The following case studies are not actual patients. They combine elements from different cases to emphasize important aspects of vitamin B12 deficiency.
Case Study 2
An 85-year-old female with a 15-year history of Parkinson disease (PD) is seen for her regularly scheduled follow up with her neurologist.
On review of symptoms, family members report that she has become more withdrawn and irritable in the last 6 months. They also report that activities she previously accomplished without difficulty, such as going to church, seem to exhaust her. She acknowledges this symptom, stating that she feels her stamina is much lower than at the time of the last visit.
She and her family do not report an appreciable difference in or worsening of her motor symptoms, but they do report that she has had some hallucinations, in the form of seeing farm animals periodically in her room. Her current medications include Stalevo™(carbidopa, levodopa, and entacapone), amantadine, Evista® (raloxifene hydrochloride), Effexor® XL (venlafaxine hydrochloride), Detrol® LA (tolterodine tartrate), Mirapex® (pramipexole dihydrochloride), and Ambien® (zolpidem tartrate).
She denies any obsessive or compulsive behaviors or any recent trauma, but she does admit having a decreased appetite and eating little or no meat. Her family describes her nutritional intake as poor, stating that she is just getting by on “tea and toast”.
Her social history reveals a widowed elderly woman who lives with her son and daughter-in-law. She had lived independently until 5 years ago when completing her activities of daily living (ADLs) became too difficult. She currently has a home health nurse visit once a day to assist with ADLs and noontime medications while her family is at work.
General exam reveals a frail, thin female with skin irritation and slight amount of saliva evident at the right corner of her mouth (the side where her PD symptoms are more pronounced). She has slight puffiness but no pitting of her ankles bilaterally.
Neurological exam reveals that she is alert and oriented to person, place, and year. She remembers 3 out of 3 items but can only recall one of three items 3 minutes later. She has definite facial masking and decreased blink rate. Cranial nerve exam reveals moderate hypophonia (low voice volume) and an intermittent tremor. She is moderately stooped with a slight tilt to the right, and she has difficulty rising from a chair without assistance even though her strength is normal. She has a mild to moderate intermittent resting tremor, worse on her right side. Sensory exam reveals decreased vibratory thresholds in both legs up to her ankles. Reflexes are 3+ out of 4 with crossed adductor spread in her legs, and her plantar reflex shows positive Babinski bilaterally.
Her neurologist orders some routine laboratory studies, including a CBC with smear and chemistry panel. In addition, the neurologist decides to get a serum B12 level because she is considered at high risk for a vitamin B12 deficiency, and many of the symptoms of PD can also be attributed to vitamin B12 deficiency. Click here to view Table 1.
Results from the CBC with smear demonstrate no evidence of anemia. The chemistry panel is within normal limits with the exception of a slightly elevated serum creatinine (1.5 milligrams per deciliter [mg/dL]). Her serum B12 level is 225 pg/mL, within the laboratory’s normal range of 180–900 pg/mL. The neurologist considers this value as “low-normal” and requests confirmatory testing with MMA and HCY levels.
Results of Confirmatory Testing
1,000 nmol/L* = 1 µmol/L
376 nmol/L = 0.376 µmol/L
*nanomols per liter
Her HCY is elevated at 18 µmols/L; however, the neurologist recognizes that this finding alone is not considered diagnostic given that Levodopa has been known to alter HCY levels. Her MMA is borderline at 0.38 µmols/L, but again, this finding is not diagnostic.
Although PD can explain most of her symptoms, vitamin B12 deficiency can also account for some of them. Her age is a risk factor for atrophic gastritis, and her diet seems to be deficient in protein so both malabsorption and malnutrition could contribute to borderline vitamin B12 deficiency.
Given the uncertain nature of the test results, her neurologist discusses vitamin B12 supplementation with her. She expresses disinterest in oral supplementation, stating “if I have to take one more pill, I will scream.” Because the laboratory findings are ambiguous, the neurologist and she agree to monitor her status rather than start injection therapy immediately.
On her return visit 6 months later, the patient’s serum vitamin B12 is 189 pg/mL, and both her Hcy and MMA levels have increased. The neurologist orders anti-parietal cell antibody and anti-intrinsic factor antibody tests to rule out pernicious anemia. Both tests are negative. She is started on 1,000 mcg of IM cyanocobalamin for 5 days, followed by monthly injections of 1,000 mcg of IM cyanocobalamin. The neurologist makes arrangements for the home health nurse to administer the injections.
At the next visit, the patient and family report she is less fatigued, less irritable, and less withdrawn. There is no worsening of motor symptoms; however, she still experiences occasional hallucinations.
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