Confirmatory Findings Research Articles

Failure to Diagnose Acute Myocardial Infarction

To the Editor.— The article written by Zarling and associates entitled Failure to Diagnose Acute Myocardial Infarction discussed the specialty of the responsible physician with respect to missing the diagnosis. They state that among the non-internal medicine specialists, the diagnostic accuracy in class I was 0%. The definition of class I was typical retrosternal chest pain with confirmatory enzymatic and/or ECG findings. When inspecting Table 3 included in the referenced article, we noted that there were no patients in class I for this group; therefore, the calculation of 0/0=0% is misleading. Another interpretation is that there was 100% accuracy in this group and, while no myocardial infarctions with typical presentations were missed by non-internal medicine physicians, the internists missed three of 27, or 11%.

Oxychlordane, HCS-3260, and nonachlor in birds: lethal residues and loss rates.

Oxychlordane reached lethal levels in birds given dietary dosages of HCS-3260 (70.75% cis-chlordane and 23.51% trans-chlordane) at 6 levels from 50 to 500 ppm. Oxychlordane ranged from 9.4 to 22.1 ppm in brains of cowbirds (Molothrus ater), grackles (Quiscalus quiscula), and red-winged blackbirds (Agelaius phoeniceus) that died on dosage and from 1.3 to 4.8 ppm in sacrificed birds, providing a clear diagnostic separation. Among starlings (Sturnus vulgaris), however, oxychlordane ranged from 5.0 to 19.1 ppm in brains of birds that died, significantly lower than in the other species, and from 1.4 to 10.5 ppm in sacrificed birds, overlapping the levels in those that died. Lethal levels, therefore, begin near 5.0 ppm, as in a previous study in which oxychlordane itself was fed, but the data from starlings emphasizes the need for confirmatory necropsy findings in diagnosis of poisoning. Nonachlor had a very low order of toxicity, killing only 1 of 12 birds dosed at 100 ppm for 35 d; 3 others died and 1 was incapacitated during a short period of food deprivation. Lethal levels of oxychlordane were present in the brains of birds that died. Oxychlordane accumulated in the bodies of birds on dietary dosage of HCS-3260 in proportion to dosage and time, but did not approach equilibrium at the levels (10, 50, and 100 ppm) that were fed. Loss rates of oxychlordane from HCS-3260, oxychlordane, or technical chlordane dosages (the last in a previous study) did not differ significantly from each other; respective half-lives were 57, 63, and 74 d. Residues of cis-chlordane in birds fed HCS-3260 were consistently lower than oxychlordane during the accumulation period and declined abruptly when dosage ceased; individual variation was high.

Role of exonuclease III in the base excision repair of uracil-containing DNA.

Mutants of Escherichia coli K-12 deficient in both exonuclease III (the product of the xth gene) and deoxyuridine triphosphatase (the dut gene product) are inviable at high temperatures and undergo filamentation when grown at such temperatures. In dut mutants, the dUTP pool is known to be greatly enhanced, resulting in an increased substitution of uracil for thymine in DNA during replication. The subsequent removal of uracil from the DNA by uracil-DNA glycosylase produces apyrimidinic sites, at which exonuclease III is known to have an endonucleolytic activity. The lethality of dut xth mutants, therefore, indicates that exonuclease III is important for this base-excision pathway and suggests that unrepaired apyrimidinic sites are lethal. Two confirmatory findings were as follows. (i) dut xth mutants were viable if they also had a mutation in the uracil-DNA glycosylase (ung) gene; such mutants should not remove uracil from DNA and should not, therefore, generate apyrimidinic sites. (ii) In the majority of the temperature-resistant revertants isolated, viability had been restored by a mutation in the dCTP deaminase (dcd) gene; such mutations should decrease dUTP production and hence uracil misincorporation. The results indicate that, in dut mutants, exonuclease III is essential for the repair of uracil-containing DNA and of apyrimidinic sites.

Renal tubular acidosis: practical guides to diagnosis and treatment.

The syndrome of renal tubular acidosis in some one of its various forms should be suspected when an infant or child has failure to thrive, metabolic acidosis, constipation, diarrhea, vomiting, anorexia, polyuria, or dehydration in infancy. Confirmatory biochemical findings include an inappropriately high urinary pH, inadequate acid excretion and/or abnormal tubular reabsorption of filtered bicarbonate. Growth can be normal when there is sustained correction of the metabolic acidosis through appropriate alkaline therapy.

Early prenatal diagnosis of Hurler's syndrome with termination of pregnancy and confirmatory findings on the fetus.

Type I mucopolysaccharidosis was diagnosed in a fetus by assay of the glycosaminoglycans of the amniotic liquor. Results are presented of biochemical and ultrastructural studies on the 18-week abortus. The evidence suggests that the liver is more severely affected than the central nervous system at this stage of gestation, and this finding agrees with the recent demonstration of the underlying enzyme defect of this disorder, with the corollary that many biochemical abnormalities previously noted in gargoylism must be pleiotropic effects of the mutant genotype.

Double outlet right ventricle: Diagnosis during life

A case of “double outlet” right ventricle is presented in which both great vessels originated from the right ventricle, a small ventricular septal defect serving as the only outlet from the left ventricle. The clinical picture was almost indistinguishable from that of a large ventricular septal defect associated with pulmonary hypertension. The correct diagnosis was suggested during left heart catheterization and confirmed by selective cineangiocardiography of the left ventricle. Death followed the latter procedure. Confirmatory necropsy findings in the heart are described.

Number 4

This patient has had edematous, red, symmetrical areas of the cheeks and chin for several weeks. She feels tired and feverish and has vague aches and pains. Pyrexia, plus a positive L.E. test, elevated sedimentation rate, albuminuria, and white blood cell count of 4,100, confirm the presence of acute, life-threatening, systemic lupus erythematosus. Slowly spreading lesions have been present for several years. There is scaling, redness, telangectasia, and atrophic scarring. With a magnifying glass, dilated follicles containing a horny plug are seen. The patient feels well. After finding that the blood count, urinalysis, serum proteins, L.E. test preparation, and serologic test for syphilis were normal, and having confirmatory histopathologic findings, a diagnosis of discoid lupus erythematosus was made. These pink papules, becoming confluent, caused only mild itching. A few scattered early vesicles could be seen with a magnifier. The process appeared in the spring of the year and the mother

A study of certain factors in the etiology of thrombophlebitis in the lower extremities following surgery

I T is generahv agreed that muItipIe factors participate -in the etiology of thromboembohsm foIlowing surgery. The apparently inconstant presence of such factors may be due, in part, to the Iack of use of known criteria for the diagnosis of periphera1 venous thrombosis.’ In a previous study it was demonstrated that shock and hypotension were present before, during or after surgery in a statisticaIIy significant number of patients who Iater died from puImonary emboIism.2 It was suggested that shock and hypotension might be etiologic factors in thromboembolic disease.2 The present study is concerned with an anaIysis of the possible etiologic roIe of shock and hypotension in postoperative thrombophlebitis. In view of the difficulties often encountered in estabIishing the presence or absence of periphera1 venous thrombosis the present study was Iimited to thrombosis of the veins of the lower extremities, which is reIativeIy easiIy diagnosed by clinica features such as pain, tenderness and sweIIing. It was thus necessary to escIude many patients with suspected but not clinically verifiabIe venous thrombosis occurring in the prostatic veins, the pelvic veins and other areas. Also excIuded were patients stated to have thrombophIebitis of one or both Iower extremities but on whose case records confirmatory cIinica1 findings had not been noted.

A case of erythroblastosis fetalis caused by isoimmunization with the agglutinogen B

A case of erythroblastosis fetalis caused by isoimmunization of an Rhpositive, type O mother by a type B baby is reported with confirmatory blood serologic findings. It is suggested that when an erythroblastotic infant is seen, whose mother is type O and her Rh factor is unknown, the baby be transfused with type O, Rh-negative blood. This would obviate the possibility of giving the infant blood to which he has circulating isoagglutinins. A case of erythroblastosis fetalis caused by isoimmunization of an Rhpositive, type O mother by a type B baby is reported with confirmatory blood serologic findings. It is suggested that when an erythroblastotic infant is seen, whose mother is type O and her Rh factor is unknown, the baby be transfused with type O, Rh-negative blood. This would obviate the possibility of giving the infant blood to which he has circulating isoagglutinins.