c-peptide has been researched along with Sjogren-s-Syndrome* in 2 studies
2 other study(ies) available for c-peptide and Sjogren-s-Syndrome
Article | Year |
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Peptide-containing nerves in labial salivary glands in Sjögren's syndrome.
The presence and spatial distribution of peptide-containing nerves in labial salivary glands from 10 Sjögren's syndrome patients were compared with those in salivary glands from 7 healthy controls.. Immunoperoxidase staining was used to demonstrate vasoactive intestinal peptide (VIP)-immunoreactive (IR) fibers, postganglionic sympathetic fibers containing the C-flanking peptide of neuropeptide Y (CPON), and sensory fibers containing calcitonin gene-related peptide (CGRP) and substance P.. Acini, intralobular ducts, small arteries, and postcapillary veins were richly innervated by VIP-IR fibers, whereas CPON-, CGRP-, and substance P-IR fibers were restricted to blood vessels. Peptide-containing nerves were found surrounding, but not in the middle of, the highly inflamed mononuclear cell areas.. This topologic distribution suggests involvement of VIP-IR fibers in vascular, motor, and secretory components of the reflex salivary secretion, whereas the distribution and the vasoactive actions of CPON, CGRP, and substance P suggest a role in the regulation of the salivary gland circulation, and thus of transcapillary flow. Excessive release may contribute to a neurogenic inflammation. Local depletion and absence of trophic neuropeptide stimuli may contribute to acinar atrophy. Topics: C-Peptide; Calcitonin Gene-Related Peptide; Humans; Immunoenzyme Techniques; Neuropeptide Y; Neuropeptides; Peripheral Nerves; Reference Values; Salivary Glands; Sjogren's Syndrome; Substance P; Vasoactive Intestinal Peptide | 1992 |
Successful immunosuppressive therapy in insulin resistant diabetes caused by anti-insulin receptor autoantibodies.
A 45-year-old, non-obese female patient with no previous history of insulin administration was found to have extreme insulin resistance and abnormally high plasma immunoreactive insulin in the absence of anti-insulin antibodies in the serum. Clinically, there was no ketonuria. The patient also had evidence of Sjogren's syndrome with several immunologic features including hypergammaglobulinemia, positive antinuclear antibodies, accelerated erythrocyte sedimentation rate and leukopenia. Plasma pancreatic glucagon and C-peptide were elevated, but other endocrinologic abnormalties were not present. In this patient the insulin resistance appeared to be due to anti-insulin receptor antibodies which could be detected even in 1:500 dilution of serum. Immunosuppressive therapy with prednisolone and cyclophosphamide resulted in a decreased level of serum gamma globulin and a concomitant decrease of blood glucose level. After immunosuppressive therapy for eight months, the diabetic syndrome disappeared completely and anti-receptor antibodies in the serum were no longer detectable. Furthermore, insulin sensitivity returned to normal. However, the patient's glucose tolerance deteriorated after the temporary termination of cyclophosphamide treatment and the lowering of prednisolone dosage. Topics: Autoantibodies; C-Peptide; Cyclophosphamide; Diabetes Complications; Diabetes Mellitus; Female; Glucagon; Humans; Immunosuppressive Agents; Insulin; Insulin Antibodies; Insulin Resistance; Middle Aged; Prednisolone; Receptor, Insulin; Sjogren's Syndrome | 1977 |