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C M Reinke

Publications and source records attributed to C M Reinke.

10 recordsLinked to original sources
PubMed1994

Update on Clostridium difficile-induced colitis, Part 2.

Clostridium difficile is a nosocomial pathogen able to survive unfavorable environments by sporulation; when conditions advantageous for rapid growth appear, the vegetative form is regenerated. Lack of conscientious hand washing and failure of health care providers to use disposable gloves facilitate transmission within institutions. Exposure to certain antimicrobials expedites C. difficile overgrowth within the colon by altering the composition of the normal gut microflora. Antineoplastic agents may also precipitate CDIC. The characteristics of the colonizing strain, the properties of the inciting drug, and individual host factors collectively seem to govern the expression of the disorder. Clinical presentations range from self-limiting diarrhea to severe diarrhea accompanied by abdominal pain, fever, and leukocytosis to potentially life-threatening PMC. A preponderance of data supports the interpretation that oral metronidazole and oral vancomycin are therapeutically equivalent for the treatment of all but the most severe cases of CDIC. Whether the two drugs are equivalent in severe CDIC is controversial and will probably remain so in the absence of a well-designed trial to expand on the findings of the study by Teasley et al. Because of the cost difference and therapeutic equivalence, oral metronidazole should be the preferred routine treatment for CDIC; oral vancomycin should be reserved for severe cases and cases that fail to respond to at least six days of oral metronidazole therapy. Another important argument, albeit a hypothetical one, for limiting institutional use of oral vancomycin is to minimize selective environmental pressure for the emergence and dissemination of vancomycin-resistant enterococci. An epidemic outbreak of CDIC caused by clindamycin-resistant C. difficile in an institution where clindamycin use was extremely high illustrates the possible consequences of such selective pressure. Oral metronidazole 250 mg four times daily will usually provide a satisfactory response, but clinicians may wish to consider increasing the total daily dose for some patients who have symptoms like fever and leukocytosis. For oral vancomycin, 125 mg four times daily is sufficient in virtually all circumstances. Ten days of therapy is usually adequate for either drug. CDIC in a patient unable to take medications orally presents a bit of a therapeutic dilemma. Two approaches that appear effective are rectal administration of vancomycin and intravenous administration of metronidazole, although intravenous metronidazole can fail to work, possibly because the colonic concentrations achieved are inadequate. Clinicians may wish to consider a total daily dose of intravenous metronidazole that is at the upper end of the adult dosage range, if this is feasible.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1994

Update on Clostridium difficile-induced colitis, Part 1.

Recent findings on the epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment of Clostridium difficile-induced colitis (CDIC) are discussed. CDIC is a gastrointestinal disorder that results from colonization by and overgrowth of C. difficile. Among patients in the community who are treated with an oral antimicrobial, only 1 to 3 individuals per 100,000 develop CDIC, compared with as many as 1 per 100 hospitalized patients treated with an antimicrobial. The requirements for CDIC are (1) a readily available source of C. difficile; (2) exposure to drugs, most commonly certain antimicrobials, that disrupt the normal colonic microflora; (3) production of the requisite cytotoxins by the C. difficile strain colonizing the colon; and (4) the presence of individual risk factors, including advanced age, severe underlying illness, and a prolonged hospital stay. Among the varied clinical manifestations of CDIC, diarrhea is predominant and is often the sole symptom. In more severe cases, fever and leukocytosis are also present. The formation of pseudomembranous plaques is pathognomonic but relatively infrequent. Presumptive diagnosis is usually based on a positive cytotoxin assay result in the symptomatic patient. Patients who respond to discontinuation of the inciting drug or drugs should not be treated indiscriminately with antimicrobials. Asymptomatic carriers should not be treated, and a period of watchful waiting may be advisable in mild cases. When treatment is necessary, oral metronidazole is the agent of choice in all but the most severe cases. Whether oral metronidazole is therapeutically equivalent to oral vancomycin in severe CDIC is controversial. Regardless of the antimicrobial used, some patients suffer a recurrence of CDIC and a few have several relapses. There have been no comparative studies of treatment for relapsing CDIC. Of the investigational treatments, the tiacumicin macrolides and the yeast Saccharomyces boulardii appear most promising. Diagnostic assays based on the polymerase chain reaction should allow more timely intervention. Health care professionals who improve their understanding of CDIC will be better able to recognize the disorder, select the best treatment, and perhaps reduce the frequency of CDIC in hospitalized patients by working to alter patterns of antimicrobial use.

Anti-Bacterial Agents↗
PubMed1987

Inhibition of herpes simplex virus DNA replication by ara-tubercidin.

Preliminary studies of the biochemical basis for the antiviral activity of the pyrrolo[2,3-d]pyrimidine nucleoside ara-tubercidin were conducted. Herpes simplex virus DNA synthesis was 3-fold more sensitive to inhibition by ara-tubercidin than was cellular DNA synthesis. Partially purified herpes DNA polymerases were more sensitive to inhibition by ara-tubercidin 5'-triphosphate than were cellular polymerases alpha and beta. Inhibition of viral DNA polymerase was competitive with dATP and noncompetitive with dTTP. The results suggest that the viral DNA polymerase plays a significant role in the antiviral activity of ara-tubercidin.

Antiviral Agents↗
PubMed1986

A systematic approach to identifying and reducing medication-related problems in family practice patients.

Because of the existence of multiple medical diseases and the concurrent use of multiple medications, many elderly patients present a therapeutically complex picture to clinicians. This pilot study evaluates a systematic approach to identifying and reducing medication-related problems in a population averaging five chronic medical problems and taking an average of eleven medications. The approach is unique in its use of an in-depth home medication history and a comprehensive review of therapy. In spite of close medical supervision, an average of ten potentially medication-related problems were identified among seventeen therapeutically complex patients. Recommendations to eliminate these problems were developed by pharmacists who reviewed the patient information. These recommendations were presented to the patient's physician who accepted 67% of the suggestions.

Aged↗
PubMed1984

DNA polymerase in nuclei isolated from herpes simplex virus type-2-infected cells. Characterization of the reaction product and inhibition by substrate analogs.

Nuclei isolated from herpes simplex virus (HSV) type 2-infected KB cells were examined for their capacity to serve as an in situ source of herpes DNA polymerase. In contrast to purified enzymes with added template, approx. 80% of the DNA synthesized in isolated nuclei was viral. The average size of DNA fragments labeled in vitro was 3.2 X 10(6) Da. Based on an increase in DNA density when nuclei were incubated in the presence of BrdUTP rather than dTTP, 16% of the nucleotides were added during the in vitro reaction. Sucrose gradient analysis of DNA polymerase activity in extracts of isolated nuclei demonstrated the nearly exclusive presence of herpes DNA polymerase. Km concentrations for the four dNTPs were from 0.14 to 0.55 microM. DNA synthesis was inhibited competitively by the 5'-triphosphates of ara-A and ara-C (Ki = 0.03 and 0.22 microM, respectively) but not by the 5'-triphosphate of dideoxythymidine. aATP also served as a substrate (Km = 0.014 microM) for the reaction. We conclude that nuclei from HSV-infected cells have significant advantages for the detailed study of inhibitors of herpesvirus replication.

Cell Nucleus↗
PubMed1983

An evaluation of certain chain-extended analogues of 9-beta-D-arabinofuranosyladenine for antiviral and cardiovascular activity.

Several nucleosides modified and chain extended at the 5'-position have been synthesized as follows: N6-benzamido- 9-(2,3-di-O-benzoyl-beta-D-arabino-pentodialdo-1,4-furanosyl)adenine, O=CHR, a leads to (E)-EtOCOCH=CHR (2) b leads to EtOCOCH2CH2R (3) c leads to H2NCOCH2CH2R (6) d leads to 1-(adenin-9- yl)-1,5,6-trideoxy-beta-D-arabino-hepto-1,4-furanuronamide (8); 3 e leads to ethyl 1-(adenin-9-yl)-1,5,6-trideoxy-beta-D-arabino-hepto-1, 4-furanuronate (5) f leads to 1-(adenin-9-yl)-1, 5,6-trideoxy-beta-D-arabino-hepto-1,4-furanuronic acid (4); 5 g leads to 9-(5,6-dideoxy-beta-D-arabino-hepto-1,4-furanosyl)adenine (7) [where a = EtOCOCH=PPh3; b = H2, Pd/C; c = Me2A1NH2; d = NH3/MeOH; e = NaOEt/EtOH; f = NaOH/MeOH; g = LiA1H4]. Both 7 and 8 show activity against herpes simplex virus type 1. The mechanism for such activity is unknown. Compounds 5 and 8 exhibited weak coronary vasodilation effects in dogs.

Adenosine Deaminase↗
PubMedDate not supplied

Apparent hemolysis in an AIDS patient receiving trimethoprim/sulfamethoxazole: case report and literature review.

OBJECTIVE: To describe a case of acute hemolysis associated temporally with administration of trimethoprim/sulfamethoxazole (TMP/SMX) in a patient with AIDS, review the available literature on TMP/SMX-induced hemolytic anemia, and discuss possible drug- and disease-related factors that may have contributed to the episode of hemolysis. CASE SUMMARY: A precipitous decrease in red blood cell count, hemoglobin, and hematocrit occurred shortly after a black woman with AIDS received a single intravenous dose of TMP/SMX for Pneumocystis carinii pneumonia. Following drug discontinuation and repeated transfusions, the patient's hematologic indices returned to baseline. LITERATURE SOURCES: References were obtained using MEDLINE searches, the bibliographies of articles identified during the searches, review articles, and standard textbooks. DATA SYNTHESIS: Of the two different mechanisms of TMP/SMX-induced hemolytic anemia, the reaction is most likely to occur via dose-related oxidative disruption of the erythrocyte membrane in subpopulations deficient in glucose-6-phosphate dehydrogenase (G6PD) activity. In the US, G6PD deficiency most frequently is encountered among blacks. The potential for hemolysis may be further increased in G6PD-deficient AIDS patients, who also appear to lack adequate intracellular glutathione, which is essential for protecting the erythrocyte membrane from oxidative damage. Although an assay for G6PD activity was not conducted, the case circumstances were consistent with TMP/SMX-induced hemolysis in a G6PD-deficient patient. CONCLUSIONS: Black patients with AIDS who are receiving relatively high (greater than or equal to 50 mg/kg/d) dosages of TMP/SMX should be monitored closely for signs and symptoms of hemolytic anemia.

AIDS-Related Opportunistic Infections↗