scholarly journals A Challenging Case of Adrenal Insufficiency Presenting with Hypertensive Crisis

2020 ◽  
Vol 5 (1) ◽  
pp. p35
Author(s):  
Ahmad Al-Abdouh ◽  
Ghazal Kooshk Jalali ◽  
Sanaz Sakiani

Adrenal insufficiency is the deficient production or action of glucocorticoids, with or without deficiency in mineralocorticoids or adrenal androgens. It usually presents with anorexia, abdominal pain, weakness, weight loss, fatigue, and hypotension. We report a case of 67 year old male, who is known to have hypertension, presented to emergency room with severe headache and was found to have high blood pressure 241/135mmHg and hypoosmolar hyponatremia. He was started on intravenous nicardipine and his blood pressure dropped suddenly, became orthostatic, and required fluid resuscitation but his headache resolved. On next day, the cosyntropin test was suggestive of primary adrenal insufficiency. The patient was started on oral hydrocortisone with improvement in his blood pressure and hyponatremia.

2006 ◽  
Vol 5 (3) ◽  
pp. 102-103
Author(s):  
Tejal Desai ◽  
◽  
Tristan Richardson ◽  

Primary Adrenal Insufficiency is due to bilateral destruction of the adrenal cortex and has a prevalence of approximately 40-60 per million adults. 1 The commonest cause is autoimmune. 1 Prompt treatment not only restores quality of life but also a normal life expectancy. 2 Here we present an unusual case of primary adrenal insufficiency, which illustrates how such an important disease often provides a diagnostic conundrum.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A108-A109
Author(s):  
Nani Oktavia ◽  
Chici Pratiwi ◽  
Jerry Nasaruddin ◽  
Muhammad Ikhsan Mokoagow ◽  
Marina Epriliawati ◽  
...  

Abstract Background: Adrenal crisis is an emergency condition in endocrinology that commonly found in primary adrenal insufficiency but also occur in chronic adrenal insufficiency triggered by various conditions such as sepsis, infection, trauma, burns, surgery, and myocardial infarction. In chronic adrenal insufficiency, adrenal crisis can be induced by excessive reductions or inadequate discontinuation of steroid treatment. Case Illustration: A 40-year old-man admitted with chief complaint abdominal pain since seven days before admission. He felt pain in the umbilical area and slowly radiated to all the part of abdomen. Other than that, he also felt nausea, had vomitus, fever, and constipation for five days. He was immobilized for four months, with muscles weakness and atrophy. He was diagnosed with Focal Segmented Glomerulosclerosis and had a high dose of methylprednisolone (48 mg) for 6 months, 40 mg for the next 2 months and methylprednisolone 12 mg for the last 2 months. The last two month, he began to have severe general weakness and hypotension. On physical examination we found hypotension, fever (38.1o C), pale conjunctiva, moon face, buffalo hump, slightly distended and tenderness of abdomen, normal bowel sound, and purple striae all over the abdomen and extremities. On laboratory examination, Hb was 8.2 (n 11.7 – 15.5 g/dl), leukocytes 10,400 (5.00 – 10.00 x 103/μL), Na 123 (n 135 – 147 mmol/L), random blood glucose 74 (n 70 – 140 mg/dL). On abdominal X ray, there was prominent faecal material and no signs of ileus. No sign of infection found in urinalysis. He had sodium correction, packed red cell transfusion, symptomatic therapy including laxative, methylprednisolone 12 mg, but no improvement of signs and symptoms beside be able to defecate. The abdominal ultrasound gave a normal result. The morning cortisol level was then examined, with the result 14.4 (n 3.7–19.4). The patient was then diagnosed with adrenal crisis based on the clinical manifestations and had hydrocortisone therapy 100 mg a day for 2 consecutive days. After hydrocortisone administration, the symptoms improved, no fever and abdominal pain, he had normotension, increased sodium level 132 (n 135 – 147 mmol/L) and blood glucose level 118 (n 70 – 140 mg/dL). On the third day the patient discharged with oral hydrocortisone 15 mg in the morning and 10 mg in the afternoon. Conclusion: Adrenal crisis was generally found in primary adrenal insufficiency but could also occur in secondary adrenal insufficiency due to inappropriate tapering off process of long term glucocorticoid use.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Shawn Esperti ◽  
Austen Stoelting ◽  
Nicolina Scibelli ◽  
David Moccia ◽  
Dveet Patel ◽  
...  

A 40-year-old male smoker with HIV was admitted for cough, hypotension, and abdominal pain for 5 days. Chest radiography showed a right lower lobe consolidation. CT of the chest, abdomen, and pelvis revealed paratracheal adenopathy, a 5.8×4.5 cm mass invading the right bronchus intermedius, and dense bilateral adrenal masses, measuring 5.4×4.0 cm on the right and 4.8×2.0 cm on the left. Laboratory studies showed white blood cell count of 18.5 K/mm3, sodium of 131 mmol/L, creatinine of 1.6 mg/dL, and CD4 count of 567 cells/mm3. The random morning cortisol level was 7.0 μg/dL, the ACTH stimulation test yielded inappropriate response, and a random serum ACTH was elevated at 83.4 pg/mL. MRI brain revealed no pituitary adenoma confirming primary adrenal insufficiency. The adrenal CT washout study was consistent with solid mass content, concerning for metastasis. Bronchoscopy with endobronchial mass and paratracheal lymph node biopsy confirmed small-cell lung cancer (SCLC). Intravenous steroids, 100 mg hydrocortisone every 8 hours, improved his hypotension and abdominal pain. PET scan revealed metabolically active right paratracheal mass, right hilar mass, and bilateral adrenal masses. Treatment included palliative chemotherapy consisting of carboplatin/etoposide/atezolizumab and chest radiation. We present this novel case to demonstrate SCLC’s ability to cause primary adrenal insufficiency, as well as evaluate clinical response to chemotherapeutics.


2016 ◽  
pp. 43-48
Author(s):  
SM Ashrafuzzaman ◽  
Muhammad Abdur Rahim

Adrenal insufficiency means hypo-function of the adrenal cortex, usually glucocorticoid, may be associated with mineralocorticoid and rarely adrenal androgen. It can be categorized into two types: Primary adrenal insufficiency, or Addison’s disease (cortisol low and ACTH high) or secondary/ tertiary adrenal insufficiency due to pituitary or hypothalamic disorders (both cortisol and ACTH are low). Identification of etiology is very important for plan of treatment. The reported incidence of adrenal insufficiency varies greatly depending on the population studied, the test and cut off levels used, and the cause. Many patients may present with adrenal crisis, some of them have subtle symptoms, hyperpigmentation, hypotension, electrolyte imbalance, shock etc. Many of them have iatrogenic adrenal insufficiency with features of Cushing’s syndrome. So, the manifestations of adrenal insufficiency are numerous and nonspecific, and clinicians should have a high index of suspicion and be alert to see important diagnostic clues, such as hyponatremia, hyperkalemia, and hypotension (that are refractory to fluids and vasopressors), diarrhea, weight loss, vomiting, fever etc. without any clear causation. Treatment of adrenal insufficiency is usually life-long, of course based on etiology. Short acting glucocorticoid is better, like hydrocortisone. Patients may be treated with prednisolone. Patients should be provided a “steroid card”. Sometimes it is essential to take patients under “withdrawal protocol”.Birdem Med J 2015; 5(1) Supplement: 43-48


Author(s):  
Avinash Suryawanshi ◽  
Timothy Middleton ◽  
Kirtan Ganda

Summary X-linked adrenoleukodystrophy (X-ALD) is a rare genetic condition caused by mutations in the ABCD1 gene that result in accumulation of very long chain fatty acids (VLCFAs) in various tissues. This leads to demyelination in the CNS and impaired steroidogenesis in the adrenal cortex and testes. A 57-year-old gentleman was referred for the assessment of bilateral gynaecomastia of 6 months duration. He had skin hyperpigmentation since 4 years of age and spastic paraparesis for the past 15 years. Physical examination findings included generalised hyperpigmentation (including skin, buccal mucosa and palmar creases), blood pressure of 90/60 mmHg, non-tender gynaecomastia and bilateral hypoplastic testes. Lower limb findings were those of a profoundly ataxic gait associated with significant paraparesis and sensory loss. Primary adrenal insufficiency was confirmed and investigations for gynaecomastia revealed normal testosterone with mildly elevated luteinising hormone level and normal prolactin. The combination of primary adrenal insufficiency (likely childhood onset), partial testicular failure (leading to gynaecomastia) and spastic paraparesis suggested X-ALD as a unifying diagnosis. A serum VLCFA panel was consistent with X-ALD. Subsequent genetic testing confirmed the diagnosis. Treatment with replacement doses of corticosteroid resulted in improvement in blood pressure and increased energy levels. We have reported the case of a 57-year-old man with a very late diagnosis of X-ALD manifested by childhood onset of primary adrenal insufficiency followed by paraparesis and primary hypogonadism in adulthood. Thus, X-ALD should be considered as a possibility in a patient with non-autoimmune primary adrenal insufficiency and neurological abnormalities. Learning points Adult patients with X-ALD may be misdiagnosed as having multiple sclerosis or idiopathic spastic paraparesis for many years before the correct diagnosis is identified. Screening for X-ALD with a VLCFA panel should be strongly considered in male children with primary adrenal insufficiency and in male adults presenting with non-autoimmune primary adrenal insufficiency. Confirmation of a genetic diagnosis of X-ALD can be very useful for a patient's family as genetic testing enables detection of pre-symptomatic female heterozygotes who can then be offered pre-natal testing to avoid transmission of the disease to male offsprings.


2019 ◽  
Vol 181 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Peter Wolf ◽  
Johanna Mayr ◽  
Hannes Beiglböck ◽  
Paul Fellinger ◽  
Yvonne Winhofer ◽  
...  

Background In patients suffering from primary adrenal insufficiency (AI) mortality is increased despite adequate glucocorticoid (GC) and mineralocorticoid (MC) replacement therapy, mainly due to an increased cardiovascular risk. Since activation of the renin–angiotensin–aldosterone system (RAAS) plays an important role in the modulation of cardiovascular risk factors, we performed in-depth characterization of the RAAS activity. Methods Eight patients with primary AI (female = 5; age: 56 ± 21 years; BMI: 22.8 ± 2 kg/m2; mean blood pressure: 140/83 mmHg; hydrocortisone dose: 21.9 ± 5 mg/day; fludrocortisone dose: 0.061 ± 0.03 mg/day) and eight matched healthy volunteers (female = 5; age: 52 ± 21 years; BMI: 25.2 ± 4 kg/m2; mean blood pressure:135/84 mmHg) were included in a cross-sectional case–control study. Angiotensin metabolite profiles (RAS-fingerprints) were performed by liquid chromatography mass spectrometry. Results In patients suffering from primary AI, RAAS activity was highly increased with elevated concentrations of renin concentration (P = 0.027), angiotensin (Ang) I (P = 0.022), Ang II (P = 0.032), Ang 1-7 and Ang 1-5. As expected, aldosterone was not detectable in the majority of AI patients, resulting in a profoundly suppressed aldosterone-to-AngII ratio (AA2 ratio, P = 0.003) compared to controls. PRA-S, the angiotensin-based marker for plasma renin activity, correlated with plasma renin activity (r = 0.983; P < 0.01) and plasma renin concentration (r = 0.985; P < 0.001) and was significantly increased in AI patients. Conclusions AI is associated with a unique RAAS profile characterized by the absence of aldosterone despite strongly elevated levels of angiotensin metabolites, including the potent vasoconstrictor AngII. Despite state-of-the-art hormone replacement therapy, the RAAS remains hyperactivated. The contribution of Ang II in cardiovascular diseases in AI patients as well as a potential role for providing useful complementary information at diagnosis and follow up of AI should be investigated in future trials.


1981 ◽  
Vol 15 (11) ◽  
pp. 904-906 ◽  
Author(s):  
Joyce A. Generali ◽  
Linda C. Hogan ◽  
Michael McFarlane ◽  
Steven Schwab ◽  
Charles R. Hartman

A hypertensive episode precipitated by avocados in a patient on tranylcypromine is described. The patient complained of severe throbbing headache, chest pain, and diaphoresis upon visiting the emergency room. Intravenous phentolamine was administered repeatedly to treat elevated blood pressure. Approximately 4 1/2 hours later, the patient's blood pressure stabilized, and he was released after a short period of observation. This is the first documented case of avocado-induced hypertensive crisis.


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