Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040425 (tonsillitis)
 1,594 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 33-year-old man (Case 1) developed scaling and erythema on the extensor side of his extremities, head, and back, 3 years before his first visit to our hospital. The lesions spread out to form several plaques and became persistent (Fig. 1a). Serum antistreptolysin O (ASO) was within the normal range and a pharyngeal culture showed normal flora. Histologic findings were compatible with psoriasis vulgaris (Fig. 1b). Topical steroid therapy was effective; however, scaling and erythema persisted. The 8-year-old daughter (Case 2) of Case 1 had suffered severe tonsillitis 2 months prior to the skin eruptions. Numerous rain drop-like scaly papules appeared on her legs and generalized rapidly (Fig. 2a). Her tonsils were swollen and reddish. Streptococcus pyogenes was detected by pharyngeal smear. The ASO value was at a high level. Histologic examination showed slightly elongated rete ridges, focal lack of the granular layer, parakeratosis, mild spongiosis, and exostosis of neutrophils (Fig. 2b). She was diagnosed with acute guttate psoriasis. Administration of oral antimicrobials reduced the ASO value and led to remission of the disease. After 1 month of antimicrobial treatment, the erythematous papules disappeared. The human leukocyte antigen (HLA) typing of the father was HLA-A24, A31, B7, B39, and Cw7, and that of the daughter was HLA-A24, A31, B39, and Cw7. Both possessed HLA-A24, B39, and Cw7. The HLA typing of other family members was also studied. The mother had HLA-A11, A24, B39, B62, Cw4, and Cw7, and her son had HLA-A11, A24, B7, B62, Cw4, and Cw7. The result of HLA typing is shown in Table 1. Lymphocyte stimulating test was performed using heat-killed S. pyogenes which were boiled at 70 degrees C for 10 min and sonicated. The stimulation index was twofold higher in the daughter than in the father (Fig. 3).
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PMID:Psoriasis vulgaris and acute guttate psoriasis in a family. 1145 89

Palmoplantar pustulosis (PPP) is a chronic inflammatory disorder characterized by sterile pustules predominantly involving the palms and soles of middle-aged women. In contrast, regions other than the palms and soles are occasionally affected, manifesting scaly erythemas which resemble psoriasis, and solitary pustules are also seen. Some of these extra-palmoplantar lesions are induced by the Koebner phenomenon or occur after focal infections like tonsillitis. The tenderness and inflammation of the extra-palmoplantar lesions in PPP are milder than in psoriasis. Histological features show mild acanthosis of the epidermis with parakeratosis and mild infiltration of inflammatory cells in the upper dermis. On the other hand, severe pustular lesions are occasionally seen in the palms and soles of the patients with pustular psoriasis. These findings suggest a close relationship between PPP and psoriasis; however, different genetic, environmental, and immunological factors are likely to be involved. Recently, understanding of psoriasis pathophysiology has greatly progressed, and the concept of psoriasis pathogenesis is currently viewed as complicated responses between infiltrating leucocytes and the resident skin, via a number of inflammatory cytokines, chemokines, and mediators produced in the skin under regulation of cellular immune systems. By contrast, the pathogenesis of PPP has been poorly investigated. This paper reviews findings of the clinicopathophysiology of PPP, making a focus on the extra-palmoplantar lesions.
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PMID:Extra-palmoplantar lesions associated with palmoplantar pustulosis. 1945 7