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S T Shulman

Publications and source records attributed to S T Shulman.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Angiogenesis in fatal acute Kawasaki disease coronary artery and myocardium.

Angiogenesis has been shown to be dysregulated in coronary artery (CA) aneurysms in the chronic phase of Kawasaki disease (KD). Neovascularization may occur in inflammatory-related vascular diseases because many angiogenesis mediators are secreted by inflammatory cells. We hypothesized that inflammation of the acute KD CA aneurysm could lead to dysregulation of angiogenesis mediators and subsequent neovascularization. To investigate this hypothesis, acute fatal KD cardiac tissues were immunostained for angiogenic inducers and inhibitors. Microvessel density was determined and the degree of inflammation assessed. Marked inflammation and angiogenesis were found in acute KD CA aneurysms and myocardium, with the highest microvessel density seen in patients who died 2-3 weeks after onset of the disease. Expression of proangiogenic proteins was higher than expression of inhibitors in KD CA aneurysms and myocardium. Angiogenesis mediators were localized to inflammatory cells in the myointima, adventitia, and myocardium. We conclude that significant neovascularization occurs in acute KD CA aneurysms and myocardium much sooner after onset of the disease than has been previously reported, that multiple angiogenesis factors are involved, and that dysregulation of angiogenesis likely contributes to KD vasculopathy.

Acute Disease↗
PubMedDate not supplied

Circulating cardiac troponin I levels in Kawasaki disease.

In addition to the vascular findings of Kawasaki disease (KD), clinical, electrocardiographic, and/or echocardiographic signs of myocarditis are recognizable in the acute phase of KD in many patients. The mechanism of myocarditis and an association with the development of subsequent coronary artery abnormalities in KD is unknown. Previous studies of serum cardiac troponin I (cTnI) measurements in pediatric populations have suggested a possible utility of measurements in diagnosis and follow-up of KD. We designed a retrospective study to evaluate cTnI measurements during acute KD and to assess the predictive value of cTnI measurements in acute KD for the subsequent development of coronary artery abnormalities. Twenty-nine children were studied. Group 1 consisted of 15 KD patients who developed coronary artery abnormalities as detected by transthoracic echocardiographic evaluation. Group 2 consisted of 14 KD patients with persistently normal coronary artery findings on echocardiograms. A control group consisted of 11 children, none of whom were known to have had clinical findings of KD or myocarditis. The mean cTnI values for all three groups were lower than the values suggestive of cardiac damage: group 1 = 0.11 +/- 0.16 ng/ml, group 2 = 0.15 +/- 0.34 ng/ml, and control = 0.04 +/- 0.08 ng/ml. The current study demonstrates that there is no significant elevation of cTnI in KD patients. Additionally, there is no correlation between cTnI measurements and the finding of myocarditis, as reflected by decreased cardiac function, or the subsequent development of coronary artery abnormalities.

Acute Disease↗
PubMedDate not supplied

Kawasaki syndrome.

Kawasaki syndrome is an acute self-limited illness of young children that may result in significant cardiovascular sequelae in 20% of patients. The etiology is unknown, but clinical and epidemiologic features strongly suggest an infectious etiology. The incidence of coronary artery abnormalities has been dramatically reduced by administration of intravenous gamma-globulin in the acute phase of illness. This paper reviews the clinical, laboratory, etiologic, epidemiologic, cardiovascular, pathologic, and therapeutic aspects of Kawasaki syndrome. Discovery of the etiology of this disorder will enable more specific diagnostic tests and therapies to be developed.

Child, Preschool↗
PubMedDate not supplied

Group C beta-hemolytic streptococcal infections in children: nine pediatric cases and review.

Streptococci of Lancefield group C colonize healthy individuals but infrequently cause invasive disease. Eight pediatric cases of infection due to group C streptococci were identified in a retrospective survey of a recent 6-year period at a children's hospital. An additional case of group C meningitis diagnosed in 1975 was included. These nine cases and 22 pediatric cases from the literature are presented to illustrate important points with respect to clinical presentations and complications and to show that these organisms can cause serious, sometimes fatal infection: pneumonitis, sinusitis, septicemia, endocarditis, osteomyelitis, and meningitis. Group C streptococci are described in terms of their biochemical properties, the infections they cause in animals, and their tendency to produce disease in humans. With increasingly frequent serologic grouping of non-group A beta-hemolytic streptococci, recognition of the role of specific non-group A streptococci is likely to increase. The antimicrobial agent of choice for infections due to group C streptococci is penicillin G. The minimum inhibitory and minimum bactericidal concentrations for the organism should be determined since penicillin tolerance may occur and may be responsible for the slow response to penicillin therapy in some cases.

Adolescent↗
PubMedDate not supplied

A nosocomial common source outbreak caused by Pseudomonas pickettii.

Pseudomonas pickettii, a Gram-negative bacillus which has been recovered rarely from clinical specimens, was isolated from the respiratory tracts of 9 of 29 (31%) pediatric intensive care unit patients. The reservoir of the organism was intrinsically contaminated single dose vials of tracheal irrigant solution. Four additional hospitals in three other states have notified the Centers for Disease Control of respiratory colonization with aerobic nonfermentative Gram-negative organisms and have associated this colonization with the use of the same tracheal irrigant solution. Because of the potential for intrinsic contamination, single dose vials must be added to the list of potentially hazardous environmental agents.

Adolescent↗
PubMedDate not supplied

Once daily ceftriaxone for central nervous system infections and other serious pediatric infections.

Ceftriaxone has a very long serum half-life and enhanced in vitro activity against common pediatric pathogens. Therefore we evaluated the efficacy and safety of once daily ceftriaxone therapy in 57 children with serious infections including: meningitis (26 patients); ventriculitis (3); pyelonephritis (7); osteomyelitis (6); abscess (4); septic arthritis (3); sepsis (2); and miscellaneous infections (6). The most common isolates were Haemophilus influenzae (23), Escherichia coli (9) and Staphylococcus aureus (8). Ceftriaxone was given intravenously or intramuscularly in a dose of 50 mg/kg for non-central nervous system (CNS) infections. Patients with CNS infections received an initial dose of 100 mg/kg followed by 80 mg/kg 12 hours later and once daily thereafter. In a limited number of patients no major differences in serum ceftriaxone concentrations were found after intravenous or intramuscular injection. Of 57 patients with pathogens isolated 55 were completely cured; in one patient with Klebsiella pneumoniae ventriculitis, intraventricular gentamicin was briefly added to the regimen. Another patient with an anaerobic liver abscess recovered after metronidazole was administered. In three patients a delayed response to ceftriaxone was noted. One patient with previous recurrent infections had a second episode of H. influenzae meningitis 22 days after cessation of therapy. Clinical side effects were noted in 10 of 71 patients (including 14 treated patients who had negative cultures). Seven patients had diarrhea, one each had fever or rash and one had fever, rash and arthralgia. Laboratory side effects in 16 of 71 patients included eosinophilia (7), thrombocytosis (7), elevated liver enzymes (4) and leukopenia and neutropenia (2).(ABSTRACT TRUNCATED AT 250 WORDS)

Abscess↗
PubMedDate not supplied

New perspectives in the drug treatment of Kawasaki disease.

Kawasaki disease (KD) has become the leading cause of acquired heart disease in developed countries. Conventional therapy for KD includes intravenous gammaglobulin (2 g/kg as a single dose over 12 hours) and aspirin (acetylsalicylic acid; high dose until the fourteenth day of illness then low dose). Therapy administered within the first 10 days of the onset of the illness has been shown to reduce arterial wall inflammation and thereby prevent the development of coronary artery aneurysm formation. The majority of patients with KD will respond to conventional therapy. However, the management of nonresponders and patients with complications (such as acute thrombosis and chronic coronary artery changes) remains controversial. In this review article, we address some of these controversies and also describe newer treatment modalities that have been used in the management of patients with KD, both in the acute and convalescent stages of the disease.

Aspirin↗