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Dr. Peter  Densen  Md image

Dr. Peter Densen Md

200 Hawkins Dr
Iowa City IA 52242
319 359-9825
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 23668
NPI: 1518949825
Taxonomy Codes:
207R00000X 207RI0200X

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Publications

A 9-year-old boy with chronic urticaria and progressive spondyloarthritis. - Allergy and asthma proceedings : the official journal of regional and state allergy societies
A 9-year-old African American boy presented with chronic urticaria and progressive spondyloarthritis. Laboratory tests were abnormal for persistently positive antinuclear antibodies and undetectable total hemolytic complement (CH50) despite normal levels of complement C2, C3, and C4. Ultimately, further testing revealed an underlying deficiency in the immune system that may be associated with autoimmune disease and thus have a bearing on the patient's urticaria and spondyloarthritis. This is a unique presentation of a rare disease and underscores the importance of evaluating for systemic disease in the workup of chronic urticaria.
Autoantibody stabilization of the classical pathway C3 convertase leading to C3 deficiency and Neisserial sepsis: C4 nephritic factor revisited. - Clinical immunology (Orlando, Fla.)
C3 deficiency is a rare disorder that leads to recurrent pyogenic infections. Here we describe a previously healthy 18 y/o Caucasian male with severe meningococcal disease. Total hemolytic activity was zero secondary to an undetectable C3. The C3 gene was normal by sequencing. Mixing the patient's serum with normal human serum led to C3 consumption. An IgG autoantibody in the patient's serum was identified that stabilized the classical pathway C3 and C5 convertases, thus preventing decay of these enzyme complexes. This autoantibody is an example of a C4 nephritic factor, with an additional feature of stabilizing the C5 convertase. Previous patients with C4 nephritic factor had membranoproliferative glomerulonephritis. Two years after presentation, this patient's C3 remains undetectable with no evidence of renal disease. We revisit the role of autoantibodies to classical pathway convertases in disease, review the literature on C4-NeF and comment on its detection in the clinical laboratory.Copyright © 2012 Elsevier Inc. All rights reserved.
The complement system in pediatric systemic lupus erythematosus, atypical hemolytic uremic syndrome, and complocentric membranoglomerulopathies. - Current opinion in rheumatology
This review summarizes the recent advances in complement biology and the evolving understanding of these contributions to the pathophysiology and treatment of predominantly pediatric disease syndromes.Identification of lupus patients with complete deficiencies of one of the plasma complement proteins enabled the field to move beyond the notion of complement as a laboratory curiosity. Clinical investigation of the manifestations observed in deficient patients has further defined the biology of the system in normal individuals. Definition of the assembly of the C3 convertases, particularly that of the alternative pathway and its regulation, has led to the appreciation that the complement system includes membrane inhibitors that are every bit as important as those in plasma. The exploration of disease states in which significant complement deposition occurs has moved the field away from consideration of this finding as a bystander effect. Dissection of these syndromes has led to the unanticipated finding of a central role for function-altering mutations in the complement proteins that form or regulate the alternative pathway C3 convertase and has opened the door to new therapeutic approaches. The disease states discussed in the review - pediatric systemic lupus erythematosus, atypical hemolytic uremic syndrome, and the complocentric membranoglomerulopathies - illustrate this evolutionary history of complement biology.This review emphasizes that both the lack of classical pathway complement activation and excessive activation of the alternative pathway contribute to distinct disease pathogenesis, and emphasizes the critical importance of homeostatic regulation, in both plasma and in tissues, of the system as a whole.
Challenges and opportunities facing medical education. - Transactions of the American Clinical and Climatological Association
Medical education is at a crossroads. Although unique features exist at the undergraduate, graduate, and continuing education levels, shared aspects of all three levels are especially revealing, and form the basis for informed decision-making about the future of medical education.This paper describes some of the internal and external challenges confronting undergraduate medical education. Key internal challenges include the focus on disease to the relative exclusion of behavior, inpatient versus outpatient education, and implications of a faculty whose research is highly focused at the molecular or submolecular level. External factors include the exponential growth in knowledge, associated technologic ("disruptive") innovations, and societal changes. Addressing these challenges requires decisive institutional leadership with an eye to 2020 and beyond--the period in which current matriculants will begin their careers. This paper presents a spiral-model format for a curriculum of medical education, based on disease mechanisms, that addresses many of these challenges and incorporates sound educational principles.
Immunoglobulin deficiencies and susceptibility to infection among homozygotes and heterozygotes for C2 deficiency. - Journal of clinical immunology
About 25% of C2-deficient homozygotes have increased susceptibility to severe bacterial infections. C2-deficient homozygotes had significantly lower serum levels of IgG2, IgG4, IgD, and Factor B, significantly higher levels of IgA and IgG3 and levels of IgG1 and IgM similar to controls. Type 1 (28 bp deletion in C2 exon 6 on the [HLA-B18, S042, DR2] haplotype or its fragments) and type II (non-type I) C2-deficient patients with increased susceptibility to bacterial infection had significantly lower mean levels of IgG4 (p < 0.04) and IgA (p < 0.01) than those without infections (who had a higher than normal mean IgA level) but similar mean levels of other immunoglobulins and Factor B. Of 13 C2-deficient homozygotes with infections, 85% had IgG4 deficiency, compared with 64% of 25 without infections. IgD deficiency was equally extraordinarily common among infection-prone (50%) and noninfection-prone (70%) homozygous type I C2-deficient patients. IgD deficiency was also common (35%) among 31 type I C2-deficient heterozygotes (with normal or type II haplotypes), but was not found in 5 type II C2-deficient heterozygotes or 1 homozygote. Thus, C2 deficiency itself is associated with many abnormalities in serum immunoglobulin levels, some of which, such as in IgG4 and IgA, may contribute to increased susceptibility to infection. In contrast, IgD deficiency appears not to contribute to increased infections and appears to be a dominant trait determined by a gene or genes on the extended major histocompatibility complex (MHC) haplotype [HLA-B 18, S042, DR2] (but probably not on type II C2-deficient haplotypes) similar to those previously identified on [HLA-B8, SC01, DR3] and [HLA-B18, F1C30, DR3].

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200 Hawkins Dr Iowa City, IA 52242
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