Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Localized scleroderma-like skin lesions which developed in two children, from 8 to 10 months after successful bone marrow transplantation for aplastic anaemia, showed histopathological features resembling those of scleroderma. This finding, like the animal models described in the literature, provides additional support for the auto-immune nature of scleroderma.
Br J Dermatol 1977 Apr
PMID:Localized scleroderma-like lesions after bone marrow transplantation in man. A chronic graft versus host reaction. 1 37

The distinctive cutaneous changes that occur in both the acute and chronic forms of the graft-vs-host reaction (GVHR) are described in two living patients in whom the GVHR developed after bone marrow transplantation for aplastic anemia. In the skin, the mild form of the acute GVHR is recognized as a subtle macular erythema, and the severe form appears as erythematous papules and violaceous macules with scale. Skin biopsy specimens in both of the acute forms show vacuolar alterations of the epidermal basal-cell layer with a perivenular infiltrate of lymphocytes. The chronic GVHR evolves from generalized scaling to diffuse areas of aclerotic and atrophic skin with a curious reticulated hyperpigmentation, ulcerations, and alopecia. Histopathologic study shows collagenization of the dermis that can be correlated with the clinical sclerodermoid changes. Owing to its visibility, the skin offers a unique opportunity for the early recognition of the GVHR.
Arch Dermatol 1977 Aug
PMID:Graft-versus-host reaction. Cutaneous manifestations following bone marrow transplantation. 1 97

Three epithelial neoplastic lesions, perineal Bowenoid papulosis, uterine cervical carcinoma, and bladder transitional cell carcinoma, which occurred in a mildly immunosuppressed patient who had aplastic anemia were studied for human papillomavirus (HPV) infection. In the Bowenoid papulosis, HPV type 16 DNA was identified by polymerase chain reaction (PCR) and by in situ hybridization (ISH). In contrast, in the uterine cervical carcinoma, HPV 16 was not detected, although possibly another unidentified type of HPV in the lesion was suggested by the ISH findings. In the bladder transitional cell carcinoma, neither papillomavirus genus-specific (PGS) antigen nor HPV DNA was found.
J Dermatol 1992 Jun
PMID:Triple cancers in the urogenital area of a patient with aplastic anemia. 140 90

A case of lichenoid drug eruption due to nandrolone furylpropionate (Demelon) is reported. A 71-year-old man with aplastic anemia developed widespread erythema and reticulation with violaceous papules and pigmentation after receiving intramuscular injections of Demelon weekly for 2 months. The eruption gradually resolved after drug withdrawal, leaving reticular pigmentation. A biopsy specimen of the skin lesion showed lichenoid-type reactions including hydropic or colloid degeneration of the basal cells, sometimes with satellite necrosis, and a band-like subepidermal lymphocytic infiltrate. Most of the mononuclear cells stained strongly for helper/inducer T lymphocytes (Leu 3a).
J Dermatol 1989 Aug
PMID:Lichenoid drug eruptions due to nandrolone furylpropionate (Demelon). 253 22

The graft-versus-host reaction (GVHR) in both mice and humans can lead to the development of a broad spectrum of clinical and pathological symptoms. These symptoms are strikingly similar to those of a number of diseases of proven or presumed immunological origin, such as systemic lupus erythematosus (SLE), other collagen vascular diseases, lymphoproliferative disease, and aplastic anemia. The purpose of our investigation was to describe the immunological and pathological events that take place in the course of graft-versus-host disease (GVHD) and to gain insight into the cellular mechanisms underlying these events. To this end, a model was employed in which nonirradiated F1 mice were used as recipients of parental lymphoid cells. By pathological manifestations, 2 basic forms of GVHD can be distinguished in such non-irradiated F1 recipients: One is acute GVHD which is often lethal. It is characterized by a variety of suppressive (hypoplastic) pathological symptoms, including a severe hypoplasia of the lymphohemopoietic system accompanied by aplastic anemia and hypogammaglobulinemia. The other basic form is characterized by stimulatory symptoms, such as persistent lymphoid hyperplasia, formation of autoantibodies, and development of pathological symptoms reminiscent of SLE and other collagen vascular diseases. The suppressive pathological graft-versus-host (GVH) symptoms are caused by T suppressor/killer (TS/K) cells of the donor which react towards allogeneic class-I-structures of the F1 recipient's major histocompatibility complex (MHC). The stimulatory pathological GVH symptoms, by contrast, are caused by donor T helper (TH) cells which react toward the recipient's allogeneic class-II-MHC structures. The possible implications of these observations for the pathogenesis of a number of GVH-like diseases in humans are discussed. The hypothesis is advanced that some of these GVH-like conditions, which arise either e causa ignota or after exposure to certain viruses or drugs, are caused by T lymphocytes reacting against self-MHC structures on lymphohemopoietic cells that were rendered "foreign". By analogy to GVHD, it is conceivable that the development of either stimulatory or suppressive GVH-like symptoms in individuals exposed to a given virus or sensitizing drug depends not on the etiologic agent per se, but on whether the predominant response is made by the individual's TH or TS@K cells. This, in turn, might depend on whether the agent becomes immunogenic in combination with class-II or class-I alloantigens.
J Invest Dermatol 1985 Jul
PMID:Pathogenesis of graft-versus-host reactions (GVHR) and GVH-like diseases. 315 4

Increasing numbers of persons are undergoing bone marrow transplantation for severe aplastic anemia and hematologic malignant neoplasms, and the proportion of those surviving has increased. Graft-v-host disease (GVHD) will, therefore, be seen with increasing frequency in the future. Graft-v-host disease occurs when immunocompetent donor lymphoid cells recognize and attack antigens of the immunocompromised host. We describe the clinical and histologic appearance of the different types of GVHD and discuss treatment, pathogenesis, and prevention of this entity.
Arch Dermatol 1983 Aug
PMID:Graft-v-host disease. 634 89

The cutaneous changes of the acute form of graft-vs-host reaction are described in two patients who underwent bone marrow transplantation for treatment of severe aplastic anaemia. One patient went on to develop a chronic reaction of the lichenoid type. Histopathology confirmed the presence of 'satellite cell necrosis' from the acute stage of the disease onwards. Direct immunofluorescence showed deposits of immunoglobulin (IgG, IgM), fibrinogen and complement on the necrotic keratinocytes, whilst the basement membrane was positive for C3. These findings suggest that humoral immunity as well as cellular immunity may play a part in the production of the rash.
Br J Dermatol 1980 Apr
PMID:Acute and chronic graft-vs-host reaction in skin: report of two cases. 699 38

A retrospective study of 26 quinacrine-treated lupus erythematosus patients failed to show evidence of drug-induced ocular changes. Although quinacrine commonly produces minor side effects, such as yellow discoloration of the skin, and may rarely produce very serious side effects, such as aplastic anemia, it appears to produce much less oculotoxicity than does chloroquine.
Int J Dermatol
PMID:Antimalarial therapy for lupus erythematosus: an apparent advantage of quinacrine. 720 69

A 12-year-old boy had striking reticulate hyperpigmentation of the neck and upper chest, dystrophic nails, patchy alopecia, and a white streak on the buccal mucosa. He was diagnosed as having chronic graft-versus-host disease (GVHD) based on clinical findings, skin biopsy findings, and his history of a bone marrow transplantation for aplastic anemia eight years earlier. Dyskeratosis congenita (DC) was not a diagnostic consideration, although the clinical findings and history of aplastic anemia made it a compelling possibility. This case highlights the clinical similarities between DC and chronic GVHD and the difficulty in arriving at an unequivocal diagnosis.
Pediatr Dermatol 1993 Dec
PMID:Dyskeratosis congenita or chronic graft-versus-host disease? A diagnostic dilemma in a child eight years after bone marrow transplantation for aplastic anemia. 830 41

The clinical and histopathological findings in a 25-year-old Japanese male patient who suffered from chronic graft-versus-host-disease (GVHD) with follicular involvement are described. The patient had been diagnosed as aplastic anemia and underwent an allogeneic bone marrow transplant (BMT). In the eighth month thereafter, pruritic follicular red papules developed over his trunk and extremities. A biopsy specimen revealed histological exocytosis of lymphocytes into the hair follicles and basal-cell vacuolization of the follicular epithelium. Analysis of T-lymphocyte subpopulations in the dermis revealed a predominance of CD4 positive cells. To our knowledge, several cases of acute follicular GVHD have been reported; however, the occurrence of chronic GVHD with follicular involvement (chronic follicular GVHD) has not been clearly documented.
J Dermatol 1993 Apr
PMID:Chronic graft-versus-host disease with follicular involvement. 831 15


1 2 Next >>