Cases reported "Diabetes Mellitus, Type 2"

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1/7. metformin retention independent of renal failure in intestinal occlusion.

    metformin is eliminated by the kidneys, and metformin accumulation has always been noticed in oligo-anuric patients. We have reported an exception to the rule with the case of a metformin-treated patient having metformin accumulation contrasting with a mild increase in serum creatinine in the context of a volvulus of the sigmoid colon. This case prompted us to examine the association between intestinal occlusion and plasma metformin concentrations. For this purpose, we developed an experimental animal model of mechanical obstruction of the intestine. rats were pre-treated during 3 weeks via drinking solution at a dose of approximately 100 mg/kg/day of metformin. They underwent at day 0 either sham-operation (n=7) or operation (n=8) to place a plastic tube around the ileum near the ileocaecal valve. metformin administration was pursued on days 1, 2, and 3 giving a single dose of 100 mg/kg by intragastric gavage. Four days after the surgery, i.e. 24 h after the last metformin administration, the surviving intestinal obstructed rats (n=8) developed overt intestinal dilation but no biochemical abnormality compared to sham-operated animals (n=7; arterial lactate concentrations respectively 4.87 /- 0.63 mmol/l and 3.97 /- 0.30 mmol/l, NS, and serum creatinine concentrations 69.0 /- 1.7 micromol/l and 68.7 /- 1.9 micromol/l, NS). By contrast, there was a striking difference with regard to metformin concentrations, decreasing from 2.95 /- 0.94 mg/l at day 0 to 0.12 /- 0.03 mg/l at day 4 (p<0.001) in the sham-operated group but remaining unchanged (1.65 /- 0.76 mg/l and 1.61 /- 0.51 mg/l) in the operation group. In conclusion, this is the first experiment showing that intestinal occlusion may be responsible for metformin retention in the absence of renal failure. Whether this observation may be relevant to other drugs remains to be established.
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2/7. onychomycosis in a diabetic patient due to trichophyton gallinae.

    A 67-year-old female suffering from diabetes mellitus type I revealed brownish-yellow discolouration, subungual hyperkeratosis, and onychodystrophy of several finger nails. Upon culturing of nail specimens, trichophyton gallinae could be repeatedly identified on Sabouraud glucose agar. To our knowledge, this is the first report of a human infection caused by this species in germany. T. gallinae is a zoophilic dermatophyte that primarily infects higher animals, but can also be transmitted to humans sporadically. Herein, clinical, diagnostic, and epidemiological aspects of this zoophilic dermatophyte are briefly reviewed.
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3/7. Resistance and allergy to recombinant human insulin.

    Insulin allergy and antibody-mediated resistance may complicate therapy with animal insulins. We describe a 53-year-old man manifesting both resistance and persistent systemic allergy despite treatment with recombinant human insulin. insulin resistance and symptoms of allergy appeared in this patient several months after initiating therapy with mixed beef-pork insulin, as is often the case. Symptoms initially improved, but persisted, and then worsened again, despite continuous human insulin therapy. Total insulin-binding capacity by Scatchard analysis, high plasma insulin-binding capacity, and specific anti-insulin antibody levels were consistent with an immunologic form of insulin resistance. Glucocorticoid therapy was required both to reduce allergic findings and to restore glycemic control. Although recently available human insulins may be less immunogenic than animal forms, immune responses to exogenous human insulin still may pose significant clinical problems.
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4/7. A case of newly diagnosed non-insulin-dependent diabetes associated with immediate-type allergy against human insulin.

    A case of newly diagnosed non-insulin-dependent diabetes mellitus with immediate-type allergy against semisynthetic human insulin is reported. She experienced immediate-type allergy 2 months after initial insulin treatment. A skin test showed that she had allergy against the insulin itself but not the additives. The amino acid sequence of the semisynthetic human insulin was identical to that of endogenous native insulin and, moreover, the patient had not been treated with animal-derived insulin previously, so a structural change to the semisynthetic formulation at the injected subcutaneous site might have antigenicity. An H1 histamine blocker markedly diminished the skin reaction to insulin, and her plasma glucose and glycosylated hemoglobin AIc became well controlled. In summary, we experienced a diabetic patient with human insulin allergy at the time of initial insulin treatment, emphasizing that the possibility of human insulin allergy should be considered whenever a patient is started on insulin therapy.
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5/7. Enzymatic, metabolic and secretory patterns in human islets of type 2 (non-insulin-dependent) diabetic patients.

    Islets were isolated by automatic digestion from non-diabetic cadaveric organ donors and from Type 2 (non-insulin-dependent) diabetic subjects. The activity of FAD-glycerophosphate dehydrogenase, but not that of either glutamate dehydrogenase, glutamate-oxalacetate transaminase or glutamate-pyruvate transaminase, was lower in Type 2 diabetic patients than control subjects. hexokinase, glucokinase and glutamate decarboxylase activities were also measured in islets from control subjects. The utilization of D-[5-3H]glucose, oxidation of D-[6-14C]glucose and release of insulin evoked by D-glucose were all lower in Type 2 diabetic patients than control subjects. The secretory response to the combination of L-leucine and L-glutamine appeared less severely affected. Islets from Type 2 diabetic patients may thus display enzymatic, metabolic and secretory anomalies similar to those often observed in animal models of Type 2 diabetes, including a deficiency of beta-cell FAD-linked glycerophosphate dehydrogenase, the key enzyme of the glycerol phosphate shuttle.
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6/7. Dangerous hyperglycemia associated with electroconvulsive therapy.

    The literature on the effect of electroconvulsive therapy (ECT) on diabetes mellitus remains controversial, with evidence of both amelioration and worsening of hyperglycemia. Both clinical reports and animal models suggest that a critical factor in glucose homeostasis may be whether or not the diabetes is insulin dependent. We present a case in which ECT was associated with extreme hyperglycemia in a patient without known preexisting diabetes. The patient subsequently required treatment with an oral hypoglycemic agent, and eventually needed insulin. The possibility of an unmasking or exacerbation of diabetic pathology during a course of ECT must be considered. Various mechanisms by which ECT may influence hyperglycemia are discussed.
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7/7. A case of a non-insulin dependent diabetic patient with regular spontaneous hypoglycemic attacks, which were due to insulin-binding antibodies induced by human insulin therapy.

    A 74-year-old diabetic patient had been treated with oral hypoglycemic agents from the age of 40 years until the age of 72, when his treatment regimen was changed to human insulin. He began experiencing hypoglycemic attacks 14 months after the initiation of insulin therapy. He continued to experience hyperglycemia every morning and hypoglycemia every day at 5:30 p.m. even after insulin therapy was withdrawn. His plasma levels of c-peptide immunoreactivity, total and free immunoreactive insulins were 4.2 ng/ ml, 740 microU/ml and 141.8 microU/ml, respectively. His 125I-insulin binding rate was 94.4%. These findings suggest that his hypoglycemic attacks may have been due to insulin antibodies. Analysis revealed that insulin binding antibodies belonged to IgG with kappa light chains. The patient's genotype was HLA-DR4. He had not received animal insulin or any medications containing a sulfhydryl group. Although the IgG antibody was produced against injected human insulin, his HLA type and the characteristics of his antibodies resembled those of a patient with insulin autoimmune syndrome (IAS). We hypothesize that this patient represented a rare instance of a patient constitutionally similar to a patient with IAS, but whose hypoglycemic attacks resulted from the antibodies induced by the administration of human insulin. This case seems to be the first one with hypoglycemic attacks due to anti-human insulin antibody produced by human insulin therapy.
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