“So you smoke and drink, correct?” I asked.
The patient was a 71-year-old man with a bit of shine still left in his bright blue eyes. He gazed at me with slight indignation.
“I overdo the bottle,” he conceded. He said he drank 10 to 12 beers and smoked a pack and a half of unfiltered cigarettes a day.
“You live by yourself?”
“Yeah, except I sometimes have lady visitors over.”
“Any family in the area?”
He had first been examined at a walk-in clinic near my office in Tampa, where he had been diagnosed with arthritis and folliculitis, an infection of the hair follicles. He had been prescribed 500 milligrams of the antibiotic cephalosporin twice a day and a strong anti-inflammatory drug. But the treatment hadn’t fixed his condition.
“I went back there again and told them I was worse,” he said. “They acted like I never took my medicines or tried to help myself. But I did. I still feel awful. I’m losing weight, my bowels are loose, and I’m frustrated with all this.”
I looked him over. He had slight pain and swelling in both of his lower legs, areas of broken blood vessels around his nails, compact nodules beneath the skin on his thighs, and islands of raised red spots on the skin around the hair follicles on his legs, buttocks, arms, and back. When I looked closely, I saw that he had malformed hairs, called corkscrew hairs, on his chest and abdomen.
“What do you like to eat?” I asked.
“Not much,” he said. “Just soup is about all I can keep down nowadays.”
“What kind of soup?”
“Just like chicken broth. That’s about it.”
“Nope. Never took those.”
I looked at his legs and feet and checked his circulation. His lower legs were a mix of ugly bruises, dry skin, and foul smell.
“So you going to do more than the last doc? Give me pills and send me away?”
“Patience,” I said. “I need to spend the time it takes to help you get better.”
Far from any seagoing vessel, this patient bore clear signs of a disease long associated with ailing sailors on long voyages. He had scurvy, the clinical state arising from a dietary deficiency of vitamin C (ascorbic acid). The term ascorbic acid comes from the New Latin scorbutus, meaning “scurvy.”
Scurvy killed more sailors than were lost in all sea battles during the age of sail. And here it was today, wreaking havoc on this unsuspecting man, who was helping the disease prosper with his alcoholism and his miserable diet.
“You don’t eat any fruits or vegetables?”
“Not in months. I know I should.”
My patient’s medical history fit the picture of scurvy today—an elderly, alcoholic man, socially isolated, and greatly in need of a normal diet. Because of his bleeding gums, it would have been painful to eat solid foods, even if he wanted to.
Any severe deficiency of vitamin C interferes with normal tissue synthesis because ascorbic acid maintains the enzymes responsible for making collagen, a material that binds cells and tissues together throughout the body. Without sufficient vitamin C, collagen breaks down, resulting in problems in connective tissue, bones, and dentin, a major constituent of teeth.
One of the well-known signs of scurvy is bleeding due to the breakdown of the walls of blood capillaries. Bleeding gums are common. And when the tiny capillaries of the hair follicles leak blood, the hair-producing cells don’t get what they need to produce normal hair. Malformed corkscrew hairs are the result. These problems appear after about five months on a diet deficient in vitamin C.
Tests of the patient’s blood showed that his fasting blood level of ascorbic acid was 0.08 milligram per deciliter, well below .2, the threshold for scurvy. A healthy person’s count would be .7 to 1.0 milligram per deciliter. A second, more accurate measure counted the concentration of ascorbic acid in his white blood cells. It was 3 milligrams per deciliter, also reflecting a state of deficiency. Other tests showed signs of anemia and reflected his alcohol abuse and liver damage.
In other words, this scurvy was advanced. My patient had probably gone without sufficient vitamin C for at least weeks, if not months. When the deficiency is slight, the first scurvy symptoms include lethargy, loss of appetite, poor weight gain, diarrhea, rapid breathing, fever, and irritability. If the deficiency is not treated, the signs of capillary breakdown begin to appear: bleeding gums, loosened teeth, soreness and stiffness of the joints and lower extremities, bleeding under the skin and in deep tissues, slow wound healing, and anemia. Although bleeding in various tissues is the most common serious problem in scurvy, sudden death due to heart failure has been reported in infants and adults with scurvy.
Treating scurvy is simple. I started my patient on 250 milligrams of vitamin C four times a day and gave him information on a balanced diet. I also gave him information on Alcoholics Anonymous and handed him a list of local counselors.
After a couple of weeks, he was taking a regular multivitamin and had improved his diet. Only 10 milligrams per day of vitamin C—easily obtained with an apple, a tomato, or a glass of citrus juice— is enough to prevent scurvy.
It is a curious legacy of evolution that only primates, guinea pigs, fruit-eating bats, and some kinds of fish are unable to produce vitamin C on their own; all lack the genetic information needed to make this crucial nutrient and must derive it from their diet. Among humans, the symptoms of vitamin C deficiency have been recorded as far back as 1550 B.C., and records from the Renaissance describe scurvy-afflicted sailors. In more recent times, scurvy claimed the lives of Arctic explorers, armies of the Crimean War and the American Civil War, workers during the California gold rush, and victims of the Irish potato famine.
Fortunately, severe vitamin C deficiency is uncommon in the United States. The vulnerable are those resembling my patient—elderly or alcoholic people who don’t eat fresh fruits and vegetables. Infants can also be susceptible if they are on restrictive diets, but the condition is rare among babies under 7 months old.
When it does occur in infancy, scurvy can be devastating. Problems arise in bone and cartilage development. Bone cells called osteoblasts fail to form bone matrix, and the normal conversion of growth cartilage to bone does not happen because capillaries fail to grow into the bone. Preexisting bone becomes brittle. Microscopic fractures occur. The membrane that clings tightly around bone—the periosteum—becomes loosened, and the ends of the long bones of the legs can bleed, causing excruciating pain. Such pathology often occurs only during periods of active bone growth in infants.
By contrast, my patient’s suffering was modest, and he rapidly recovered. As he started to feel better, he became less resentful of my exams and questioning. He was no longer accused of being noncompliant or a malingerer. Instead he was being treated for the symptoms of his unrecognized vitamin deficiency.
We are lucky to have a grapefruit tree at our home in Florida, and I loaded up a dozen to bring to the office. When I last saw this patient, I gave them to him.
“Thanks,” he said. “I’ll make sure to eat one every day.”
Robert A. Norman is a dermatologist in Tampa, Florida, and author of The Woman Who Lost Her Skin and Other Dermatological Tales (Routledge, 2004). The cases described in Vital Signs are true stories, but the authors have changed some details about the patients to protect their privacy.