La anemia perniciosa se desarrolla cuando el cuerpo no es capaz de absorber la vitamina B12 que necesita de los alimentos debido a la falta de una proteína. DISCUSSION: It was proven that atrophic gastritis with positive intrinsic anti-factor envolvendo diabetes, tireoidites, gastrite atrófica, anemia perniciosa, vitiligo. sobre todo en la anemia perniciosa (con anticuerpos anti-factor intrínseco), que gastrectomía / cirugía bariátrica y gastritis atrófica metaplásica autoinmune .
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Polyglandular syndrome is characterized by the association of autoimmune, organ-specific, endocrine and non-endocrine diseases. To present a case of polyglandular syndrome type III b accompanied by pernicious anemia and autoimmune thyroiditis.
Report the clinical case of a young patient that developed progressive and disabling peripheral neuropathy framework, triggered by vitamin B12 deficiency. There was a progressive neurological improvement after parenteral cyanocobalamin replacement, keeping the patient at ambulatory, under maintenance therapy. The importance of suspecting on polyglandular syndrome in the presence of autoimmune frameworks is important, especially those involving diabetes, thyroiditis, atrophic gastritis, pernicious anemia, vitiligo, among others.
Autoimmune polyglandular syndrome APS was first described in by Schmidt, through necropsies on patients with adrenal insufficiency, in which destructive and non-specific lymphocyte infiltration was found both in the thyroid gland as in the cortex of adrenal glands.
The Gastrltis is characterized by the association of organ-specific autoimmune diseases, endocrine and nonendocrine. The polyglandular syndrome type III, in turn, can be subdivided according to the autoimmune disease associated: This article reports a case of a young woman with polyglandular syndrome type III bwhich developed a progressive and disabling peripheral neuropathy with myelopathy, triggered by vitamin B12 deficiency.
It was proven that atrophic gastritis with positive intrinsic anti factor antibody lead to pernicious anemia that regressed after cyanocobalamin administration. Female patient 34 years old, was referred from neurologist to gastroenterologist after six months of symptoms. She had initiated the neurological symptoms with paresthesia in gastfitis lower limbs, ascending and progressive, in the hallux region which advanced gradually to the thoracic region.
After 4 months when she could no longer walk, having dizziness, loss of proprioceptive atroficz and ataxia. There was no history of alcoholism, hypertension, diabetes mellitus, hepatitis, use of illicit drugs and tattoos. There is reference to a anemi transfusion 3 years ago due to a miscarriage. Reported swimming in the river in childhood.
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At clinical examination, with regular condition, conscious, color, eutrophic, with paraesthesia and motor deficit in the lower limbs, impaired gait, using wheelchair for mobility.
The cerebrospinal fluid examination revealed no alterations. The MRI of the spine in its thoracic and lumbar regions showed multiple cold areas and modification of signal involving the cord at various levels, showing hyperintense signal on T2 at its periphery. This finding is more pronounced near the tenth thoracic vertebra region, predominantly in the anterior-medial region of the medulla. Electromyography showed polyneuropathy with pattern of axonal impairment in the lower limbs.
The patient had no gastrointestinal symptoms, but as the blood count showed anemia with hemoglobin of Pathologic result of antral biopsy revealed it to be a mild chronic atrophic gastritis in antrum with incomplete interstitial metaplasia. The intrinsic anti-factor antibody was positive and the anti-parietal cell antibody negative; the total abdominal ultrasonography revealed no alterations.
The rheumatoid factor was negative and anti-thyroglobulin anti-TGanti-tpo antibodies were positive. The dosage of vitamin B6 was 6. The serum vitamin B12 levels normalized after parenteral administration, with progressive neurological improvement.
This article reports the case of a previously healthy young patient, who starts with neurological manifestations, evolving progressively to neuropathy with myelopathy. Following, it was detected the presence of autoimmune diseases such as pernicious anemia with vitamin B12 deficiency positive intrinsic anti-factor antibody and thyroiditis with anti-thyroglobulin antibodywhich led to the diagnosis of autoimmune polyglandular syndrome type III b.
In a more advanced stage of the disease, pernicious anemia may occur as a result of vitamin B12 deficiency. Myelopathy due to vitamin B12 deficiency is manifested initially by paresthesia and weakness, affecting all four limbs in a symmetrical pattern. In advanced stages, there are paraplegia and varying degrees of spasticity, associated with hyper- or hyporeflexia, ataxia, paresthesia, alterations of deep sensitivity, cognitive dysfunction, pelvic floor disorders, decreased visual acuity.
The occurrence of sensory level is rarely observed. Response to treatment is related to the severity and time between onset of symptoms and treatment. In this case the neurological manifestations presented were consequence of pernicious anemia based on the good response to cyanocobalamin and the histological demonstration of atrophic gastritis and the presence of the intrinsic anti-factor antibody.
Few reports in the literature have described the transverse myelitis by cyanocobalamin deficiency, with welldefined sensory level, as in our case. According to Vasconcellos, the presence of sensory level denotes severe case of vitamin B12 deficiency and may be considered a finding associated with a bad prognosis. In the case presented here, the patient had flaccid and arreflex paraplegia with sensory level at T10; however, contrary evidence, it evolved with a favorable prognosis after replacement of cyanocobalamin.
The electroneuromyography in cases of polyneuropathy reveals, in general, decreased or absent sensory nerve action potentials and normal conduction velocity.
Polyglandular Syndrome Type III and Severe Peripheral Neuropathy: An Unusual Association.
This finding is most commonly found in the posterior cord of the marrow. The radiological changes may take up to 12 months to disappear. In the blood count is observed anemia and less commonly leukopenia, besides thrombocytopenia.
A bone marrow biopsy is usually hyperplastic, with a predominance of red cell precursors. In the present case there was normalization of the MCV with treatment. The dosage of the intrinsic anti-factor antibody is positive in cases of pernicious anemia. Laboratory diagnosis of vitamin B12 deficiency can be accomplished through the dosage of atroficaa or homocysteine and methylmalonic hastritis in the urine.
The detection of antibodies atroficw sufficient for the diagnosis of autoimmune disease of the thyroid. The treatment is based on the parenteral replacement of cyanocobalamin. The recovery becomes evident after months of treatment; after this period the recovery is slow and can last up to years.
In conclusion, spinal presentation of vitamin B12 deficiency in the form of transverse myelitis, as synchronous manifestation of polyglandular syndrome type III b is a rare condition, one should suspect the vit B12 deficiency when certain neurological changes are evident. The presence of sensory level is explained oerniciosa the spinothalamic tract impairment as observed in the present case gastrritis.
The most commonly cause implicated in this deficiency, according to the literature, is pernicious anemia. It is a treatable disease, if diagnosed early, have a good prognosis. Our patient showed with severe disabilities gastrittis neurological symptoms for 6 months which could explain the reversal of the neurological status. Still, the patient had sensory level, considered a poor prognostic factor in cases of myelopathy due to vitamin B12 deficiency, but that progressed well after replacement therapy.
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Gastritis Atrofica Anemia Perniciosa Failure Liver Failure Kidney / pirineosostenible report
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Sensitivity of serum methylmalonic acid and total homocisteine determination for diagnosis cobalamin and folate deficiencies. Subacute combined degeneration with high serum vitamin B12 level and abnormal vitamin B12 binding protein. Neurology in clinical practice. Clinical practice vitamin B12 deficiency. N Engl J Med. Protection of human and animal subjects.
The authors declare that no experiments were performed on humans or animals for this study. Gastritos authors declare that they have followed the protocols of their work center on the publication of patient data. Right to privacy and informed consent.
The authors have obtained the written informed consent of the patients or subjects mentioned in the article.
The corresponding author is in possession of this document. Introduction Autoimmune polyglandular syndrome APS was first described in by Schmidt, through necropsies on patients with adrenal perniclosa, in which destructive and non-specific lymphocyte infiltration was found both in the thyroid gland as in the cortex of adrenal glands. Clinical case Female patient 34 years old, was referred from neurologist to gastroenterologist after six months of symptoms.
Discussion This article reports the case of a previously healthy young patient, who starts with neurological manifestations, evolving progressively to neuropathy with myelopathy.
Ethical disclosures Protection of human and animal subjects. Conflicts of interest The authors have no conflicts of interest to declare. Received 5 February ; accepted 5 August Como citar este artigo.