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M Maislos

Publications and source records attributed to M Maislos.

28 records · Page 2Linked to original sources
PubMed1990

[A simple qualitative method for assessing microalbuminuria in diabetics].

Diabetes mellitus is one of the most important causes of kidney diseases, the first sign of which is albuminuria. It is now possible to detect microalbuminuria before the appearance of larger quantities. We compared a simple qualitative test for microalbuminuria (change in color of a tablet containing bromphenol blue on addition of urine) with a more elaborate quantitative immunoturbidometric method. Of 109 samples tested 31 were positive by the quantitative method and 29 of these were positive by the tablet method. Out of the 78 negative by the quantitative method only 4 were positive by the qualitative test. The sensitivity of the tablet test was 93.5%, specificity 94.0%, positive predictive value 87.9%, negative predictive value 97.4%, false positive rate 5.2%, and false negative rate 6.2%. We conclude that the tablet test is simple and accurate and is suitable both for screening of large populations and for the diagnosis of individual cases of microalbuminuria.

Albuminuria↗
PubMed1988

Pharmacokinetic model of circulating covalent aggregates of insulin.

Covalent aggregates of insulin in blood of insulin-treated diabetic patients account for as much as 70% (mean 28 +/- 3.6%) of serum insulin immunoreactivity. These aggregates may originate in therapeutic insulin, because similar substances account for 0.1-3% of these preparations. Larger amounts in blood imply that aggregates accumulate as a result of delayed clearance. To test and quantify this speculation, we calculated the plasma kinetics of this material in four normal volunteers who received large intravenous doses (30 mU.kg-1.min-1) of beef-pork crystalline zinc insulin for 120 min. Insulin aggregate and monomer concentrations were measured in blood samples obtained at regular intervals throughout the infusion and during 4 h after discontinuation of insulin. Pharmacokinetic parameters were calculated from the data. Insulin aggregate and monomer serum t 1/2 were 63.6 +/- 6.9 and 34.3 +/- 2.8 min, respectively, and clearances were 101 +/- 10 and 232 +/- 47 ml/min. Volume of distribution (V beta) and volume at steady state (Vss) were 9.1 +/- 1.8 and 8.2 +/- 2.2 L for insulin aggregate and 11.6 +/- 2.8 and 12.2 +/- 3.6 L for insulin monomer, respectively. Mean residency time was 141 +/- 14 and 114 +/- 10 min for insulin aggregate and monomer, respectively [P less than .01 for all parameters except V beta (.014) and Vss (.012), aggregate vs. monomer]. Thus, in relation to insulin monomer, calculated pharmacokinetic parameters of the aggregate predict accumulation after insulin injection. Plasma t 1/2 of the aggregate was almost double that of monomeric insulin; total-body clearance and the corresponding volumes of distribution were smaller.

Adult↗
PubMed1987

Bile salt deficiency and the absorption of vitamin D metabolites. In vivo study in the rat.

We studied the effect of the absence of bile salts on the absorption of vitamin D metabolites in vivo, in the biliary duct-ligated rat. The mesenteric, lymphatic absorption of the metabolites studied (vitamin D3, 25-hydroxyvitamin D3, and 1,25-dihydroxyvitamin D3) was almost completely abolished in the experimental animals. These results differed significantly (P less than 0.001) from those of the control rats. The 1,25-dihydroxyvitamin D3 absorption into the portal vein system was unaffected by the lack of biliary salts. The absorption of 25-hydroxyvitamin D3 was decreased and that of vitamin D3 was negligible, under the same experimental conditions. These data show that the more polar vitamin D metabolites, like 1,25-dihydroxyvitamin D3 and to some extent 25-hydroxyvitamin D3, are absorbed directly into the portal blood without the involvement of bile salts and micelle formation. Thus, the use of polar vitamin D metabolites should be considered in correcting hypovitaminosis D and osteomalacia in cases of chronic biliary salt depletion.

Animals↗
PubMed1986

The source of the circulating aggregate of insulin in type I diabetic patients is therapeutic insulin.

Circulating insulin immunoreactivity (IRI) in type I diabetic patients (insulin-dependent diabetes mellitus [IDDM]) includes a covalent aggregate about twice the size of insulin. These studies were designed to determine the source and conditions promoting the accumulation of this material. Among 31 IDDMs, the aggregate made up 28 +/- 3.6% of the mean fasting plasma IRI. Five of these patients were restudied after 5 d of treatment with equidose intravenous insulin. The relative amount of the aggregate during subcutaneous treatment (40 +/- 8.0%) was indistinguishable (P greater than 0.7) from that at the termination of intravenous treatment (41 +/- 6.8%). To determine whether previous exposure to therapeutic insulin influenced the appearance and accumulation of the aggregate, we intravenously or subcutaneously infused insulin for 5 h in nine healthy volunteers (euglycemic clamp). At the termination of the high-dose intravenous infusion (10 mU X kg-1 X min-1), the concentration of the aggregate was 81 +/- 18 microU/ml, and it accounted for 2.9% of total IRI. At the conclusion of the other infusion protocols, the absolute amounts of aggregate were somewhat less, but they accounted for similar percentages. On polyacrylamide gel electrophoresis, the circulating aggregate was indistinguishable from a material of similar molecular weight contaminating commercial insulin. We conclude that the insulin aggregate found in the blood of IDDMs originates in commercial insulin. Its appearance is independent of the route of insulin administration. Prolonged and continuous use of insulin may increase its concentration but is not necessary for its appearance. The potential biologic and immunologic consequences of the aggregate are important matters that need to be addressed.

Chromatography, Gel↗
PubMed1985

Leiomyoblastoma associated with intractable hypercalcemia and elevated 1,25-dihydroxycholecalciferol levels. Treatment by hepatic enzyme induction.

A 42-year-old woman, with a previously resected jejunal leiomyoblastoma, was first seen with liver metastases 31/2 years after the tumor resection. Intractable malignant hypercalcemia appeared eight months later, together with renal insufficiency. No osteolytic lesions were detected. Levels of parathyroid hormone, cyclic adenosine monophosphate, and 1,25-dihydroxycholecalciferol (1,25[OH]2D) were not useful in distinguishing between the hypercalcemia of malignancy and concurrent hyperparathyroidism. Despite renal insufficiency, hypercalcemia, and subtotal parathyroidectomy, the 1,25(OH)2D levels remained elevated, consistent with the speculation that a tumor product stimulated 1-alpha-hydroxylation of 25-hydroxycholecalciferol. Phenytoin and phenobarbital (enzyme induction therapy), in combination with phosphorus and glucocorticoids, appeared to be useful in controlling the hypercalcemia.

Adult↗
PubMed1985

Transitory hypocalcemia complicating measles.

During an epidemic of measles, 12 young adults developed hypocalcemia associated with a decrease in parathyroid hormone level. Calcium and parathyroid hormone levels returned to normal in five of the 12 patients for whom convalescent data were available.

Acute Disease↗
PubMedDate not supplied

Massive splenomegaly responsive to proguanil and with features of hairy cell leukaemia.

A recent Ethiopian immigrant to Israel presented with pneumococcal sepsis, massive splenomegaly and lymph-adenopathy. Investigations revealed many features of both hairy cell leukaemia (HCL) and hyperreactive malarious splenomegaly (HMS). Proguanil therapy for HMS was followed by rapid, marked decrease in spleen size, disappearance of the tartrate-resistant acid phosphatase-positive cells characteristic of HCL, and increasing eosinophilia, but unchanged lymphadenopathy.

Adult↗