ABSTRACT
La vacunación contra el SARS-CoV-2 no está exenta de efectos adversos. Se presenta dos casos de afectación endocrina asociada a la vacunación por la COVID-19. Mujer de 46 años que, luego de la primera dosis, presentó fiebre persistente y signos de tirotoxicosis, tras el diagnóstico de tiroiditis subaguda asociada a vacunación por la COVID-19, el cuadro remitió con el uso de corticoides. Varón de 71 años, que luego de la vacunación por la COVID-19, presentó hipoglicemias hiperinsulinemicas, con resultado positivo de anticuerpos antiinsulina. Se le diagnosticó con una hipoglicemia autoinmune asociada a la vacunación por la COVID-19 y recibió tratamiento con prednisona, controlando los episodios de hipoglicemia. En conclusión, las enfermedades endocrinas asociadas a vacunación por la COVID-19 son extremadamente raras y su detección oportuna permite su tratamiento adecuado.
SARS-CoV-2 vaccination is not free of adverse effects. We present two cases of endocrine involvement associated with COVID-19 vaccination. A 46-year-old woman who, after receiving the first COVID-19 vaccination dose, presented persistent fever and signs of thyrotoxicosis after being diagnosed with subacute thyroiditis associated with COVID-19 vaccination; the condition remitted with the use of corticoids. A 71-year-old male, who after COVID-19 vaccination, presented hyperinsulinemic hypoglycemia, testing positive for anti-insulin antibodies; he was diagnosed with autoimmune hypoglycemia associated with COVID-19 vaccination and received treatment with prednisone, controlling the episodes of hypoglycemia. In conclusion, endocrine diseases associated with COVID-19 vaccination are extremely rare and their timely detection allows adequate treatment.
Subject(s)
Humans , Male , Female , ThyrotoxicosisABSTRACT
Objetive: To analyze the hematological changes of systemic lupus erythematosus (SLE) and the clinical characteristics of immune-related hypoglycemia, and to provide the basis for the diagnosis and treatment of SLE complicated with autoimmune hypoglycemia (AIH). Methods: The clinical data a patient with SLE complicated with AIH with pancytopenia as the first manifestation were collected and the relevant literatures were reviewed. Results: A 70-year-old man was admitted to hospital because of dizziness and fatigue, and suffered from more than 3 months, aggravated for 2 weeks. The physical examination results showed pale conjunctiva, moist rales over the both lower lung and there were no other obvious positive signs. The blood test showed pancytopenia and the fasting blood glucose 2. 34 mmol · L-1 The pathomorphology of tissue was observed by bone marrow puncture; rheumatism examinations, glucose metabolism indexes, insulin autoantibodies (IAA) and other assistant examinations were performed, and the patient received the related treatment. The patient had a history of photosensitivity. Admission examinations indicated multiple serous effusions, urinary protein >). 5 g · 24 h-1, pancytopenia, abnormal antinuclear antibody (ANA) titer, pancreatic CT (-), and the patient was diagnosed as SLE complicated AIH finally. After treatment of prednisone, the symptoms of the patient were improved; the the whole blood count and fasting blood glucose responded well to the therapy of prednisone. After discharge from the hospital, the patient was treated with prednisone continuously and was required to regularly monitor the blood test and the blood glucose level. The patient's whole blood count was gradually increased and no hypoglycemia occurred. Conclusion: SLE with hematological changes as the first manifestation is easily misdiagnosed. And autoantibody-mediated glucose homeostasis should be considered when SLE is complicated with hypoglycemia.
ABSTRACT
We describe an unusual case of systemic lupus erythematosus with pulmonary manifestations presenting as hypoglycemia due to anti-insulin receptor antibodies. A 38-year-old female suffered an episode of unconsciousness and was admitted to hospital where her blood glucose was found to be 18 mg/dL. During the hypoglycemic episode, her serum insulin level was inappropriately high (2,207.1 pmol/L; normal range, 18 to 173) and C-peptide level was elevated (1.7 nmol/L; normal range, 0.37 to 1.47). Further blood tests revealed the presence of antinuclear antibodies, anti-double-stranded DNA antibodies, and anti-Ro/SSA, anti-La/SSB, anti-ribonucleoprotein, and anti-insulin receptor antibodies. A computed tomography scan of the abdomen, aimed at tumor localization, such as an insulinoma, instead revealed ground-glass opacities in both lower lungs, and no abnormal finding in the abdomen. For a definitive diagnosis of the lung lesion, video-associated thoracoscopic surgery was performed and histopathological findings showed a pattern of fibrotic non-specific interstitial pneumonia.
Subject(s)
Adult , Female , Humans , Autoantibodies/blood , Autoimmunity , Biomarkers/blood , Blood Glucose/metabolism , Hypoglycemia/blood , Insulin/blood , Insulin Resistance , Lung Diseases, Interstitial/diagnosis , Lupus Erythematosus, Systemic/complications , Receptor, Insulin/immunology , Thoracic Surgery, Video-Assisted , Tomography, X-Ray Computed , Treatment OutcomeABSTRACT
Se informa el caso de una mujer de 42 años quien desarrolla pancreatitis autoinmune, colangitis esclerosante y probable hipoglucemia autoinmune, asociada con hiperparatiroidismo primario. (Acta Med Colomb 2012; 37: 80-82).
Abstract We report the case of a 42 year old woman who developed autoimmune pancreatitis, sclerosing cholangitis and probable autoimmune hypoglycemia associated with primary hyperparathyroidism. (Acta Med Colomb 2012; 37: 80-82).
ABSTRACT
BACKGROUND: Type B insulin resistance syndrome is a manifestation of autoantibodies to the insulin receptor that results in severe hyperglycemia and acanthosis nigricans. However, the mechanisms by which these autoantibodies induce hypoglycemia are largely unknown. In this paper, we report the case of patient with type B insulin resistance syndrome who presented with frequent severe fasting hypoglycemia and acanthosis nigricans. METHODS: To evaluate the mechanism of hypoglycemia, we measured the inhibition of insulin binding to erythrocytes and IM9 lymphocytes in a sample of the patient's dialyzed serum before and after immunosuppressive therapy. RESULTS: In the patient's pre-treatment serum IgG, the binding of 125I-insulin to erythrocytes was markedly inhibited in a dose-dependent manner until the cold insulin level reached 10-9 mol/L. We also observed dose-dependent inhibition of insulin binding to IM9 lymphocytes, which reached approximately 82% inhibition and persisted even when diluted 1:20. After treatment with glucocorticoids, insulin-erythrocyte binding activity returned to between 70% and 80% of normal, while the inhibition of insulin-lymphocyte binding was reduced by 17%. CONCLUSION: We treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine. We characterized the patient's insulin receptor antibodies by measuring the inhibition of insulin binding.
Subject(s)
Humans , Acanthosis Nigricans , Antibodies , Autoantibodies , Azathioprine , Cold Temperature , Erythrocytes , Glucocorticoids , Hyperglycemia , Hypoglycemia , Immunoglobulin G , Insulin , Insulin Resistance , Lymphocytes , Receptor, Insulin , SteroidsABSTRACT
Autoimmune hypoglycemia is characterized by insulin autoantibody, hyperinsulinemia and fasting hypoglycemia without previous insulin immunization. Negative results on the anatomic studies of the pancreas and an inability to reproduce hypoglycemia during a prolonged fast may be helpful in excluding insulinoma. Autoimmune hypoglycemia is self-limited disorder. We recently experienced a case of autoimmune hypoglycemia in a patient with insulin antibody, and the patient was without previous insulin injection therapy or any evidence of insulinoma, during treatment with anti-tuberculosis drugs. We present this case along with a review of the literature.
Subject(s)
Humans , Hyperinsulinism , Hypoglycemia , Immunization , Insulin , Insulinoma , PancreasABSTRACT
Autoimmune hypoglycemia is characterized by hyperinsulinemia, fasting hypoglycemia, and the presence of insulin auto- antibodies without previous exposure to exogenous insulin. We experienced a case of autoimmune hypoglycemia without diabetes mellitus or any evidence of insulinoma. The insulin auto-antibody and insulin receptor auto-antibody were present. We diagnosed the patient as having autoimmune hypoglycemia and treated with glucocorticoid. After treatment, the hypoglycemic symptoms were resolved. However, four months later, the patient was readmitted with transient diabetic ketoacidosis. After recovery, he showed no signs of diabetes mellitus. We believe that insulin auto-antibodies may play a role in autoimmune hypoglycemia and diabetic ketoacidosis, but its role and mechanism are not precisely known. Further studies are needed to define the action mechanisms and the functions of insulin auto-antibodies: here we present case with a relevant literature.