdominal lymphoma, these symptoms are often attributed to progression of the lymphoma or to chemotherapy of the lymphoma. Since there is an established relationship between gluten-sensitive enteropathy and intestinal lymphoma, the differential diagnosis of steatorrhoea or diarrhoea developing in the course of malignant intestinal lymphoma must include gluten-sensitive enteropathy as well. In the investigation for gluten-sensitive enteropathy HLA typing can be used as a screening test in addition to routine malabsorption tests and small bowel biopsy
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