ABSTRACT
The association between proton pump inhibitor (PPI) therapy and hypomagnesaemia has been recognized since 2006. We report the case of a 51-year-old woman who developed severe symptomatic hypomagnesaemia after a long-term PPI therapy given for recurrent peptic ulcer disease. Hypomagnesaemia could only partially be resolved during substitution therapy, but was corrected after withdrawal of the PPI. Recurrence of hypomagnesaemia occurred after retreatment with PPIs, supporting the causal relationship. An underlying gastric acid hypersecretion (Zollinger-Ellison syndrome) was highly suspected and eventually controlled by a combination of a histamine 2-receptor antagonist and octreotide, without the need for further PPI therapy after 2 years of follow-up.
Subject(s)
Magnesium Deficiency/chemically induced , Proton Pump Inhibitors/adverse effects , Zollinger-Ellison Syndrome/drug therapy , Blood Chemical Analysis , Female , Humans , Middle AgedABSTRACT
The frequency of HLA DR3 in patients with Addison's disease is increased and the relative risk factor rises to 10 when adrenocortical failure is part of a polyendocrinopathy.
Subject(s)
Addison Disease/immunology , Autoimmune Diseases/immunology , Adrenal Cortex/immunology , Diabetes Mellitus, Type 1/complications , Diabetes Mellitus, Type 2/complications , Endocrine Glands/immunology , Endocrine System Diseases/complications , Gene Frequency , Genes, MHC Class I , Genes, MHC Class II , HLA Antigens/analysis , HLA-B8 Antigen , HLA-DR Antigens/analysis , Humans , Islets of Langerhans/immunology , Thyroid Diseases/complicationsABSTRACT
Thyroid hormones occasionally appear less effective when administered alone to patients with panhypopituitarism, and manifestations suggestive of hypothyroidism have been reported in patients suffering from untreated Addison's disease. In the latter condition, thyrotropin secretion is increased: this occurs already after as little as 2 days of temporary withdrawal of therapy with substitution doses of corticosteroids while circulating levels of thyroid hormones remain within normal limits. Therefore, a possible role of cortisol in interaction between triiodothyronine and its nuclear receptors was examined at the level of circulating lymphocytes obtained from patients with primary or secondary adrenocortical failure. The affinity of these receptors was found to be decreased, by more than 50% on average, in the absence of cortisol treatments. This change was promptly corrected upon resumption of therapy. The number of binding sites was not significantly modified. The influence of cortisol on thyroid hormone receptors discussed here might account for the clinical observations mentioned above.
Subject(s)
Adrenal Cortex Hormones/deficiency , Cell Nucleus/metabolism , Hydrocortisone/physiology , Receptors, Thyroid Hormone/metabolism , Thyrotropin/metabolism , Triiodothyronine/metabolism , Addison Disease/drug therapy , Female , Humans , Kinetics , Lymphocytes/metabolism , Male , Thyrotropin-Releasing Hormone/therapeutic useSubject(s)
Addison Disease/complications , Diabetes Complications , Adult , Aged , Female , Humans , Male , Middle AgedSubject(s)
Addison Disease/therapy , Addison Disease/diagnosis , Addison Disease/etiology , Addison Disease/metabolism , Adrenal Cortex Hormones/therapeutic use , Adult , Autoimmune Diseases/complications , Catecholamines/urine , Female , Humans , Hydrocortisone/blood , Male , Middle Aged , Steroids/urine , Tuberculosis/complicationsABSTRACT
Out of a score of patients known as suffering from Addison's disease, tuberculosis was the cause in 7, and their serum fasting gastrin levels were normal, averaging 52 pg/ml. For the 14 remaining cases, with the auto-immune variety of the disease, there were high gastrin levels in 3; in 2 out the 11 others, with values within the normal range, there was total achlorhydria. Could it be that gastrin-secreting cells might occasionally be involved in auto-immune endocrine disorders?
