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Acanthosis nigricans is well recognized in its clinical association with several types of insulin-resistant syndromes, and skin involvement is usually unresponsive to local treatment or management of diabetes. A young woman with a lipodystrophic form of diabetes, hypertriglyceridemia, and severe generalized acanthosis nigricans was placed on a diet with fat supplementation in the form of omega-3-fatty-acid-rich fish oil. She was observed to have striking improvement in the appearance and extent of acanthosis nigricans while receiving this regimen. This occurred despite continued therapy with niacin (nicotinic acid), an agent associated with acanthosis nigricanslike skin changes.
Arch Dermatol 1988 Jul
PMID:Improved acanthosis nigricans with lipodystrophic diabetes during dietary fish oil supplementation. 338 52

We report the clinical features of 62 consecutive patients with lichen planus observed in 18 months. The largest number of cases occurred between 50 and 70 years of age. Thirty-four patients had lichen planus only. In the remainder, lichen planus was associated with chronic liver diseases (16 cases), immune-related disorders (7 cases), and diabetes (5 cases). Mucous-erosive lichen planus was significantly more frequent in cases with lichen planus and other diseases. In all patients with liver diseases the histological features always showed a severe liver involvement. No relationship was observed between lichen planus and the etiology of the liver diseases. Females were more affected by immune-related disorders than males. The above data, together with the increased levels found of IgA, auto-antibodies, and cryoglobulins, even in cases with lichen planus only, suggest that lichen planus results from an immune imbalance, often associated with systemic involvement.
Arch Dermatol Res 1988
PMID:Lichen planus, chronic liver diseases, and immunologic involvement. 340 60

In a 56-year old woman progressive partial lipodystrophy began at the age of 6 years on the face, thereafter extending slowly down to mid-thigh level (fig. 1 and 2), with moderate hypertrophy of the subjacent fatty tissue and a fatty macroglossia (fig. 3). Histological examination of the lipodystrophic skin not only showed an absence of fatty tissue, but also abnormalities at the dermis-epidermis junction with hyaline bodies (fig. 4). At the age of 23 she developed purpura, predominantly on the legs, which rapidly became chronic (fig. 5); histological examination showed leucocytoclasic vasculitis of dermal vessels (fig. 6) with granular deposits of C3 on the vessels and of IgM at the dermis-epidermis junction. Episodes of polyarthralgia and headaches were frequent. Regressive neuritis of the external popliteal nerve occurred when she was 53-year old. Renal function tests proved normal, but renal biopsy was not performed. There was no diabetes mellitus, but an oral glucose tolerance test and a somatostatin insulin glucose test elicited definite resistance to insulin. A search for a serum factor inhibiting insulin receptors was negative. Permanent abnormalities in serum were a very deep fall in C3, a pronounced fall in CH50 and a low C4 level. Besides, a C3 nephritic factor (NeF) at a high level and circulating immune complexes were present (table I); a mixed IgM-IgG cryoglobulin was found intermittently (fig. 7). Clearance of the immune complexes by splenic macrophages was extremely slow. During a series of plasma exchanges, serum C3 increased transiently, whereas serum C4 remained unchanged (fig. 8).(ABSTRACT TRUNCATED AT 250 WORDS)
Ann Dermatol Venereol 1987
PMID:[Barraquer and Simons lipodystrophy. Complement anomalies and cutaneous leukocytoclasic vasculitis]. 343 45

A 65-year-old man with insulin-dependent diabetes developed intractable pruritus preceding weight loss and increasing fatiguability. Esophagogastroduodenoscopy revealed infection with Candida, cytomegalovirus, and Cryptosporidium. His T cell helper/suppressor ratio was inverted, and the serum human immunodeficiency virus (HIV) antibody was positive. Results of an extensive evaluation for internal malignancy were negative. Despite optimal care, the patient died 12 weeks after his initial hospitalization. We believe that HIV infection should be added to the list of underlying disorders that may present with pruritus.
J Am Acad Dermatol 1987 May
PMID:Pruritus as a presenting sign of acquired immunodeficiency syndrome. 358 90

We treated two patients with dermatitis herpetiformis and Addison's disease, and one patient with celiac disease without the rash, but with Addison's disease and juvenile diabetes. In two of the patients, the concomitant diseases also included a thyroid disease. The predisposing factors to the multiple endocrine disorders in these patients with gluten-sensitive skin and/or small intestinal disease remained unknown. Two of the three patients had HLA-B8, none was known to have affected relatives, and the Addison's disease appeared before, at the same time, or after the patients contracted dermatitis herpetiformis or celiac disease.
Arch Dermatol 1987 Jul
PMID:Dermatitis herpetiformis and celiac disease associated with Addison's disease. 360 72

We observed three children with a clinically similar presentation of erythematous nodules that expanded centrifugally leaving lipoatrophy. Areas of lipoatrophy coalesced, resulting in clinical pictures similar to partial or total lipodystrophy. Histologic study revealed a lobular panniculitis with a mixed infiltrate of lymphocytes and mononuclear phagocytes. Of these three children, one had insulin-dependent diabetes mellitus and Hashimoto's thyroiditis, one developed juvenile rheumatoid arthritis, and the third developed insulin-dependent diabetes mellitus, suggesting that the pathogenic mechanism may be an expression of autoimmunity.
Arch Dermatol 1987 Dec
PMID:Lipoatrophic panniculitis: a possible autoimmune inflammatory disease of fat. Report of three cases. 368 6

Pruritus was present in one half of our cases and ran parallel to the disease, thereby suggesting a causal relationship between it and PCT. Moreover, no correlations could be established between pruritus and the patients' sex, associated treatments (oestrogens, etc.) or underlying disease (liver damage, diabetes mellitus, cancer, hypersideraemia), nor between pruritus and the form of PCT (sporadic or familial) and the levels of urinary porphyrins. Pruritus localized to sun-exposed skin areas belongs to the category of phototoxic symptoms, although a burning sensation is more often observed in such cases, but this cannot explain the generalized pruritus. Immunoglobulin and complement deposits in the vessel walls have been demonstrated in PCT. In addition, the serum of PCT patients may, when irradiated, activate the classical complement pathway, thus promoting the release of mediators. Pro-inflammatory enzymes probably play a secondary role.
Ann Dermatol Venereol 1986
PMID:[Pruritus and tardive cutaneous porphyria]. 371 63

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

Ten patients with necrobiosis lipoidica lesions were studied. Five patients had diabetes mellitus. The age of the patients varied from 15 to 73 years and the duration of the skin lesions was from 2 to 20 years. Histologically, the lesions were characterized by degeneration of collagen and elastin. In some lesions elastin fibers could be seen in areas devoid of normal-looking collagen. Electron microscopy revealed loss of cross-striation of collagen fibrils and a marked variation in the diameter of individual collagen fibrils. The concentration of collagen, measured by assay of hydroxy-proline, a collagen-specific amino acid, was markedly decreased in the lesional skin, but the ratio of type I/III collagen was unchanged in the affected skin. Fibroblasts established from affected skin synthesized less collagen than cells derived from healthy-looking skin. The decreased collagen synthesis was due to a decreased amount of messenger RNA for type I procollagen, measured by hybridization with a specific human cDNA clone. The production of collagenase by these fibroblasts was not increased. Our results thus indicate that in necrobiosis lipoidica lesions, collagen fibrils are defective and the amount of collagen is reduced, probably due to decreased synthesis of collagen by affected fibroblasts.
J Invest Dermatol 1987 Feb
PMID:Necrobiosis lipoidica: ultrastructural and biochemical demonstration of a collagen defect. 380 59

An edematous rash developed on the abdominal skin of a 76-year-old woman who had had diabetes mellitus for ten years. Some months later, the affected skin became thickened and indurated. Histopathologic examination revealed marked dermal fibrosis with excessive deposition of collagen. The patient also had IgA (k-type) paraproteinemia. Fibroblast cultures from the affected and unaffected skin were studied for collagen metabolism. Procollagen synthesis was elevated about sixfold on fibroblasts derived from the affected skin. A similar increase was detected in messenger RNA (mRNA) levels using a complementary DNA clone specific for human pro alpha 1(l) collagen mRNA. The elevated mRNA level could be the result of increased transcriptional activity of collagen genes or decreased degradation of collagen mRNAs. Our findings suggest that increased collagen deposition may account for the marked dermal fibrosis that we observed in this patient.
Arch Dermatol 1987 Feb
PMID:Scleredema and paraproteinemia. Enhanced collagen production and elevated type I procollagen messenger RNA level in fibroblasts grown from cultures from the fibrotic skin of a patient. 381 96


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