Bo Norberg
How we wish to be cited:
Norberg B. Oral high-dose cobalamin for B12-dependent polyneuropathy [case 11]. Rondel
2002; 11. URL: http://www.rondellen.net
Oral high-dose cobalamin for B12-dependent polyneuropathy
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Summary. Advanced deficiency of vitamin B12 with polyneuropathy may occur in the absence of anemia. Such a deficiency may successfully be treated with oral high-dose cobalamin. Since B12 deficiency in the aged is often combined with folate defieciency, the combination of oral high-dose cobalamin with oral high-dose folic acid is suggested. This case report describes the career of a modern post-industrial patient. | |
Bo Norberg |
An educational problem
One stumbling-block of medical pedagogy is that the typical patient of the textbooks
– usually the sickest still alive – is rare. The problem is prominent in the
management of cobalamin deficiency, which in contemporary Sweden generally is discovered
and treated in early stages (cf 1).
An active man with brittle body
An active scientist, a man born 1924, passed the lobby of the university hospital in a
January day, 1998. In passing, he told a younger coworker, who crossed his track, that he
was just fine, that his present mistress was fantastic, his psychotherapist wonderful, and
that he had scheduled a program for his own personal rehabilitation.
The coworker felt that something was wrong and offered a consultation in an outdoor clinic for student training. The scintist accepted and turned up at the clinic 10 weeks later, a vigorous 74-year-old man, length 160 cm, weight 70 kg. During the preceding year, he had voluntarily slimmed himself 15 kg and was now able to walk 5 km in one hour.
History
The patient had suffered from tuberculosis in his teens, was later nursed in special
hospitals for periods, and at least one "therapeutic pneumothorax" had been
performed on his right lung. The patient was a smoker between 13-56, at worst 30-40
cigarettes daily. He stopped smoking in an advanced stage of emphysema. "Now, Mr.
Smith, you have to choose between smoke and air!"
The patient had a coronary by-pass 1987. Now he had 14 medicines for bronchospasm, angina pectoris, high blood pressure, low back pain, enlarged prostate gland with difficulties of urine voiding, and impotence due to erectile dysfunction.
Physical examination
The patient had signs of emphysema, bronchospasm, and chronic bronchitis. To the surprise
of the physician, the patient did not respond, when his plantar reflexes were tested
– he only appeared absent-minded. With the temperament of the patient in mind, the
physician had expected him to jump up on to his pillow, when his foot soles were
scratched. Nor did the patient react, when his vibration sense was tested by a tune fork
against the external protuberances of his ankles.
Laboratory tests
Laboratory tests verified the suspicion of vitamin B12 deficiency. The hemoglobin value
was 137 g/L with macrocytes, mean corpuscular volume (MCV) 105 fL. Serum cobalamins were
low, 31 pmol/L. Serum folates were close to the lower limit of the reference range, 10
nmol/L. The plasma homocysteine in fasting state was elevated, 60 micromol/L, with a
pathological increase four hours after a methionine load, 110 micromol/L. Serum gastrin
was high, 1,360 ng/L (i.e. ten times the upper reference limit), suggesting a chronic
atrophic gastritis. "My digestion is perfect! I can always drink as much coffee as I
wish."
Diagnosis and management
The state of the patient was interpreted as cobalamin deficiency with polyneuropathy. The
deficiency was supposed to be due to an atrophic gastritis with vitamin B12 malabsorption.
As remission therapy, the patient was treated with oral high-dose cyanocobalamin
(Behepan), 2 mg daily, oral high-dose folic acid (Folacin), 10 mg daily, and pyridoxine 40
mg daily. At follow-up 6 weeks later, the sensitivity of foot soles and vibration sense in
the ankles had returned, although still impaired. Serum cobalamins had risen tenfold to
352 pmol/L.
Monitoring six months after the start of remission treatment showed that red blood cells were normalized with mean corpuscular size 92 fL. Serum cobalamins had risen to 522 pmol/L. Plasma homocysteine, fasting and after methionine loading, was normal. Twelve months after therapy start, the sole sensitivity and the vibration sense were deemed normal. Maintenance therapy was continued with oral high-dose cobalamin, 1 mg daily, and oral high-dose folic acid, 5 mg daily.
In correlation with cobalamin/folate therapy, the patient improved and tidied up in mind and life. Some research was completed. However, his body tapered off. Attacks of angina pectoris and atrial fibrillation became more frequent and worse. About 30 months after the first encounter, he died suddenly by a heart infarct.
Discussion
The present case report supports the view that polyneuropathy due to vitamin B12
deficiency may be treated by oral high-dose cyanocobalamin (1-5). The present patient had
no obvious signs of folate deficiency and pyridoxine deficiency. However, combined
deficiencies are common in old age and block the effects of cobalamin monotherapy (cf 2,
6). Thus, combination therapy with oral high-dose cyanocobalamin and oral high-dose folic
acid is recommended (cf 1,2,5).
The career of the present patient suggests that
The majority of patients with vitamin B12 deficiency in a post-industrial society are above 70 years of age (7). An ordinary Swedish patient is managed by his general practitioner (8). The present patient had direct access to all hospital specialists and was able to get all investigations and medicines fancied. On a personal level, he demonstrated increasing insight and adaptation until the inescapable end.
Bo Norberg
Referenser
Published May 15, 2002