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Addison's disease is an uncommon endocrine condition manifested by a variety of nonspecific symptoms, such as malaise, anorexia and nausea. Symptoms usually do not occur until most of the adrenal gland has been destroyed. Autoimmune disease has surpassed tuberculosis as the primary cause of Addison's disease. Nevertheless, tuberculosis still accounts for a significant proportion of cases. The rapid adrenocorticotropic hormone (ACTH) stimulation test is useful for identifying adrenal insufficiency. Maintenance therapy consists of hydrocortisone and fludrocortisone.
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PMID:Addison's disease. 200 21

A 69-year-old female was admitted because of a febrile state, somnolence, nausea and diarrhea. Addison's disease known to have developed several years earlier after adrenal tuberculosis suggested Addisonian crisis triggered by an acute infection. Therapy with steroids and substitution of electrolytes and fluid led to rapid improvement. Streptococcus bovis was identified as causative agent. The known association of this germ with cancer of the colon led to further investigation which revealed cancer of the sigmoid and incidental cancer of a salpinx. After surgical removal of both cancers, the patient has remained free of complaints under substitution of steroids.
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PMID:[Fever, somnolence, vomiting, diarrhea]. 212 19

We reported a case of Addison's disease, caused by adrenal tuberculosis. The patient was female, seventy four years old. She complained cough and body weight loss. She complained cough from June, 1989, but her home doctor didn't take care of her symptoms. September 1989, she felt appetite loss, and easy fatigue, so her home doctor suspected her disease as pulmonary tuberculosis, so he introduced our hospital, and she admitted. When she admitted, her chest roentogenogram revealed bIII2. Sputum smear examinations were negative. Laboratory data on admission, we observed slightly eosinophilia, severe iron deficiency anemia, and accenturation of blood sedimentation rate. Immediately after admission, she complained nausea, vomiting, coldness, and powerless. On 25 days after admission, she lost her senses suddenly, and her blood pressure fell 5 days after, she fell in shock state, too. We found out her blood sugar data was 29. After blood examinations, we found out that ACTH was high, cortisole, 17-KS, 17-OHCS were low. So we thought she got acute hypoadrenocorticism. We found her abdominal CT revealed calcification in her right adrenal gland. We diagnosed her disease as Addison's disease caused by adrenal tuberculosis so we began to give prednisolone, 7.5 mg per day. After giving, her state made better. We thought her disease as Addison's disease caused by adrenal tuberculosis, revealed acute hypoadrenocorticism.
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PMID:[A case of Addison's disease caused by adrenal tuberculosis, and revealed acute hypoadrenocorticism]. 826 25

Primary adrenal insufficiency (PAI) is a relatively rare but serious condition that can lead to signs and symptoms ranging from mild generalized weakness and fatigue to fulminant shock and death. We present the case of a previously healthy 31-year-old man who developed PAI while undergoing rehabilitation after a severe traumatic brain injury (TBI). The patient suffered a TBI with comminuted skull fractures, bifrontal confusions, and bilateral epidural hematomas in a jet-ski accident. Acute hospitalization was prolonged by several medical complications, and the patient was admitted for subacute rehabilitation 1 month after his injury with cognitive deficits, persistent agitation, confusion, generalized weakness, and poor endurance for therapy. His weakness, fatigue, and orthostasis did not improve with attempts at gradual remobilization. The patient also had persistent anorexia, nausea, and hyponatremia despite various treatment regimens. Endocrinology workup showed normal anterior pituitary function but an abnormal response to adrenocorticotropic hormone (ACTH) stimulation, leading to the diagnosis of PAI. The patient was treated with prednisone and fludrocortisone, which resulted in improvement in clinical symptoms followed by rapid gains in all functional areas. No previous descriptions of PAI following head injury were found in the medical literature. It is important for physiatrists to be aware of this entity because symptoms of adrenal insufficiency can be similar to those commonly seen with TBI alone. PAI may also be confused with other endocrine disorders more frequently seen after TBI such as the syndrome of inappropriate antidiuretic hormone secretion. Recognition and appropriate management of adrenal insufficiency can lead to significant clinical and functional gains.
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PMID:Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. 908 56

Clinical features and the management of adrenal insufficiency are considered with reference to etiology, diagnosis, and treatment. Specifically considered are the management of patients with Addison's disease and metastases. Adrenal insufficiency may go unrecognized in the cancer patients because features such as nausea, vomiting, anorexia as well as orthostatic hypotension are not specific and may be mistakenly attributed to advancing malignancy or side effects of therapy. Prompt recognition and treatment of adrenal insufficiency can avert potentially life-threatening situations.
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PMID:[Adrenal cortex insufficiency caused by metastatic tumors]. 948 26

An 18-year-old white woman had nausea, vomiting, weight loss, and a diagnosis of anorexia nervosa. Copper-colored skin was noted on physical examination, and serum chemistry values were normal. Subsequent fever, disorientation, and confusion led to the discovery of Addison's disease, which responded well to corticosteroid replacement therapy. Addisonian and anorexic patients exhibit clinical similarities, including nausea, vomiting, weight loss, abdominal pain, cold intolerance, hypothermia, and orthostasis. Other commonalities include prolongation of electrocardiographic PR and QT intervals and generalized slowing on electroencephalogram. Important differences include a brown color to the skin in Addison's disease instead of a yellowish color in anorexia. Addisonian patients also display hypocortisolism, hypoglycemia, and hyperkalemia, in contrast to the hypercortisolism, hyperglycemia, and hypokalemia seen in anorexia.
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PMID:Prompt differentiation of Addison's disease from anorexia nervosa during weight loss and vomiting. 949 78

Addison's disease due to adrenal lymphoma usually manifests as bilateral adrenal enlargement. We report a patient with Addsion's disease in whom the initial overt primary adrenal insufficiency was accompanied by an only slightly enlarged right adrenal gland. The 80-year-old man presented with nausea, anorexia, weight loss, and hyperpigmentation of the skin and buccal mucosa. Addison's disease was diagnosed based on this clinical presentation and laboratory findings of low cortisol and high adrenocorticotropin levels. Computerized tomography (CT) of the adrenal glands revealed a small right adrenal tumor. His family refused to allow percutaneous or surgical biopsy to determine the nature of the tumor. His general condition improved after steroid supplementation. However, about 1 year later, dizziness, fever, night sweats, and edema of the lower legs developed, and adrenal CT scanning revealed that the left adrenal gland had enlarged and now exceeded the size of the right one. Left adrenalectomy was performed and pathology showed a diffuse large B-cell lymphoma. Staging work-up using whole-body CT scanning suggested a stage IIIb lymphoma. Chemotherapy was given, but the disease still progressed and the patient died 4 months after diagnosis. Primary adrenal lymphoma should be considered in the differential diagnosis of Addison's disease, even if only slight enlargement of the adrenal glands is found initially.
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PMID:Adrenal lymphoma and Addison's disease: report of a case. 1263 19

Pituitary coma is a rare case of emergency and primarily due to ACTH and TSH deficiency. Pituitary coma occurs more often in patients with well-known pituitary deficiency than in patients with intrasellar tumor. Clinical manifestations are hypotonia, bradycardia, decreased skin and nipple pigmentation, muscle weakness, vomitus, nausea, obstipation, hypothermia, and hypoventilation. A postpartal agalactia is often the first sign of Sheehan's syndrome. Unlike primary adrenal insufficiency (Addison's disease) ACTH deficiency does not cause hyperpigmentation, hyperkalemia, or salt loss. The suspicion of pituitary coma requires replacement with 100 mg hydrocortisone iv, 200 mg hydrocortisone iv/24 h, 500 micro g levothyroxine iv and fluid substitution. Since thyroxine accelerates the degradation of cortisol and can precipitate adrenal crisis in patients with limited pituitary reserve, hydrocortisone replacement should always precede levothyroxine therapy. ACTH stimulation test, CRH stimulation test and insulin tolerance test (optional) should be performed after therapeutic compensation to determine pituitary function.
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PMID:[Hypophyseal coma]. 1468 87

A 50-year-old woman complained of nausea, diarrhoea, tiredness and dizziness five weeks after a visit to Egypt. She was deeply tanned with hyperpigmentation on the metacarpophalangeal joints, palm of hand creases and buccal mucosa, due to Addison's disease.
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PMID:[Diagnostic image (303). A deeply tanned woman]. 1719 6

In literature different cases of polyglandular autoimmune type II syndrome (PGA II) are reported, where Addison's disease is associated with gonadal insufficiency. The lack in the production of sexual steroids causes a severe postmenopausal osteoporosis. The case we report is related to a 38-year-old woman we met in 1988 and who was suffering from deep asthenia, cramps, cutaneous hyperpigmentation, nausea, vomiting, abdominal pain, weight loss and hypotension. The biochemical data were indicative for autoimmune adrenal failure. Between 1988 and 1997 the patient developed a progressive insufficiency of other endocrine glands, leading to the classic feature of PGA II. In 1998, this clinical status was complicated by a severe osteoporosis. We thought that the sudden decrease in the bony mineral density was due to the lack of the protective role played by adrenal gland androgens in postmenopausal osteoporosis. They would directly act on the bony tissue, independently from oestrogens peripheral conversion, thus producing a stimulant effect on the bone formation. A new therapeutical approach, in case of osteoporosis, is today represented by DHEA replacement therapy in women showing low hormone levels.
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PMID:Polyglandular autoimmune endocrine insufficiency complicated by severe osteoporosis. 1721 95


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