Objectives: Adrenal gland hypertrophy can be related to acute stress with abnormal adrenal function tests. It may not always need treatment. Material and methods: An acute presentation of adrenal gland hypertrophy following an abdominal emergency, with subsequent hypoadrenalism was investigated. Results: Adrenal medullary and cortical function fully recovered without treatment. Conclusions:We postulate that the adrenal glands became enlarged and hypertrophied during an acute stress event, possibly caused by acute adrenal medullary hypersecretion and subsequent cortical hyposecretion. A wait and watch policy should be followed if no other clinical symptoms and signs of adrenal disease are present. CT scan remains an important diagnostic tool. LEARNING POINTS• Abnormal adrenocortical function tests and hypertrophy can occur in an acutely ill patient as a stress response.• It is possible to have both hypersecretion and hyposecretion of adrenal hormones.• A wait and watch policy should be followed if no other clinical symptoms and signs of adrenal disease are present in an acutely ill patient. KEYWORDS Adrenal gland hypertrophy, transient adrenal insufficiency, reversible adrenal dysfunction, transient adrenal medullary hyperactivity, stress related hypertension. INTRODUCTIONThe adrenal medulla and cortex participate in the response to acute stress
Henoch-Schönlein purpura (HSP), also known as immunoglobulin A (IgA) vasculitis, is a small-vessel vasculitis characterized by IgA deposits in various organs in the body producing a unique constellation of symptoms. This disease predominantly affects the skin (palpable purpura), joints (arthritis/arthralgia), gut (abdominal pain), and kidneys (nephritic syndrome-IgA nephropathy [IgAN]). The pathogenesis of HSP in children is usually secondary to an immune reaction after viral infections. In adults, few cases of HSP/IgA vasculitis have been reported secondary to altered metabolism of IgA in patients with alcoholic liver cirrhosis.Here, we report an unusual case of HSP/IgA vasculitis. The patient presented with signs of alcoholic liver cirrhosis with abdominal pain and ascites along with a lower extremity purpuric rash. The patient had significant findings of liver cirrhosis with radiographic evidence of cirrhotic liver with esophageal varices and splenorenal shunt and elevated serum ascites albumin gradient. Urinalysis revealed proteinuria with microscopic hematuria, further evaluated with a kidney biopsy. Microscopic analysis revealed focal segmental endocapillary and extracapillary proliferative glomerulonephritis with focal necrotizing features, consistent with IgAN/HSP nephritis. Treatment was initiated with high-dose steroids and cyclophosphamide infusions.Alcohol-induced endotoxin release and inflammation lead to high amounts of circulating IgA due to increased intestinal permeability and reduced hepatic clearance. Further disease development is caused by IgA deposits in affected organs (skin and kidney in our case). We hypothesize that the development of disease for the patient was secondary to altered IgA processing in decompensated alcoholic cirrhosis.
A 76 year old gentleman not known to be diabetic presented with confusion and agitation. On admission he had a blood glucose reading of 2.1mmol/l and clinical examination confirmed an abdominal mass. He was initially resuscitated with intravenous dextrose but continued to experience hypoglycemic episodes. Urine sulphonylurea, serum insulin, pro-insulin and c-peptide levels tested at the time of hypoglycemia were satisfactory. There was no ketonaemia and the short synacthen test showed adequate response. His IGF 2 and IGF2:IGF1 ratio was elevated. An abdominal Ultrasound and CT scan were inconclusive as to the nature of the mass, so biopsy and histology were organized which confirmed a spindle cell neoplasm. To maintain euglycaemia, he had dietician input for complex carbohydrate meals and regular scheduled snacks, but as this failed to sustain his euglycaemia, he was then started on steroid therapy. He had a good response to the dexamethasone. Unfortunately, as curative therapy of the spindle cell tumor was not an option for him, he was referred for palliative follow-up.
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