Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These guidelines for the treatment of patients who have sexually transmitted diseases (STDs) were developed by the Centers for Disease Control and Prevention (CDC) after consultation with a group of professionals knowledgeable in the field of STDs who met in Atlanta on September 26-28, 2000. The information in this report updates the 1998 Guidelines for Treatment of Sexually Transmitted Diseases (MMWR 1998;47 [No. RR-1]). Included in these updated guidelines are new alternative regimens for scabies, bacterial vaginosis, early syphilis, and granuloma inguinale; an expanded section on the diagnosis of genital herpes (including type-specific serologic tests); new recommendations for treatment of recurrent genital herpes among persons infected with human immunodeficiency virus (HIV); a revised approach to the management of victims of sexual assault; expanded regimens for the treatment of urethral meatal warts; and inclusion of hepatitis C as a sexually transmitted infection. In addition, these guidelines emphasize education and counseling for persons infected with human papillomavirus, clarify the diagnostic evaluation of congenital syphilis, and present information regarding the emergence of quinolone-resistant Neisseria gonorrhoeae and implications for treatment. Recommendations also are provided for vaccine-preventable STDs, including hepatitis A and hepatitis B.
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PMID:Sexually transmitted diseases treatment guidelines 2002. Centers for Disease Control and Prevention. 1218 49

Idiopathic CD4+ T lymphocytopenia is a very rare condition characterized by persistent depletion of circulating CD4+ T lymphocytes, without evidence of HIV or HTLV infection, or other identifiable causes of immunodeficiency. The syndrome can present with dermatological diseases, including viral, fungal and bacterial infections, as well as Kaposi's sarcoma, epithelial cell malignancies, lymphoma and inflammatory dermatoses. We report the case of a 47-year-old woman with idiopathic CD4+ T lymphocytopenia who presented with a 10-year history of disseminated and refractory flat warts from which human papillomavirus type 3 DNA was identified. The patient also had alopecia areata.
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PMID:Idiopathic CD4+ T lymphocytopenia associated with disseminated flat warts and alopecia areata. 1243 98

Imiquimod, an imidazoquinoline amine, is approved for the topical treatment of external anogenital warts induced by human papilloma virus. Several clinical trials have shown imiquimod to be an effective and safe drug for treatment of anogenital warts. Consequently, it was considered that imiquimod might be effective on warts caused by the same aetiological agent located on other skin areas. We describe the favourable outcome of a case of multiple facial verrucae in a human immunodeficiency virus (HIV)-infected patient treated with imiquimod 5% cream. This is a promising finding which supports those of two previous reports. We feel that imiquimod could be used in HIV-infected patients with multiple facial warts in whom conventional therapies are ineffective or produce significant side-effects.
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PMID:Successful treatment of multiple filiform facial warts with imiquimod 5% cream in a patient infected by human immunodeficiency virus. 1278 Jul 7

Human immunodeficiency virus (HIV) infects and destroys crucial components of the immune system, leaving patients susceptible to a number of viral, bacterial and fungal diseases. Viral warts are caused by human papillomavirus infection and are a common skin disease that afflicts HIV-infected patients. Treatment modalities currently rely on destruction of the infected tissue or interruption of cell division; however, frequent recurrence is a particular challenge in HIV-infected patients. We report the case of a 41-year-old HIV-positive man with multiple common warts located on his hands and feet. Following 5 months of treatment with imiquimod, an immune response modifier, as a 5% cream, complete clearance of all warts was achieved. Mild erythma, itching and burning at the application site was observed in the early stages of treatment. The patient showed no relapse of warts at the 30-month follow-up visit.
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PMID:Topical treatment of common warts in an HIV-positive patient with imiquimod 5% cream. 1461 16

The possibility of increases in both oral and anogenital pathologic conditions due to human papillomavirus (HPV) in patients infected with the human immunodeficiency virus (HIV) is of concern and is the focus of numerous current research studies. HIV-infected women are at higher risk for cervical HPV detection, for infection with high-oncogenic-risk types of HPV, for persistent HPV infection, for cervical cytologic abnormalities, and for cervical intraepithelial neoplasms. HIV-infected men are at increased risk for anal HPV infection, for anal infection with high oncogenic-risk types of HPV, for persistent anal HPV infection, and for anal intraepithelial defects. Recent studies have shown an increased risk of oral warts in HIV-infected individuals despite treatment with highly active antiretroviral therapy (HAART). Oral HPV infection rates have not declined since the initiation of HAART, and evidence suggests that the rates may have actually increased in white HIV-infected males.
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PMID:Human papillomavirus infection and disease in HIV-infected individuals. 1525 42

A 55-year-old white man with a history of hypertension, fibromyalgia, and colonic polyps presented with unrelenting plantar warts on his hands and feet for the past 4 years. He was otherwise healthy and without a history of recurrent infections. Physical examination was unremarkable except for extensive warts on his hands and feet. Pertinent laboratory findings included hypoalbuminemia, hypogammaglobulinemia, and lymphopenia most severely affecting CD4(+) T cells. Testing for HIV infection was negative. This clinical and laboratory presentation suggested a combined humoral and cellular immunodeficiency syndrome that could be best explained by loss of lymphocytes, immunoglobulins, and other serum proteins. Additional immunologic testing revealed a marked reduction in peripheral blood naive (CD4(+)CD45RA(+)) T cells. A 24-hour stool collection showed a markedly elevated alpha(1)-antitrypsin level. These findings were most consistent with the diagnosis of intestinal lymphangiectasia, a type of protein-losing enteropathy associated with hypoalbuminemia, hypogammaglobulinemia, and lymphopenia, characterized by a preferential loss of naive CD4(+) T cells into the gastrointestinal tract. This case illustrates the importance of considering intestinal loss of immunoglobulins and lymphocytes in the differential diagnosis of the adult patient who presents with laboratory evidence of a combined humoral and cellular immunodeficiency. It also underscores the diagnostic utility of the clinical immunology laboratory and how flow cytometry, in particular, can contribute to an understanding of pathogenic mechanisms.
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PMID:A 55-year-old man with hypogammaglobulinemia, lymphopenia, and unrelenting cutaneous warts. 1531 25

The WHIM syndrome is a rare immunodeficiency disorder characterized by warts, hypogammaglobulinemia, infections, and myelokathexis. Dominant heterozygous mutations of the gene encoding CXCR4, a G-protein-coupled receptor with a unique ligand, CXCL12, have been associated with this pathology. We studied patients belonging to 3 different pedigrees. Two siblings inherited a CXCR4 mutation encoding a novel C-terminally truncated receptor. Two unrelated patients were found to bear a wild-type CXCR4 open reading frame. Circulating lymphocytes and neutrophils from all patients displayed similar functional alterations of CXCR4-mediated responses featured by a marked enhancement of G-protein-dependent responses. This phenomenon relies on the refractoriness of CXCR4 to be both desensitized and internalized in response to CXCL12. Therefore, the aberrant dysfunction of the CXCR4-mediated signaling constitutes a common biologic trait of WHIM syndromes with different causative genetic anomalies. Responses to other chemokines, namely CCL4, CCL5, and CCL21, were preserved, suggesting that, in clinical forms associated with a wild-type CXCR4 open reading frame, the genetic anomaly might target an effector with some degree of selectivity for the CXCL12/CXCR4 axis. We propose that the sustained CXCR4 activity in patient cells accounts for the immune-hematologic clinical manifestations and the profusion of warts characteristic of the WHIM syndrome.
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PMID:WHIM syndromes with different genetic anomalies are accounted for by impaired CXCR4 desensitization to CXCL12. 1553 53

A 11-year-old female admitted to our hospital because of erythema of the face and the trunk, and a wide and dense cluster of verruca vulgaris on the right sole. She had no family history of immunodeficiency, no perinatal abnormality, no growth abnormality, or no history of severe infections. From the age of 4 years, she noticed erythema around her nose. At the age of 9 years, small erythema and papules appeared on her chest. In January, 2003, erythema around her nose and papules of the trunk spread rapidly, and she also felt fatigue and effort dyspnea. Laboratory examinations revealed near absence of serum IgG, and IgE, high serum IgM (525 mg/dl), and normal IgA and IgD. Thl/Th2 ratio was 36.9. We diagnosed her as having hyper-IgM syndrome. Histological examinations of a skin biopsy showed the infiltration composed of mainly histiocytes,and mildly atypical CD8 + T cells around the blood vessels in the dermis. We concluded her skin manifestations as reactive lymphohistiocytic infiltration at the base of immunodeficiency and durable stimulation of various antigens. Her skin manifestations improved transiently by the intravenous immunogrobulin and corticosteroids therapy.
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PMID:[A female case of hyper-IgM immunodeficiency syndrome with uncommon skin manifestations]. 1555 25

We have developed an immunization platform which combines heat shock proteins (Hsp) with protein antigens, such as viral or cancer targets, into a single recombinant fusion protein. Pre-clinical data demonstrate the ability of Hsp fusion proteins to induce antigen-specific cytotoxic T lymphocytes, Type 1 cytokines and anti-tumour immunity. One Hsp fusion protein, HspE7, is now in clinical development for therapy of diseases caused by human papillomavirus (HPV). HPV infection is associated with development of proliferative lesions (papillomas or warts) as well as malignant lesions (anogenital dysplasia and cancer). HspE7 has been shown in efficacy trials to be active against genital warts and anal dysplasia, and a trial is underway in another HPV indication, recurrent respiratory papillomatosis. Having observed therapeutic activity for our lead product HspE7 in humans, we are currently developing Hsp fusion proteins as therapeutic vaccines for other chronic viral infections. Potential targets include hepatitis B, herpes simplex, hepatitis C, and human immunodeficiency virus.
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PMID:CoVal fusions: a therapeutic vaccine platform using heat shock proteins to treat chronic viral infection and cancer. 1560 93

The vast majority of known primary immunodeficiencies (PIDs) are autosomal or X-linked recessive Mendelian traits. Only four classical primary immunodeficiencies are thought to be autosomal-dominant, three of which still lack a well-defined genetic etiology: isolated congenital asplenia, isolated chronic mucocutaneous candidiasis, and hyper IgE syndrome. The large deletions on chromosome 22q11.2 associated with Di George syndrome suggest that this disease may be dominant but not Mendelian, possibly involving several genes. The clinical and genetic features of six novel autosomal-dominant primary immunodeficiencies have however been described in recent years. These primary immunodeficiencies are caused by germline mutations in seven genes: ELA2, encoding a neutrophil elastase, and GFI1, encoding a regulator of ELA2 (mutations associated with severe congenital neutropenia); CXCR4, encoding a chemokine receptor (warts, hypogammaglobulinemia, infections and myelokathexis syndrome); LCRR8, encoding a key protein for B-cell development (agammaglobulinemia); IFNGR1, encoding the ligand-binding chain of the interferon-gamma receptor; STAT1, encoding the signal transducer and activator of transcription 1 downstream from interferon-gammaR1 (Mendelian susceptibility to mycobacterial diseases); and IKBA, encoding IkappaBalpha, the inhibitor alpha of NF-kappaB (anhidrotic ectodermal dysplasia with immunodeficiency). These recent data suggest that many more autosomal-dominant PIDs are likely to be identified in the near future.
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PMID:Autosomal-dominant primary immunodeficiencies. 1560 87


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