¶ … Hyponatremia in a 38-year-Old male
The constellation of signs and symptoms the patient presented with is consistent with a diagnosis of adrenal insufficiency (Betterle, Pra, Mantero, and Zanchetta, 2002, p. 330-331). These include a recent history of gastric distress, partial loss of consciousness, lethargy, dizziness, disorientation, weight loss, hyponatremia, borderline hyperkalemia, low serum and free cortisol levels, and the lack of a rapid cortisol response to ACTH stimulation (Wilson, 2008). Signs and symptoms that may not support a diagnosis of adrenal insufficiency include no mention of hyperpigmentation or pallor, and an unremarkable abdominal CT scan. A discussion of these signs and symptoms, and the possible relevance to a diagnosis of adrenal insufficiency follows.
True Hyponatremia Diagnosis
There are a large number of conditions and diseases that can lead to the development of hyponatremia, so this symptom alone has limited diagnostic utility (Wilson, 2008, p. 519). The combination of severe hyponatremia and low serum osmolality suggest the neurological symptoms are being caused in part by cerebral edema (Porter and Kaplan, 2010). This would develop due to an osmotic shift of water into cells within the central nervous system, thus creating hypotonic conditions that would interfere with a cell's ability to function normally. The osmotic gradient between the extracellular and intracellular compartments would also tend to pull potassium out of cells to compensate for low sodium levels, which may explain the finding of borderline hyperkalemia. Together these findings suggest the patient is suffering from true hyponatremia (Milionis, Liamis, and Elisaf, 2002).
The elevated serum potassium and low serum bicarbonate levels are consistent with compensatory mechanisms attempting to resolve metabolic acidosis, a condition that sometimes develops in persons suffering from primary adrenal insufficiency (Follin and Lenker, 2004, p. 522). Hyponatremia alters serum pH because the sodium (cation) concentration is lowered, unless the concentration of the other cations and anions compensate to maintain pH within the normal range. Evidence that a condition of metabolic acidosis exists is also supported by the neurologic symptoms of partial loss of consciousness, lethargy, and disorientation. The recent history of gastric distress is also consistent with metabolic acidosis.
Panhypopituitarism, Hypothyroidism and Hypovolemia are Excluded
The patient's urine osmolality is within the normal range for a person not suffering from hyponatremia. This finding suggests the kidneys are not functioning appropriately, because they are not excreting excess body water to bring the serum sodium concentration back within the normal range (Milionis, Liamis, and Elisaf, 2002). A number of different conditions can lead to this problem, including hypovolemia, hypothyroidism, adrenal insufficiency, syndrome of inappropriate anti-diuretic hormone secretion (SIADH), reset osmostat syndrome, and renal salt wasting. Laboratory testing revealed normal TSH and free thyoxine (T4) levels, which argues against the anterior pituitary and thyroid as possible causes of this patient's symptoms (Follin and Lenker, 2004, p. 431).
Low blood volume, or hypovolemia, typically causes the kidneys to conserve sodium and water. Hypovolemic patients would be expected to have urine sodium levels below 20 mEq/L/d (Milionis, Liamis, and Elisaf, 2002). With a urine sodium concentration of 53 mEq/L/d, it's unlikely this patient is hypovolemic. Testing for adrenal insufficiency is the next step.
Adrenal Insufficiency Diagnosis
The patient's baseline serum cortisol level of 7 mcg/dL is equal to the lower limit of the morning normal range, and well within the afternoon normal range (Andrews, Johnson, Kothare, and Weinstock, 1999, p. 226). This value alone does not suggest adrenal insufficiency is the cause of hyponatremia. Serum cortisol levels can be misleading though, because different conditions can lead to an increase in serum cortisol-binding protein concentrations, thus creating a reservoir of non-biologically active cortisol that can mask low levels of the biologically active (free, i.e., unbound) from of cortisol (Al-Aridi, Abdelmannan, and Arafah, 2011, p. 9). The combination of below normal urinary (free) cortisol levels and normal thyroid function, confirms the need to dynamically test for adrenal hypofunction. Al-Aridi, Abdelmannan, and Arafah (2011, p. 10) report that they typically view serum cortisol levels below 12 mcg/dL as justification for further testing for adrenal insufficiency, because any patient who is critically ill would be expected to produce more than 15 mcg/dL. This patient, who is obviously critically ill, therefore has an unexpectedly low serum cortisol level even though...
A bolus of cosyntropin is injected and serum cortisol levels are measured at baseline, 30, and 60 minutes later. Serum cortisol levels in a healthy person would be expected to rise at least 7 mcg/dL by the 60 minute time point, to a value above 18 mcg/dL (Andrews, Johnson, Kothare, and Weinstock, 1999, p. 197-198). This patient's serum cortisol levels failed to respond to the cosyntropin injection, which supports a diagnosis of adrenal insufficiency and provides an explanation for most of the patient's symptoms (Follin and Lenker, 2004, p. 22).
Further Testing Required
The ACTH stimulation test alone can't distinguish between primary and secondary adrenal insufficiency, therefore further testing is needed to exclude one or the other (Follin and Lenker, 2004, p. 22). Differentiating between primary and secondary adrenal insufficiency can be done by measuring serum aldosterone and cortisol levels during a prolonged ACTH stimulation test. If aldosterone levels are within the normal range, then secondary adrenal insufficiency is the likely cause of the symptoms, otherwise a diagnosis of primary adrenal insufficiency (Addison's disease) is appropriate. The test should be prolonged over several days to assess whether adrenal function can recover with prolonged exposure to cosyntropin. If cortisol levels do eventually increase, then secondary adrenal insufficiency is the more appropriate diagnosis.
If Addison's disease is diagnosed, then the patient's serum should be screened for autoantibodies specific for adrenal cortex antigens (ACA), and P450c21, P450SCC, and P450C17, as part of testing for autoimmune adrenal insufficiency (Ten, New, and MacLaren, 2001). Autoimmune Addison's is the most common form in developed countries where tuberculosis has been aggressively treated (Betterle, Pra, Mantero, and Zanchetta, 2002, p. 337). Prior to the development of effective treatments for tuberculosis, Addison's was primarily caused by this infectious agent. For this reason, the patient should be tested for tuberculosis. Less common causes of Addison's include HIV infection, mycosis, bacterial infections, and metastatic cancer, and these should be excluded as well. Addison's can be part of an autoimmune polyglandular syndrome that involves multiple conditions, including mucocutaneous candidiasis, hypoparathyroidism, diabetes mellitus, and thyroid disease. If autoimmune Addison's is eventually diagnosed, tests for these conditions should be performed and the patient monitored for the possible emergence of this syndrome.
Significance of the Unremarkable CT Scan Results and no Report of Hypopigmentation
The patient's symptoms did not include any remarks about hyper- or hypopigmentation, and if the absence of such a remark indicates that no change in pigmentation was observed, this supports a diagnosis of secondary adrenal insufficiency (Al-Aridi, Abdelmannan, and Arafah, 2011). Hyperpigmentation is caused by elevated corticotropin and MSH levels driving increased production of melanin in melanocytes. High serum levels of cortocotropin occur because cortisol levels fail to provide a negative feedback signal to the anterior pituitary. If the patient is hyperpigmented, then a diagnosis of Addison's disease is warranted, pending completion of further laboratory tests for adrenal function. The absence of hyperpigmentation does not preclude a diagnosis of Addison's disease though, because in some patients it can take months of elevated corticotropin levels to cause visible signs (Betterle, Pra, Mantero, and Zanchetta, 2002, p. 346).
A small percentage of Addison's patients do not develop hyperpigmentation due to a genetic defect in melanin metabolism. Such a defect could have predisposed a family with a history of adrenal insufficiency to a series of misdiagnoses (Ten, New, and MacLaren, 2001). For example, acute adrenal insufficiency has been reported to cause psychosis in some patients (Anglin, Rosebush, and Mazurek, 2006), which could explain the patient's family history of schizophrenia. Patients with severe adrenal insufficiency often experience a substantial decline in cardiac function and if the patient is also suffering from atherosclerosis then the risk of an adverse cardiac event would be increased. This may explain the older brother's myocardial infarction. His inability to survive the cardiac emergency would also have been impaired because of a compromised cortisol response (Iribarren et al., 2010).
If the patient's family has a heritable defect in melanin metabolism that exposed them to a series of misdiagnoses, then this would suggest a heritable predisposition for adrenal insufficiency exists in this patient's family as well. Autoimmune polyendocrine syndromes (APS) and isolated Addison's disease have a genetic component that frequently involve mutations in HLA DR3, and invariably include primary adrenal insufficiency (Betterle, Pra, Mantero, and Zanchetta, 2002, p. 337). If the patient does suffer from genetic defects in both systems, then the age of the patient would favor a diagnosis of APS II or isolated Addison's disease. As mentioned above, the patient should be screened for the presence of serum autoantibodies specific for the adrenal cortex pending the results of further endocrine…
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