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Biomedical subjects

M M Bern

Publications and source records attributed to M M Bern.

At least 37 records · Page 2Linked to original sources
PubMed1983

Bleomycin-induced fatal hyperpyrexia.

Bleomycin is a frequently used antitumor agent with adverse effects usually involving the lungs, skin, and bone marrow. An acute hyperpyrexic reaction has also been noted with this agent, usually after the initial injection. Thus a test dose is recommended before therapy is begun. A case of fulminant hyperpyrexia and death in a patient with lymphoma who had previously received multiple courses of bleomycin without prior hyperpyrexia is reported. Fever was associated with the patient's lymphoma and may have effectively reduced the patient's "margin" for tolerating the additional drug-induced pyrexia. It is suggested that attempts be made to lower fevers before therapy with this agent is initiated.

Adolescent↗
PubMed1983

Disseminated varicella-zoster virus infection with the syndrome of inappropriate antidiuretic hormone.

A patient with non-Hodgkin's lymphoma who was previously treated with chemotherapy and radiotherapy was seen with intestinal pseudoobstruction due to paralytic ileus associated with herpes zoster (varicella zoster) infection. The infection was accompanied by a polydermatomal rash with typical morphologic characteristics, followed by cutaneous dissemination and the syndrome of inappropriate antidiuretic hormone (SIADH), as well as myotomal paresis. The diagnosis was supported by cytology and by culture of the virus from the CSF. The isolation of the virus from the CSF, coupled with abnormalities of the patient's mental status and CSF, indicate that meningoencephalitis occurred and probably accounted for the SIADH. The patient had a spontaneous and complete recovery. To our knowledge, this is the first report of SIADH associated with herpes zoster infection.

Aged↗
PubMed1983

Effects of low-dose warfarin on antithrombin III levels in morbidly obese patients.

Morbid obesity has been associated with increased risks for thrombotic diseases. Patients with morbid obesity are shown to have decreased activity and decreased concentration of antithrombin (AT) III. This deficit can be corrected by giving the patients low doses of the oral anticoagulant warfarin. The same beneficial effect was not observed in normal lean control volunteers in whom the levels of AT III were normal at all times. Thus, it may be possible to offer prophylactic protection against the effects of having depressed levels of AT III in patients at increased risk for thrombotic diseases without using full anticoagulant doses of warfarin, including morbidly obese patients.

Antithrombin III↗
PubMed1982

Effect of sulfinpyrazone upon antithrombin III and platelet factor 4 in chronic renal failure.

Despite the suppressive effects of uremia upon platelet function, patients with chronic renal failure are at increased risk for thrombotic diseases. This increased risk is linked to lowered concentrations of antithrombin III (AT III) and increased platelet release in vivo, as indicated by increased plasma concentrations of platelet factor 4 (PF4). Sulfinpyrazone, a drug capable of reducing the frequency of thrombotic events in uremic patients, allows return toward normal of the AT III while reducing to normal the plasma concentration of PF4. Thus, suppression of platelet function by sulfinpyrazone appears to reduce in vivo clotting, and thus reduces consumption of AT III.

Adult↗
PubMed1982

Cultured endothelial cells derived from the human iliac arteries.

Cells derived from the endothelium of human iliac arteries were cultured in vivo. The cells were isolated, grown, and subcultured in HEPES buffered Medium 199 supplemented with 20% heat inactivated human whole blood serum, human alpha-thrombin, and commercial endothelial cell growth supplement derived from bovine brain. The cells were viable in culture for 8 to 10 passages at a split ratio of 1:3. After the 10th passage, the cells began to enlarge and their growth rate was reduced. No cultures were viable after the 12th passage. The cells were determined to be of endothelial origin by their morphology at confluence; their ultrastructural characteristics, including the presence of Weibel-Palade bodies; the production and release of factor VIII-related antigen; and by their maintenance of a surface that prevented platelet attachment. The cultured arterial endothelial cells released prostacyclin in response to challenge with thrombin and protamine sulfate but not in response to bradykinin or the platelet-derived growth factor. Although the cultures described in this report were derived from patients with varying degrees of atherosclerotic disease, there were no significant differences in morphological or physiological parameters among these cultures or in comparison with commonly studied cells derived from human umbilical veins.

Antigens↗
PubMed1981

Noncirrhotic portal hypertension in adults.

Of 366 cases of portal hypertension in adult patients referred for evaluation and management in the past 15 years, the cause was not related to cirrhosis or hemochromatosis in 41. No specific cause was demonstrated for portal hypertension in four cases, which were excluded from further evaluation. Of the remaining 37 patients, 26 had a presinusoidal block characterized primarily by bleeding from esophagogastric varices, and 9 had a postsinusoidal block characterized by the rapid development of intractable ascites. In two cases an arteriovenous fistula was the cause of portal hypertension. Treatment was operative or nonoperative depending on the nature and prognosis of the basic disease. The various approaches to therapy include shunting procedures for the control of ascites or esophagogastric varices, the use of a type of portal-azygous disconnection and a direct approach to a valve or a fistula. In the absence of a rapidly fatal primary disease, portal hypertension is not a threatening problem and may be controlled with minimal mortality by appropriate surgical management.

Adult↗
PubMed1981

Insulin resistance and monoclonal gammopathy.

Two maturity-onset diabetic patients developed severe insulin resistance during the course of monoclonal gammopathies. One patient had Waldenström macroglobulinemia and the other had multiple myeloma with IgA gammopathy. The maximum insulin binding capacity (MIBC) was 121 U/liter and 54.7 U/liter, respectively, during insulin resistance. The clinical courses of insulin resistance paralleled the activity of the monoclonal gammopathies (MG) with the insulin resistance disappearing after the monoclonal gammopathies were controlled. Six other diabetic patients with concurrent insulin resistance and monoclonal gammopathies are reviewed.

Aged↗
PubMed1981

Thrombocytopenia complicating preeclampsia: data to support a new model.

Thrombocytopenia can be associated with preeclampsia without evidence of consumptive coagulopathy and may contribute to placental insufficiency. In the case reported here, the patient's platelets agglutinated in vitro in the presence of her serum when the serum had been preincubated with her placental cells. The reaction was calcium and, probably, complement dependent. Mixtures of sera and placentas from normal APO-matched control pregnancies caused no agglutination of the patient's platelets. The capacity of her serum and placental cells to agglutinate her own platelets was not found in the sera obtained 60 days post partum. These findings suggest that in some cases of preeclampsia the platelets may be involved in an immune-mediated phenomenon that can induce platelet agglutination and is probably accentuated in the placenta, thus attenuating placental blood flow.

Adult↗
PubMed1978

Intraaterial hepatic infusion and intravenous adriamycin for treatment of hepatocellular carcinoma: a clinical and pharmacology report.

Four patients received intraarterial (ia) hepatic infusion and 10 received intravenous (iv) adriamycin for hepatocellular carcinoma. Four of each group are evaluable. The remaining 6 patients died within 14 days of intravenous therapy and are, therefore, considered nonevaluable. Patients received 2 to 9 courses of adriamycin every 3 weeks. One half of each group of evaluable patients had partial responses (pr). The group had pr for 22.5 weeks (range 8 to 37). The iv group had pr 27.2 weeks (range: 16 to 38.5). Mean survival was 21 weeks for nonresponders, and 43 weeks for responders. Intraarterial infusion did not protect patients from adriamycin toxicity. Cardiac and liver toxicity were not seen, but marrow and gastrointestinal toxicity developed at 1.2 X 10(-7)M adriamycin serum level. Adriamycin disappearance curves after ia and iv therapy were similar for similar bilirubin levels, and prolonged with hyperbilirubinemia. Ascites fluid did not accumulate detectable adriamycin. Pharmacokinetics are described in this report.

Adolescent↗
PubMed1978

Selective platelet immune retention.

Inbred rats were immunized with Freund's Adjuvant containing proteins of Mycogacterium tuberculosis, Mycobacterium butyrium, or dinitrochlorobenzene (DNCB). Native arterial blood was then passed over glass beads coated with those antigens. The platelet retention on the glass beads was measured. Rats immunized with Complete Freund's Adjuvant developed accelerated platelet retention on beads coated with protein derivatives of tuberculosis (PPD) after just 18 seconds of blood flow. Rats immunized twice maintained selective retention longer than those immunized once. The test animals developed no cutaneous hypersensitivity nor precipitin lines on Ouchterlong gels against PPD. Rats sensitized to DNCB had accelerated platelet retention on DNCB-coated beads. Results were temperature and complement dependent, and antigen-specific. Heparin caused a dose-dependent inhibition of the accelerated retention. PPD potentiated the ADP-induced aggregation of plateletrich plasma (PRP) from immunized rats. These experiments suggest that platelets react selectively to antigens in the intravascular spaces in immune reactions.

Animals↗
PubMed1975

Variable response of activated partial thromboplastin time to heparin therapy during hemodialysis.

The consistency of the anticoagulant effect of intravenously administered heparin was studied. The activated partial thromboplastin time (APTT) was measured for six patients hourly during three consecutive hemodialysis sessions each. Cephaloplastin was the plasma-activating agent. The time required to form a clot was measured by a light-sensitive electronic timer and confirmed within +/- 5% by the tilt tube method. Results are reported in second relative to units of heparin given to patients per kilogram body weight. The range of APTT's measured 55 minutes after each heparin dose greatly exceeded the range of technical variability of the assay method. The probably mechanisms and consequences for this variability after a constant heparin dose are discussed. The anticoagulation effect of heparin during hemodialysis in an otherwise stable clinical situation is not constant. The risks of having too much or too little anticoagulation are not eliminated by having determined a therapeutic heparin dose during one dialysis rung.

Blood Coagulation Tests↗