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S Sollberg

Publications and source records attributed to S Sollberg.

45 records · Page 3Linked to original sources
PubMed1990

HLA-antigen frequencies in patients with progressive systemic sclerosis and morphea.

A possible HLA disease association was investigated in 40 patients (38 female, 2 male) with progressive systemic sclerosis (PSS) and 42 patients (32 female, 10 male) with morphea. The HLA A, B, C, DR phenotypes of patients were compared with 193 healthy controls. The following relative risk (RR) values were determined in PSS: A1 (1.38), A2 (1.39), B8 (1.67), B15 (3.22), DRw8 (6.30) and in morphea patients: A3 (1.43), B7 (1.39), B40 (1.81), Bw60 (2.49), DR2 (2.38) and DRw8 (2.55), indication a relatively weak, HLA-linked genetic predisposition for the manifestation of the disease. The HLA "risk" antigens for the two clinically different subtypes of the disease are also different: raised A1/B8 frequencies, like in our PSS group, correlate with a high, pathological immune response (autoimmune disorders). In contrast, A3/B7/DR2 prevalence, like in our morphea group, correlates with a low immune response. HLA typing may contribute to clinical differential diagnosis and possibly also prognosis.

Adult↗
PubMed1989

Association of HLA antigens with progressive systemic sclerosis and morphea.

The HLA phenotype frequencies of 40 patients with progressive systemic sclerosis (PSS) and 42 patients with morphea (sclerodermia circumscripta) indicate a weak, HLA-linked genetic predisposition of the affected individuals (70 female, 12 male). An "opposite" HLA A1, B8 (high immune response) vs A3, B7, DR2 (low immune response) constellation in PSS and morphea supports the clinical subdivision of scleroderma into these different nosological entities, and may serve as a differential diagnostic tool and prognostic marker.

Female↗
PubMed1989

[Scleroderma and HLA antigens].

A possible HLA disease association was investigated in 40 patients (38 female, 2 male) with progressive systemic scleroderma (PSS), and 42 patients (32 female, 10 male) with morphea. HLA ABCDR/DQ, glyoxalase and properdin factor B (GLO and BF) phenotypes of patients were compared with 193 healthy controls. Four PSS family studies were performed. The following relative risk (rR) values were determined in PSS: A1 (1.38), A2 (1.39), B8 (1.67), B15 (3.22) and in morphea: A3 (1.43), B7 (1.39), B40 (1.81), BW60 (2.49), DR2 (2.38) and DRW8 (2.55), indicating a relatively weak, HLA-linked genetic predisposition for the manifestation of these dermatological disorders. The HLA "risk" antigens for the two clinically different subtypes of the disease are also different: raised A1/B8 frequencies such as those in our PSS group are related to high (or pathologic) immune response (autoimmune disorders). In contrast, A3 B7 DR2 elevations such as those recorded in our morphea group correlate with low immune response. Following exposition to certain suspected environmental factors (quartz, chemical solvents, drugs, viral fragments), the HLA phenotype may thus predipose some individuals--predominantly women--to different clinical patterns of the disease. HLA typing may thus be useful in clinical differential diagnosis (recent subtyping protocols) and possibly also for determination of the prognosis, i.e. HLA-B8 seems to be related to an acute, inflammatory course of PSS, and HLA-B7/DR2, to rather mild morphea patterns.

Adult↗
PubMed1987

[Classification of progressive systemic scleroderma].

A new classification of forms of progressive systemic scleroderma (PSS) is presented. Compared with previous classifications, it includes not only frequent, typical forms of PSS, but also rarer manifestations. For the first time, it considers pathogenetic factors, such as the phenomena which have become known concerning the immunological system, and distinguishes between noninflammatory and inflammatory subtypes. Etiological (in this case, immunogenetic) criteria are also considered. This classification is open to further differentiation and development.

Antibodies, Antinuclear↗
PubMed1987

[Urticaria pigmentosa--an obligate systemic disease? Results of nuclear medicine studies and etiopathogenetic significance].

The objective of the present investigation was to establish the frequency of systemic spreading of urticaria pigmentosa by means of bone and bone marrow scintigraphy as a noninvasive imaging technique with a low radiation exposure. Bone scintigraphy: Seven of nine patients investigated showed diffuse and focal nuclide accumulation. After exclusion of other causes by reference to the case history and the clinical and chemical laboratory findings, these nuclide accumulations were regarded as mastocytosis-specific in accordance with the atypical localization. Bone-marrow scintigraphy: All the patient investigated showed a peripheral expansion of the bone marrow. This must be interpreted as an expansion of the macrophages of the bone marrow on the basis of the method used. Since the mast cell is regarded as a more highly differentiated form of the same cell-type as macrophages/monocytes, on the basis of the scintigraphic results presented, urticaria pigmentosa can be regarded pathogenetically as a hyperplasia of the macrophages of the bone marrow organ, with increased differentiation in mast cells. The extent of this differentiation and its pathological quality then determine the clinical signs and symptoms (cutaneous, systemic, or malignant mastocytosis). Urticaria pigmentosa thus has the character of a systemic disease.

Adult↗
PubMed1986

[Kyrle's disease in diabetes mellitus and chronic terminal kidney failure].

The diagnosis of Kyrle's disease is based on both clinical and histological findings. The penetration of the keratin plug into the dermis is no pathognomonic feature but the result of pathologic events. Kyrle's disease may be caused and promoted by association with other diseases going along with hyperkeratosis and causing damage to tissue proteins by non-enzymatic glycosylation (e. g., diabetes mellitus and renal failure).

Adult↗