Miliary Tuberculosis with Addisons Disease - in old case of pulmonary tuberculosis, and tuberculosis of seminal vesicles - A rare case report

Addison's disease is a rare endocrinal disorder that was first described by Thomas Addison in 1855. Addison抯 disease occurs as a result of a lack of production of adrenocortical hormones, which is a rare but fatal disease if left untreated. The two most common causes of Addison's disease are autoimmune adrenalitis and tuberculosis which refer to hypoadrenalism caused by total or near total destruction or dysfunction of both adrenal cortices. Usual manifestations involve chronic fatigue, muscle weakness, loss of appetite, nausea, vomiting, diarrhoea, hypotension, and hyper pigmentation of the skin. A substantial proportion of patients presenting with extra-pulmonary tuberculosis (TB) have urogenital TB (UG-TB), which is easily under diagnosed because of non-specific symptoms, which are chronic and have cryptic protean clinical manifestations. Most of the clinician are not aware of the possibility of UG � TB. Calcification of seminal vesicle found in this case is a rare condition, which is commonly associated with diabetes, hyperparathyroidism, and genitourinary tuberculosis. We here in report a rare case of adrenal insufficiency due to miliary tuberculosis involving adrenal gland, old pulmonary tuberculosis and genitourinary tuberculosis (seminal vesicles calcification) in a 31 year old male person. He presented with multiple episodes of vomiting, and giddiness which wasalso accompanied with atypical hyperpigmentation. His symptoms resolved after starting anti tuberculous therapy.

A Case of Type II Autoimmune Polyglandular Syndrome: Acute adrenal crisis presented as the first manifestation of Addison's disease in a patient with diabetic ketoacidosis and hypgonadism / 대한내분비학회지

Type II autoimmune polyglandular syndrome typically presents in adulthood. Insulin dependent diabetes mellitus and thyroid dysfunction are the most frequent manifestations. Addison's disease is the third major endocrine component of this disorder. In this report, we described a thirty-two year-old male patient who had hypogonadism, insulin dependent diabetes mellitus, and mild Addison's disease presenting its first manifestation as an acute adrenal crisis due to diabetic ketoacidosis. The ACTH concentration will be elevated early in the course of Addisons disease even before a significant reduction in the basal cortisol level or its response to exogenous ACTH occurs. Therefore, plasma ACTH measurements serve as a valuable screening study for Addisons disease.

A Case of Addison's Disease: Partial Recovery of Adrenocortical Function Following Antituberculous Medication / 대한내분비학회지

Addisons disease is relatively rare than secondary adrenal insufficiency and result from progressive adrenocortical destruction. The common causes are idiopathic autoimmune atrophy and tuberculosis of adrenal glands. It is generally regarded as incurable in the sense that substitution therapy is required for the rest of the patients life. We report a case of tuberculous primary adrenal insufficiency which was confirmed by biopsy. This case was treated with antituberculous medication and showen to have improved adrenocortical function after six months.

A case of Addison's disease / 대한피부과학회지

Addisons disease is the defieient production of glucocorticoid or mireralocorticoid or both, due to the destruction of the adrenal cor tex. We report a case of Addiaons disesse in a 26-year-old male who complained only of skin and oral mucosal hyperpigmentations without other constitutional symptorns, Physical examinations showed scanty pubic and axillary hsirs. On adrenocorticoid funtion study, the ACTH stimulstion test failed to rise the bassl plasme cortisol level and basal ACTH level was marked elevated st PM 6:00. Routine laboratory and other endocrinologic evaluations exhibited within normal limits. Radiologic findings showed negative on both cheet X-ray and abdominal MRI films. Gradisl disapperance of skin snd mucosal hyperpigmentation were noted following administration of phosiologic dose of corticosteriods. Almost normal appearance was obtaineg after 26 months treatment.