PubMed Health⌕ Search

Biomedical subjects

M I Malik

Publications and source records attributed to M I Malik.

7 recordsLinked to original sources
PubMed1992

Distribution of biotin in human plasma: most of the biotin is not bound to protein.

Estimates of the plasma concentration of biotin differ considerably. Variation in detectability of biotin bound covalently to protein is one potential source of disagreement. In this study we determined the amount of biotin covalently bound to plasma protein. First, greater than 99% of free and reversibly bound biotin was removed by dialysis; then greater than 90% of covalently bound biotin was released by acid hydrolysis. For plasma samples from 11 normal adults, the ratio of covalently bound biotin to free biotin was 0.15 +/- 0.09 (mean +/- SD). Taking into account the additional biotin that is reversibly bound to protein, this study provides evidence that approximately 12% of total biotin in plasma is covalently bound, 7% is reversibly bound, and 81% is free. We conclude that covalently bound biotin cannot account for the reported sixfold increase in biotin detected after acid hydrolysis. We speculate that the reported increase was an artifact caused by substances produced during acid hydrolysis of plasma.

Adult↗
PubMed1992

A case of percutaneous industrial methanol toxicity.

Methanol (CH3OH) is a chemical feedstock of increasing importance as well as a commonly used solvent. In the early 1980s methanol production was introduced at a new petrochemical complex in the Saudi port of Jubail. A case is presented of a consultant supervising tank cleaning prior to methanol loading. He wore positive pressure breathing apparatus but no protective clothing. After 2-3 hours working in the confined space of the tank, he worked on deck and continued to wear his methanol-soaked clothing which eventually dried out. Visual symptoms of acute methanol toxicity presented some 8 hours after exposure. The appropriate treatment (with ethanol provided by the ship bond) was carried out in hospital and the individual recovered completely. Most reported cases of methanol toxicity are social in origin, arising from ingestion. This particular case, though unusual, does present some interesting lessons.

Adult↗
PubMed1990

Syringomyelia presenting as cricopharyngeal pseudostricture.

A 14-year-old boy was referred for evaluation of a cervical esophageal "stricture" diagnosed by upper gastrointestinal radiograph, which had been performed for evaluation of dysphagia and dysphonia of several months' duration. Neurological examination revealed several cranial nerve abnormalities and hyperreflexia, raising the suspicion of a cervicomedullary junction lesion. However, computed tomography of the head, neck, and spine was completely normal. Findings on the swallowing videofluoroscopy were interpreted as consistent with a stricture (a "tight constriction distal to the pyriform sinus"). However, no evidence for this was found by either esophagoscopy or esophageal manometry, which revealed a low-pressure cervical esophageal sphincter. Neurologic evaluation was pursued with magnetic resonance imaging, which revealed a large syrinx extending from C2 to T2 segments. We report this case to point out the importance of considering neurologic disease in the differential diagnosis of "stricture" of the cervical esophagus.

Adolescent↗
PubMed1986

T-cell chronic lymphocytic leukemia with pure red cell aplasia: laboratory demonstration of persistent leukemia in spite of apparent complete clinical remission.

A 40-year-old woman presented with splenomegaly, macrocytic anemia, and red cell aplasia. Although lymphocytosis was absent in the peripheral blood, large atypical lymphoid aggregates were present in the bone marrow. Splenectomy resulted in partial remission of red cell aplasia, but a gradual increase in the number of peripheral blood lymphocytes followed during the next 36 months. Flow cytometric analysis demonstrated that the majority of these peripheral blood lymphocytes had suppressor, natural killer T-cell phenotype. No other treatment was given until red cell hypoplasia worsened 42 months after initial presentation. Repeat bone marrow evaluation again demonstrated severe erythroid hypoplasia and large abnormal lymphocytic infiltrates. Cyclophosphamide given for 8 months resulted in complete resolution of the red cell aplasia and complete clinical remission of CLL. However, flow cytometric analysis revealed persistent increase in bone marrow T-cells, and bone marrow co-culture studies demonstrated residual ability of peripheral blood mononuclear cells to inhibit erythropoiesis in vitro, suggesting that residual, clinically undetectable leukemia persists in spite of complete clinical remission.

Adult↗
PubMed1984

Cardiopulmonary bypass for patients with previously documented heparin-induced platelet aggregation.

Heparin-dependent intravascular coagulation is a widely recognized syndrome in which heparin acts as a hapten for an antiplatelet antibody and causes accelerated intravascular thrombosis and thrombocytopenia that may culminate in organ loss, hemorrhagic diathesis, and even death. Diagnosis is made in vitro by observing heparin-stimulated aggregation of normal platelets suspended in the patient's platelet-poor plasma. Treatment consists of cessation of heparin and use of antiaggregating agents with or without warfarin sodium. Management of patients with prior heparin-dependent intravascular coagulation who require cardiopulmonary bypass has not been reported. We now have successfully managed three such patients and herein present guidelines for management. Each patient was undergoing heparin therapy and manifested hallmark heparin tachyphylaxis, thrombocytopenia, and increased thrombotic symptoms (further venous thrombosis after cardiac catheterization in two cases and exacerbation of unstable angina in the other). In vitro aggregation studies were abnormal. Heparin was stopped, and antiaggregative therapy was begun with good response in each instance. In vitro studies were done serially until the antiplatelet antibody reaction had vanished (usually 4 to 8 weeks), and coronary revascularization was then conducted with full heparinization. Further heparin exposure postoperatively was avoided. There was no perioperative evidence of intravascular thrombosis or bleeding diathesis, and in vitro heparin-dependent aggregation did not recur. We conclude that patients with previously documented heparin-dependent intravascular coagulation can safely sustain the massive heparin rechallenge of cardiopulmonary bypass, provided that in vitro aggregation has ceased and rechallenge therapy is not prolonged.

Aged↗