Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old woman visited our hospital with a five month history of persistent pustulation, crusting, and alopecia on the vertex of the scalp. No pathological organisms were isolated from the lesions. Histological examination revealed non-specific changes of chronic inflammation with destroyed follicles. Antibiotic therapy produced no response, but steroid therapy was effective. From these observations, a diagnosis of erosive pustular dermatosis of the scalp (EPDS), as described by Pye et al., was made. The patient also had Hashimoto's thyroiditis, autoimmune hepatitis, and Takayasu's aortitis. The laboratory studies revealed an increased erythrocyte sedimentation rate, C-reactive protein 3+, hypergammaglobulinemia, and various auto-antibodies, suggesting the possibility of a pathogenesis common to both this dermatosis and the autoimmune diseases.
J Dermatol 1989 Oct
PMID:Pustular dermatosis of the scalp associated with autoimmune diseases. 257 30

Two patients with secondary new syphilis are described, abusing alcohol, developing early syphilitic hepatitis. The manifestations of this condition are similar to those of viral hepatitis. This necessitates a thorough examination of the skin integument, visible mucosae, genitals and perianal area, and of the peripheral lymph nodes in the patients with suspected viral hepatitis, in order to timely detect a possible liver involvement in Treponema infection. When such patients consult a doctor, specific serologic tests should be carried out and case history be carefully recorded.
Vestn Dermatol Venerol 1989
PMID:[Liver involvement in early secondary syphilis]. 260 68

Hepatitis B is now the most commonly reported hepatitis in the United States and the physician's greatest infectious occupational hazard. Although dermatologists are at increased risk for contracting and transmitting hepatitis B virus, surveys continue to indicate that a substantial number do little to decrease this risk. We have summarized the recent developments regarding the transmission, diagnosis, and clinical presentation and course of hepatitis B virus infection, and have offered specific preventive measures to assist the dermatologist in keeping hepatitis B out of his medical practice. By employing these measures, dermatologists can do their part in contributing to the future eradication of this disease.
Arch Dermatol 1989 Feb
PMID:Prevention of hepatitis B. 264 27

The finding of hepatitis B surface antigen in systemic polyarteritis nodosa is well recognized. We described a case of cutaneous polyarteritis nodosa associated with hepatitis antigenemia and a medium-sized vessel vasculitis on skin biopsy, with no evidence of systemic involvement.
J Am Acad Dermatol 1986 Nov
PMID:Cutaneous polyarteritis nodosa associated with hepatitis B surface antigen. 287 14

A 6-year-old girl with mild hepatitis was found to have an elevated urinary level of vanillylmandelic acid (VMA), but no cause for the elevation was found. The patient was receiving griseofulvin for treatment of tinea capitis, and this drug was suspected of causing a falsely elevated urinary VMA level. Four other patients receiving griseofulvin were also found to have elevated urinary VMA levels. In one patient, urinary VMA level determined by an alternate method was normal.
Arch Dermatol 1989 Feb
PMID:Falsely elevated urinary level of vanillylmandelic acid induced by griseofulvin. 291 64

Erythema multiforme is said to be rare in childhood and especially in early infancy. Three infants, none older than 1 year, were seen with this condition; all showed typical clinical features. In one of the three infants, no distinctive etiological factor(s) could be found. One was suffering from congenital hepatitis (cause unknown) and another from a staphylococcal infection.
Pediatr Dermatol 1986 Feb
PMID:Erythema multiforme in childhood and early infancy. 293 29

Human hypersensitivity angiitis is an immune complex disease in which patients present with palpable purpuric lesions of the skin and may often have multiple organ involvement. The antigen may be derived from an infectious organism such as the hepatitis virus, streptococcus, or a drug, and complexes with antibody. Under circumstances of vascular turbulence or vessel wall dilatation this complex may become fixed, activating the complement sequence with elaboration of chemotactic factors for neutrophils. These cells release lysosomal enzymes resulting in vessel wall destruction. Red blood cells leak into the tissue producing purpura and the inflammatory infiltrate accounts for the palpability. Although many patients have skin lesions only, others may have involvement of joints, gastrointestinal tract, kidneys, and even the lungs. The central question in the pathogenesis of this disease is why the immune complex is so selective in its site of deposition. Part of the reason must be related to the lattice formation of a particular complex, while other reasons are related to host factors of altered vascular permeability, integrity of clearance mechanisms or even a genetically determined defect of the phagocytic system.
J Invest Dermatol 1985 Jul
PMID:Human hypersensitivity angiitis, an immune complex disease. 315 5

The origin of leukocytoclastic vasculitis (LV) being often difficult to determine, we have undertaken since 1980 a prospective study of factors associated with LV. We selected 53 patients whose LV was clinically predominant, and excluded patients in whom LV was an expected phenomenon in a known autoimmune or infectious disease. Twenty-eight of the 53 patients presented with a typical Gougerot-Ruiter disease, 15 with a bullous or necrotic form of the disease and 10 with urticarial lesions. Detail of the prospective laboratory tests performed is given in table I. Correlations between laboratory values and LV-associated factors were significant with the decrease of complement but not with the presence of circulating immune complexes, rheumatoid factor, cryoglobulin or direct immunofluorescence test positivity. Most of the associated factors in our series were infectious agents (streptococci, hepatitis virus), immunological agents (rheumatoid factor, cryoglobulin) or drugs known to be potential LV-inductors; other factors were less common or quite recently described (enterovirus, Yersiniae, cirrhosis, primary liver cancer, Chlamydiae, refractory anemia with an excess of myeloblasts. We do not feel that a large series of laboratory tests should be performed in every case of LV. The clinical context and simple laboratory tests, such as blood cell count, complement assay, plasma electrophoresis and a search for rheumatoid factor should be enough to guide the clinician and help him decide whether further investigations are needed. However, it should be noted that in some cases without clinical pointers only full virological evaluation enabled us to determine that enteroviruses may be involved in the pathogenesis of LV.
Ann Dermatol Venereol 1988
PMID:[Prospective study of factors associated with leukocytoclastic vasculitis]. 336 10

Persistent viral infections have been postulated to be trigger factors for the development of autoimmune disease. We report the development of vitiligo in four patients with human immunodeficiency virus (HIV)-related conditions and in one patient with hepatitis who later developed both psoriasis and acquired immunodeficiency syndrome (AIDS). Other common features were hepatitis and multiple other viral infections. Ribavirin was associated with repigmentation in one patient. Vitiligo may be an example of an autoimmune disease triggered by viral infection in a genetically predisposed host.
J Am Acad Dermatol 1987 Oct
PMID:Human immunodeficiency virus-associated vitiligo: expression of autoimmunity with immunodeficiency? 366 11

A 50-year-old man suffering from cholestatic hepatitis and diabetes mellitus with hyperlipoproteinaemia had small, painful, slightly elevated, reddish, firm indurated plaques on his soles. Histologically, the lesions were composed of a centrally located cutaneous nerve surrounded by concentric layers of xanthoma cells. Electron microscopy showed the cutaneous nerves to be unmyelinated, their axons were vacuolated and contained dense bodies. The xanthoma cells had the same ultrastructural features as those observed in usual xanthomatous lesions. We suggest that this entity be named perineural xanthoma.
Br J Dermatol 1986 Dec
PMID:Perineural xanthoma. 380 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>