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Jack: More than just hypertension

When I first met Jack in 2002, he was 57 years old and had been on multiple medications for high blood pressure for over 15 years. We were unable to obtain a family history of premature hypertension, as he was adopted. He was in fairly good health except he recalled that years ago he was told by a physician to make a habit of donating blood regularly, perhaps due to borderline high iron levels, but was uncertain of the details. He maintained an active lifestyle, and routinely drank 2-4 glasses of alcohol beverage per day.

Despite almost maximum doses of 4 different medications to lower his blood pressure, Jack's blood pressures were still not optimally controlled, ranging 140-150's systolically and 90's diastolically. I performed routine blood work and found that Jack's serum potassium level was low, despite the fact one of his anti-hypertensive medication (Prinivil) carried the side effect of raising potassium levels, if anything. I was suspicious that he may have an adrenal gland tumor producing too much aldosterone, one of the key hormones involved in blood pressure as well as electrolyte balance, rather than simply age-related essential hypertension (usually due to hardening of the arteries). My index of suspicion remained high even though a CAT scan of his adrenal glands was negative for the presence of tumor. I performed a specialized saline-challenge test in Jack to see if I could appropriately suppress the production of aldosterone after a salt load, since one of aldosterone's main tasks in the kidneys is to retain sodium in balance with the excretion of potassium. Too much retention of sodium (such as from a tumor or enlargement of the adrenal glands producing too much aldosterone), can lead to hypertension. His results came back highly suggestive of adrenal-mediated hypertension, which was later confirmed when I referred him to an endocrinologist. Once the mechanism of his hypertension was illuminated, he was placed on the medication Aldactone, to specifically block the actions of his own aldosterone, which allowed us to discontinue 3 of his other anti-hypertensive medications. His blood pressures continue to be very well-controlled today, with low dosage Aldactone and a much lower dose of a second medication.

Jack subsequently embarked on a long road tour for close to 2 years, but came back to me recently for evaluation of diarrhea, which he had been experiencing for 6 months. He was initially seen by a physician who gave him antibiotics to treat presumed giardia infection (although no stool tests were done) since his symptoms began shortly after a camping trip. His symptoms did not improve, so stool tests were done, which were negative. He then saw another physician, who did additional stool testing, which were still negative. Jack was convinced that he did not have a gut infection, since he had no fevers, bloody stools, or abdominal pain. I performed initial general lab tests, and found that his fasting blood sugar was now diabetic range at 141, triglycerides were very high at 349, and liver labs now indicated liver injury, all of which were new findings. I suspected that Jack's diet had contributed to his high blood sugar, which often correlate with high triglycerides, which in turn, can cause "fatty liver" damage to the liver. I told him that "fatty liver" damage was not benign, and could lead to eventual scarring, very similar to the damage done by excess use of alcohol. He admitted that his diet had not been the best given he was traveling, and his wife was also concerned that his alcohol consumption might be more than what his body could handle. I counseled Jack and his wife on how the wrong diet, such as that high in processed carbohydrates, trans fats, and excess alcohol (which is rapidly absorbed as sugar after ingestion), could contribute to his current problems. Furthermore, excess sugar consumption can lead to excess gas formation by our gut bacteria and disturb our normal gut flora. I also suspected that Jack may have lactose intolerance, and asked him to go on an elimination trial, which later confirmed that he was, indeed, intolerant of dairy products.

Jack and his wife took my advice very seriously, and dramatically changed his diet, cutting down on processed foods and alcohol. Within 2 months, his blood sugar and triglycerides had both normalized. I performed additional testing to further evaluate other potential causes of liver injury. I was suspicious of the disorder hemochromatosis (based on the history of him being told years ago to donate blood regularly), which is a disorder of excess iron absorption, often leading to the production of excess red blood cells, and scarring within multiple organ sites. Such scarring can prominently happen in the pancreas, leading to diabetes, or the liver, eventually leading to liver failure. Specialized genetic testing (which have only become available within the last 10 years) subsequently documented that Jack was a carrier for both mutations for this disease tested. Because he had 1 copy of each gene mutation, he was at much higher risk than the average population for clinical manifestations of iron overload, even though he did not formally have hemochromatosis, the disease. This meant that Jack had to be much more vigilant about not consuming excess iron, and once again, could probably benefit from regularly donating blood.

This case points to the importance of really understanding the body as a system with a multitude of interrelated connections, as well as looking for the root cause of symptoms, rather than simply suppressing them. The presentation of premature hypertension and a slightly low serum potassium were clues in Jack's history which later led to the correct underlying cause and therefore, targeted treatment for his hypertension. There are many anti-hypertensive medications in our armamentarium, but simply applying more medications in the hopes of lowering his numbers without first investigating the root cause of his hypertension was not the solution. Although indiscretionary dietary practices on his part definitely contributed to Jack's lab abnormalities, we now know through specialized genetic testing, that his risk for eventual diabetes and liver damage are actually much higher than the average patient. This piece of information, in turn, will allow Jack to be even more careful with his diet, which will ultimately prevent the manifestation of his genetic tendencies. Jack's situation also nicely demonstrates that most diseases are preventable, starting with the appropriate diet and lifestyle practices, even in the presence of certain genetic tendencies.