Cases reported "Vitamin B Deficiency"

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1/16. Acute axonal polyneuropathy in chronic alcoholism and malnutrition.

    In contrast to the classic, slowly progressive polyneuropathy in alcoholic patients, acute forms, clinically mimicking guillain-barre syndrome, are rare. We present a patient who developed motor weakness and sensory loss in all four limbs within four days. Laboratory data were consistent with long-term alcohol abuse and documented thiamine deficiency. Repeated cerebrospinal fluid examinations were normal. Electrophysiological studies showed an acute sensorimotor polyneuropathy with predominantly axonal involvement. We conclude that acute alcoholic neuropathy has to be distinguished from guillain-barre syndrome and other forms of acute polyneuropathy by using clinical, laboratory, and electrophysiological data. Both ethanol toxicity and vitamin deficiency could play a role in the pathogenesis. ( info)

2/16. Potential association of thyrotoxicosis with vitamin B and folate deficiencies, resulting in risk for hyperhomocysteinemia and subsequent thromboembolic events.

    OBJECTIVE: To describe a patient with severe thyrotoxicosis attributable to Graves' disease who had a thrombotic cerebrovascular accident and hyperhomocysteinuria, which resolved on correction of the thyrotoxicosis, and to present findings in a pilot study undertaken to investigate the relationship among thyrotoxicosis, homocysteine, folate, and vitamin B(12). methods: We present a case report of the index case, with clinical and laboratory details. For the investigative analysis, 21 patients who were 18 to 50 years old and had newly diagnosed, untreated Graves' disease and 10 age-and sex-matched euthyroid control subjects were studied. Of the patients with Graves' disease, 11 underwent studies both at diagnosis and after treatment. fasting blood tests were performed for thyrotropin, free thyroxine, homocys-teine, vitamin B(12), folate, and methylmalonic acid, a marker of vitamin B(12) deficiency. RESULTS: Vitamin B(12), folate, homocysteine, and methylmalonic acid levels were not significantly different between the thyrotoxic and control or posttreatment groups. In patients with thyrotoxicosis, however, free thyroxine was positively correlated with both homocysteine (r = 0.67; P = 0.03) and methylmalonic acid (r = 0.89; P = 0.003). CONCLUSION: The positive correlation between free thyroxine levels and both homocysteine and methylmalonic acid suggests that thyrotoxicosis may be associated with functional vitamin B(12) deficiency. Such a deficiency may result in clinically important hyperhomocysteine-mia. ( info)

3/16. Large-artery stroke in a young patient with Crohn's disease. role of vitamin B6 deficiency-induced hyperhomocysteinemia.

    An increased incidence of ischemic stroke has been reported in patients with Crohn's disease. Cerebral infarcts are usually considered as a complication of the hypercoagulable state associated with this inflammatory bowel disease (IBD). The association between Crohn's disease, hyperhomocysteinemia and large-artery stroke of the young has rarely been reported. A 39-year-old woman, with prior medical history of Crohn's disease and hypertension, presented with an ischemic stroke of the left internal carotid artery (ICA) territory. Etiological workup disclosed bilateral high-grade ICA stenosis and atheroma of the subclavian and vertebral arteries. Exhaustive search for prothrombotic factors showed inflammation, with an increased level of fibrinogen and factor ix, and a marked hyperhomocysteinemia. Both vitamin B1 and vitamin B6 plasmatic levels were decreased. Heterozygous C677T methylene-tetrahydrofolate reductase gene mutation was present. This observation highlights the combined proatherogenic effect of vitamin b deficiency-induced hyperhomocysteinemia and inflammation leading to large-artery stroke of the young in the setting of Crohn's disease. Our case report stresses the importance of vitamin deficiency screening in patients with IBD in terms of stroke prevention. ( info)

4/16. sodium valproate -- induced skeletal myopathy.

    The authors report a case of skeletal myopathy in a four-year-old boy on long-term sodium valproate therapy for secondary epilepsy due to neurocysticercosis. He presented with clinical features of limb girdle weakness. EMG revealed features of myopathy. carnitine deficiency due to sodium valproate was suspected and plasma carnitine levels were found to be low. sodium valproate was withdrawn. L-carnitine supplementation resulted in marked clinical recovery as well as rise in plasma carnitine levels. ( info)

5/16. Imerslund-Grasbeck syndrome associated with recurrent aphthous stomatitis and defective neutrophil function.

    Vitamin B(12) deficiency is a well-known cause of recurrent aphthous stomatitis (RAS). However, the mechanism by which this deficiency causes the stomatitis is not well understood. Imerslund-Grasbeck syndrome (IGS) causes vitamin B(12) deficiency and proteinuria due to a defect in the vitamin B(12) receptor. We sought to determine whether the RAS observed in IGS patients is associated with neutrophil dysfunction. We report 3 infants with vitamin B(12) deficiency due to IGS, who presented with borderline or normal hemoglobin concentrations, RAS, and a neutrophil function defect. All 3 patients were homozygous for a splice site mutation affecting exon 4 of the AMN gene. A direct correlation was observed between low serum vitamin B12 levels and defective neutrophil function (low chemotaxis and elevated superoxide production) in the patients. Vitamin B(12) therapy led to an immediate resolution of aphthous stomatitis and full correction of neutrophil function. We demonstrated that serum vitamin B(12) deficiency is associated with a neutrophil chemotactic defect and RAS in IGS patients. We suggest that the RAS observed in these patients is due to this defect. ( info)

6/16. Vitamin deficiency in the elderly.

    The oral manifestations of vitamin deficiencies are often the first indications of malnutrition. This is especially true among the elderly, whose more frequent physical and/or psychological disorders may prevent them from eating a balanced diet. The following is a guide to the dentist, who is often the first health professional to recognize nutritional deficiencies in this age group. ( info)

7/16. vitamin b deficiency neuropathy. case reports.

    Poor nutrition is common throughout the third world. The US also has examples among recent Asian and Latin American immigrants, alcoholics, the homeless, and former prisoners of war. All of these groups are susceptible to long-term pathologic damage, depending on the degree of malnutrition which they experience. The peripheral nervous system is quite vulnerable to impairment and damage from vitamin B loss. ( info)

8/16. hyperpigmentation in megaloblastic anemia.

    hyperpigmentation of the hands and feet developed in a 65-year-old Korean woman who had undergone a total gastrectomy and esophagojejunostomy due to early gastric cancer 7 years previously. A diagnosis of megaloblastic anemia due to vitamin B12 deficiency was made. In the areas of pigmentation, there were abnormally large nuclei in the keratinocytes. All of these findings were reversible upon the administration of vitamin B12. Ultrastructurally, there were many intracytoplasmic desmosomes, numerous aggregated bundles of tonofilaments, and highly condensed keratohyalin granules. The pathophysiologic mechanism of vitamin B12 deficiency associated with pigmentary disturbances and change of nuclear size is discussed. ( info)

9/16. Vitamin B 1, B 2 and B 6 deficiency in neurological disorders.

    The activities of the red blood cell enzymes transketolase, glutathione reductase, and glutamic oxaloacetate transaminase were measured with and without in vitro addition of their respective coenzyme components thiamine, riboflavin, and pyridoxine in a group of patients with neurological disorders which may have been caused by malnutrition, intestinal malabsorption, hepatic failure or neoplasms arising outside the nervous system. The incidence of thiamine deficiency was 31%, of riboflavin deficiency 22% and of pyridoxine deficiency 6%. alcoholics in particular suffered from deficiencies of vitamin B 1, and B 2. There was a correlation of vitamin B 1 and B 2 deficiency and signs of a cerebellar and/or brainstem lesion. The most frequent symptoms in this connection were gait disturbances and oculomotor signs like spontaneous and gaze nystagmus, disturbed eye tracking, diminished optokinetic nystagmus, decreased ability to suppress vestibular nystagmus by fixation. These signs hardly ever occurred in alcoholic patients who showed no deficiency of vitamin B 1, B 2 or B 6. Whenever they do appear, a vitamin B supplementation has to be performed in order to prevent the manifestation of Wernicke's encephalopathy, cerebral or cerebellar atrophy. alcoholics showed the same incidence of polyneuropathy, whether they suffered from a deficiency of B vitamins or not. Deficiencies of vitamin B 1, B 2 or B 6 were also found in patients with intestinal malabsorption and polyneuropathy, diabetic polyneuropathy, optic atrophy, myelopathy and cerebellar ataxia of unknown etiology, neurological manifestations of neoplasms arising outside the nervous system, B 12 myeloencephalopathy and Thevenard's syndrome. ( info)

10/16. Strachan's syndrome 30 years after onset.

    While a prisoner-of-war in Malaya from 1942-1945, a 29-year-old man developed a painful sensorimotor neuropathy, bilateral central scotomata and sensorineural deafness. Examination 34 years later, after a long period of adequate nutrition, revealed considerable residual deficit. Nerve conduction studies suggested axonal degeneration with prominent collateral reinnervation. This case of Strachan's syndrome is reported to draw attention to the limited functional recovery and to focus attention on this condition at a time when famine conditions are rife in Southeast asia. ( info)
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