Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight patients with giant cell arteritis (6 with Horton's disease and 2 with polymyalgia rheumatica) were investigated for abnormalities in glycoregulation, previously reported in Horton's disease, using oral glucose tolerance tests with measurement of insulinaemia and C-peptide response to glucagon to evaluate pancreatic function. The results were compared with those obtained in an age and weight matched population of patients with inflammatory syndromes of other origins. All patients with giant cell arteritis had abnormal glucose tolerance tests, with diabetes mellitus in 6 and impaired glucose tolerance in 2. Insulinaemias at all stages of the test, insulin response areas and basal C-peptide values were elevated; C-peptide response to glucagon was normal. Similar results were observed in patients with other inflammatory syndromes. It is concluded that glycoregulation disorders are not incidental in giant cell arteritis, that the normal pancreatic function seems to exclude immune pancreatic vasculitis, and that the abnormal glycoregulation is probably due to insulin-resistance. Since these abnormalities cannot be explained by the patients' advanced age alone, the part played by the inflammatory syndrome, which was common to both groups, is discussed. Its responsibility for inducing insulin-resistance may account for the fact that corticosteroids, which are rapidly effective against giant cell arteritis, normalise oral glucose tolerance tests.
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PMID:[Glycoregulation disorders in giant-cell arteritis]. 316 17

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)
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PMID:[Barraquer and Simons lipodystrophy. Complement anomalies and cutaneous leukocytoclasic vasculitis]. 343 45

Using chlorotetracycline (CTC) as a probe we studied calcium homeostasis of platelets in various disorders. Studied were healthy subjects and patients with disorders where platelets play an important role. These included thromboses, hypertension, diabetes mellitus, vasculitis, immune thrombocytopenia, thrombotic thrombocytopenic purpura, myelofibrosis, hemolytic anemias and uremia. Significant elevation of calcium levels were observed in all of these disorders except uremia. Nifedipine reduced or normalized the increased levels in most patients and its discontinuation resulted in a return of the abnormality. We propose that platelets in thromboses and related disorders are exposed to subcritical concentrations of activating factors, leading to enhanced calcium influx and elevated free cytoplasmic calcium followed by elevated resting dense tubular calcium. Nifedipine appears to protect platelets from these stimuli and coupled with their known action on vessel walls, calcium channel blockers show promise as antiatherogenic as well as antithrombotic agents.
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PMID:Increased platelet calcium in thrombosis and related disorders and its correction by nifedipine. 356 79

A type of mastopathy is unique to insulin-dependent diabetic patients. The characteristic change is a connective tissue overgrowth with vasculitis and some proliferation of duct epithelium. It is not the type of change typically associated with an increased risk of breast cancer. Clinically this change is indistinguishable by physical or radiographic findings from breast malignancy. Eleven biopsies showing these characteristics were performed on insulin-dependent patients who had diabetes mellitus from childhood. Every patient had some major complication of diabetes mellitus, usually diabetic retinopathy. In every instance the mastopathy continued to manifest itself as a part of the healing process. The probability is that this is an evidence in the breast of collagen cross-linking changes seen in patients with diabetes mellitus. This observation should help in the supervision of patients with a clinical background compatible with this study.
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PMID:Mastopathy in insulin-dependent diabetics. 357 1

Serum amyloid P-component (SAP) is a normal plasma protein and is a constituent of normal human glomerular basement membrane. Immunofluorescence with anti-SAP antibody produced characteristic linear staining along the glomerular basement membrane in normal kidney. Distinctive abnormal staining patterns were seen in renal biopsy specimens from patients with diabetes, membranous glomerulonephritis, mesangiocapillary nephritis, systemic vasculitis, Goodpasture's syndrome.
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PMID:Amyloid P-component in human glomerular basement membrane. Abnormal patterns of immunofluorescent staining in glomerular disease. 615 7

Six patients had a syndrome of painful lumbosacral plexopathy and elevated erythrocyte sedimentation rate. Sural nerve biopsy in each case showed axonal degeneration and epineurial arterioles surrounded by mononuclear inflammatory cells. Differential fascicular involvement suggested an ischemic cause in three nerves, but no patient had a necrotizing vasculitis. None of the six patients had vasculitis or cancer. Three of the six were diabetic and were initially thought to have diabetic plexopathy, but deterioration continued despite control of the diabetes. These six patients appeared to have an ischemic neuropathy with an immunological basis. Five were treated with immunosuppressant drugs, and in four the plexopathy improved or was arrested. The pathogenesis is unclear, but postmortem findings in one case suggest that the syndrome does not stem from an underlying vasculitis.
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PMID:Painful lumbosacral plexopathy with elevated erythrocyte sedimentation rate: a treatable inflammatory syndrome. 632 73

Fifteen patients with symptomatic cryoglobulinaemia were subjected to apheretic treatment when acute renal insufficiency, glomerulonephritis, severe generalized vasculitis and polyneuropathy unresponsive to conventional therapy or complications due to steroids, such as vertebral collapse, peptic ulcer and steroid diabetes, had appeared. Treatment was performed by discontinuous flow centrifugation or cascade filtration: when discontinuous flow centrifugation was employed, a mixture of saline, gelatin and fresh frozen plasma was used for replacement. Cytotoxic drugs were administered to patients with lymphoma (4 patients) or chronic active hepatitis (5 patients) and also to patients suffering from essential mixed cryoglobulinaemia. Exchanges were organized into courses of 3 to 5 sessions over 5 to 10 days and employed as a supportive measure. No patient underwent long-term treatment. A complete resolution of kidney damage, skin involvement and neurologic signs was observed when treatment was started early in the course of the disease, whereas unequivocal but moderate improvement was obtained in the case of long-lasting symptoms such as polyneuropathy. Relapses were seen in most patients when cytotoxic drugs had been discontinued abruptly. In 8 patients the solubility of cryoglobulins was studied by a recently developed turbidimetric assay. Following treatment the solubility increased; when solubility decreased, 2 patients of this group had a relapse. On the basis of these preliminary observations it appears that the possibility of predicting relapsing disease or the need of continuing therapy can eventually be achieved.
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PMID:Plasmapheresis and cytotoxic drugs for mixed cryoglobulinemia. 653 39

Many diseases in children are associated with thrombotic tendencies either as a complication or as part of the pathophysiologic process. Disorders in which platelet consumption and/or activation occur include myeloproliferative syndromes, sickle cell disease, cardiac prostheses, arteriovenous shunts, vasculitis, diabetes mellitus, and hemolytic-uremic syndrome and other renal diseases. Platelet involvement can be demonstrated by several indicators, including an increase in platelet release product levels in the plasma (beta-thromboglobulin, platelet factor 4, and thromboxane B2). The agents that have the greatest success in thrombotic disorders where platelet involvement is prominent include the prostaglandin pathway cyclo-oxygenase inhibitors aspirin and sulfinpyrazone, as well as dipyridamole. Although indications and dosages for the use of antiplatelet agents in children can be suggested, the treatment of each patient should be individualized in light of current knowledge.
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PMID:Use of antiplatelet agents in pediatric hypercoagulable states. 670 78

The second case in the medical literature of hypersensitivity vasculitis induced by glybenclamide is reported, and for the first time vasculitic lesions are demonstrated in the histopathological study of liver tissue. The case was a male patient admitted because of a febrile illness and generalized malaise of long duration. He had diabetes mellitus that was being treated with glybenclamide. Physical examination disclosed fever, poor general condition, hepatomegaly, and red nodes in the finger-tips of both hands. Abnormal laboratory parameters included normochromic normocytic anemia, leukocytosis with a high eosinophil count, and markedly elevated erythrocyte sedimentation rate. There was as well slight cytolysis and marked elevation of cholestatic serum enzymes without hyperbilirubinemia. Biopsy of the skin lesions demonstrated anular granulomata, a common lesion in diabetics. The histopathological study of the liver revealed a vasculitic hypersensitivity reaction with conspicuous granulomata located in the vicinity of blood vessels and in the wall of portal arterioles, the endothelium of the latter being disrupted at different levels. Glybenclamide withdrawal resulted in a clinical, biological and histopathological cure of the disease. Unlike the previously reported case, the patient remains alive, and this may partly have been due to early institution of corticosteroid therapy.
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PMID:[Hypersensitivity vasculitis and granulomatous hepatitis induced by glybenclamide: a case report (author's transl)]. 677 55

We studied 20 patients with Vogt-Koyanagi-Harada syndrome. They represented 3.7% of referred patients with uveitis. American Indian ancestry appears to be the link to Oriental racial type. Five patients had a forme fruste retinal detachment. After extensive treatment with corticosteroids, detachments flattened within an average of two to three months. Anterior inflammation continued to persist chronically. Seven of our patients had retinal vasculitis. Pregnancy had a beneficial effect on disease activity. Those patients with diabetes mellitus and sickle cell hemoglobin did not have an adverse effect. Visual outcome was good; of 20 patients, 16 had visual ascuity of 6/21 (20/70) in at least one eye.
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PMID:Vogt-Koyanagi-Harada syndrome. 719 Mar 60


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