Cases reported "Diabetes Mellitus"

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1/12. Isolation of a virus from the pancreas of a child with diabetic ketoacidosis.

    A healthy 10-year-old boy was admitted to the hospital in diabetic ketoacidosis within three days of onset of symptoms of a flu-like illness. He died seven days later and post-mortem examination showed lymphocytic infiltration of the islets of langerhans and necrosis of beta cells. Inoculation of mouse, monkey and human cell cultures with homogenates from the patient's pancreas led to isolation of a virus. Serologic studies revealed a rise in the titer of neutralizing antibody to this virus from less than 4 on the second hospital day to 32 on the day of death. Neutralization data showed that the virus was related to a diabetogenic variant derived from Coxsackievirus B4. Inoculation of mice with the human isolate produced hyperglycemia, inflammatory cells in the islets of langerhans and beta-cell necrosis. Staining of mouse pancreatic sections with fluorescein-labeled antiviral antibody revealed viral antigens in beta cells. Both the clinical picture and animal studies suggested that the patient's diabetes was virus induced.
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2/12. Repair of the corneal epithelial adhesion structures following keratectomy wounds in diabetic rabbits.

    In corneal tissue from a diabetic patient 15 months after delayed epithelial healing following vitrectomy surgery, electron microscopy revealed a discontinuous basement membrane; immunohistochemically, fibronectin was present in the basement membrane zone. To determine whether alterations in repair of the basement membrane, anchoring fibrils and hemidesmosomes occur in wounds in diabetics, we studied the pattern of histochemical localization of bullous pemphigoid antigen (the intracellular hemidesmosome plaque component), laminin and type VII collagen (the anchoring fibril collagen) in alloxan-induced diabetic rabbits following superficial keratectomy. Ultrastructural studies of basal laminae and hemidesmosomes also were performed. Epithelial wound closure was complete by 66-72 h after 7-mm superficial keratectomies. Type VII collagen localized at the base of the epithelium at the wound periphery by 66 h, appearing as a beaded line underlying the epithelium; at 1 week, as in control rabbits, the localization zone extended across the wound bed. Polyclonal antibodies to laminin and bullous pemphigoid antigen showed similar localization. Small segments of basal laminae were noted by electron microscopy of the wound periphery as early as 66 h post-keratectomy. By 2 weeks, an increase in hemidesmonsomes associated with segments of discontinuous basal lamina was apparent. No obvious differences in the time or pattern of re-appearance of the adhesion complex in keratectomy wounds could be discerned between normoglycemic and hyperglycemic rabbits. Thus, healing defects in diabetics may be due to factors other than reassembly of adhesion structures.
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3/12. Fatal yersinia enterocolitica septicemia complicated by unique hemosiderosis. A case report.

    A fatal case of yersinia enterocolitica septicemia which was complicated by unique hemosiderosis is reported. On admission, the patient had diabetes and showed unusual hyperferritinemia. Postmortem examination revealed that the liver was studied with abscesses, and Yersinia antigen was expressed in foamy macrophages within these abscesses. Moreover, the cadaver showed generalized hemosiderin deposition, which was mainly observed in the liver and, to lesser degrees, in the pancreas, spleen, lymph nodes, brain, thyroid and kidneys. Since there was no apparent cause of the hyperferritinemia and generalized hemosiderosis, consideration was given to possible primary hemochromatosis. However, no liver or pancreatic fibrosis was demonstrated. kupffer cells were also loaded with hemosiderin, and therefore it was considered that these cells had lost their ability to phagocytize the microorganism adequately, leading to major liver involvement. Interestingly, hemosiderin deposits in the kidneys were mostly present in glomerular epithelial cells. To our knowledge, this unique presentation has not been previously described in humans.
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4/12. A new type of transient diabetes mellitus of infancy?

    Two male siblings with transient diabetes mellitus were of normal birth weight, were asymptomatic, and did not require treatment with insulin. This may be a previously undescribed disorder or part of the range of transient diabetes mellitus of infancy. Previously reported infants with transient diabetes mellitus of infancy have usually been small for gestational age and have presented with glycosuric dehydration, infections, or growth failure. Insulin concentrations after oral glucose challenge showed inadequate insulin secretion with respect to the degree of hyperglycaemia in these children. Autosomal dominant inheritance may occur in some families with this disorder, and parents of some affected children may also have had asymptomatic or unrecognised transient diabetes mellitus of infancy. Leucocyte histocompatibility antigen typing of this family did not show any association of specific antigens with transient diabetes mellitus of infancy in the affected children.
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5/12. A syndrome of immunoglobulin a deficiency, diabetes mellitus, malabsorption, a common HLA haplotype. Immunologic and genetic studies of forty-three family members.

    Three persons in a kindred of 43 had variable expression of a syndrome consisting of immunoglobulin a deficiency, diabetes mellitus, malabsorption, and a common HLA haplotype. Findings from the proband included life-threatening malabsorption; idiopathic intestinal mucosal atrophy with infalmmation; iga deficiency and antibodies to multiple endocrine organs; insulin-dependent diabetes mellitus; and the major histocomptability antigens HLA-A2, B8, and DW3. In addition to the described syndrome other conditions present in the family include Graves' disease, vitiligo, hypocomplementemia, rheumatic fever, multiple sclerosis, and a high frequency of antibodies to endocrine tissue. Since Graves' disease, diabetes mellitus, and idiopathic Addison's disease have all been described in association with HLS-B8 and DW3, we believe that the occurrence of these diseases in this family suggests that a single immune response gene or gene complex is linked with HLA-B8 and DW3.
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6/12. Coexistence of a circulating IgG-albumin complex and a gamma heavy chain in the same patient.

    A patient with an IgG-albumin complex and a gamma heavy chain in his serum was studied by crossed immunoelectrophoresis. The IgG-albumin complex was not dissociated after incubation with 2-mercaptoethanol but it was after incubation with sodium dodecyl sulfate. Evidence was obtained that the IgG and albumin were held together by noncovalent bonds, possibly due to an antigen-antibody reaction.
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7/12. insulin resistance: definition and treatment.

    Two cases of insulin resistance are described, and recent developments in the pathogenesis and treatment of insulin resistance are reviewed. Both immune and nonimmune types of insulin resistance have been described. Immune resistance is related to the presence of circulating antibodies directed against exogenous insulin or the insulin receptor sites. Nonimmune resistance is associated with obesity, ketoacidosis, infection, or endocrinopathies. Treatment of insulin-resistant diabetics can include proper diet and weight control; use of insulin in large quantities; selection of less antigenic forms of insulin, such as pork, fish, or sulfated insulin; oral hypoglycemics such as tolbutamide; and immunosuppressive therapy with corticosteroids. The production of human insulin by recombinant dna technology promises benefits to patients with high levels of antibodies directed against insulin from animal sources. True insulin resistance is a rare phenomenon, which must be documented adequately before vigorous treatment is considered.
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8/12. diagnosis of self-induced hyperinsulinism in an insulin-dependent diabetic patient by radioimmunoassay of free c-peptide.

    On the basis of results of simultaneous determinations of plasma free insulin and free c-peptide, episodes of hypoglycemia in an insulin-dependent diabetic were attributed to surreptitious self-administration of insulin. Immunoreactive c-peptide values were falsely increased and diagnostically misleading when measured in unextracted plasma. After preliminary removal of antigen/antibody complexes from the plasma by extraction with polyethylene glycol, the c-peptide values, referred to as "free c-peptide," were suppressed. We suggest that insulin antibodies formed complexes with proinsulin-like material in the plasma of this patient, which accounted for most of the c-peptide immunoreactivity in her unextracted plasma. These complexes must be removed if c-peptide measurements are to be accurate.
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9/12. Immune competence and diabetes mellitus: pyogenic human hand infections.

    An unexpectedly high incidence of diabetes mellitus was found in 12 patients with pyogenic hand infections. Three patients had overt diabetes, four had latent diabetes, and only five were normal when tested after resolution of the acute inflamatory state. Cellular immunity, assessed in five patients by intradermal injections of common antigens and the topical application of the neoantigen, dinitrochlorobenzene, appeared to be grossly normal in all patients. If changes in immunity were present, it is likely that the skin tests were not sensitive enough to detect these alterations.
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10/12. Histologic observations of pleomorphic corynebacterium-like microorganisms in diabetic scleredema adultorum.

    Diabetic scleredema adultorum is a rare connective tissue disorder characterized by scleroderma-like changes, usually affecting the skin of the neck, shoulders, and upper back in diabetics. Presented herein are two cases in which pleomorphic, but predominantly coccoid forms, were observed in acid-fast, Giemsa, and Gram-stained tissue, sections of the affected skin. culture of the skin was positive for a microaerophilic, corynebacterium-like organism in one case and an anaerobic propionibacterium (corynebacterium) sp in the other case. The morphologic appearance of the bacterial isolates greatly resembled the morphologic forms observed in the tissue sections, suggesting that bacteria, possibly in a cell-wall-deficient phase, may play a role in the pathogenesis of this disorder. Findings of similar bacteria in previously reported cases of other connective tissue disorders such as sclerodermiformis, and rheumatoid arthritis, might support our idea that bacteria could supply the antigenic stimulus for the production of scleredema.
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