Cases reported "Anemia, Pernicious"

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1/30. Relationship between pernicious anaemia and gastric neuroendocrine cell disorders.

    The incidence of gastric carcinoid tumours is increasing. This rise is probably due to the number of gastroscopies and improved histological techniques. The majority (65%) of these gastric tumours is associated with chronic atrophic gastritis and pernicious anaemia. In this article two patients are presented, one with pernicious anaemia and gastric neuroendocrine cell hyperplasia and one with pernicious anaemia and multiple gastric carcinoids. These neuroendocrine cell disorders have a relatively favourable prognosis. Therefore, a wait-and-see policy was preferred. The pathogenesis, clinical symptoms, diagnosis, prognosis and treatment of these different neuroendocrine cell manifestations are discussed. We recommend performing a gastroscopy at the time of diagnosis for young patients with pernicious anaemia, and whenever abdominal problems, unexplained weight loss or aggravation of the anaemia arise.
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2/30. Coexistent lymphoid interstitial pneumonia, pernicious anemia, and agammaglobulinemia.

    immunologic factors have been incriminated in the pathogenesis of lymphoid interstitial pneumonia. The discovery of a patient with coexistent lymphoid interestitial pneumonia, pernicious anemia, and common variable hypogammaglobulinemia focused attention on the possible autoimmune nature of this pulmonary disease. Extensive immunologic studies demonstrated a noticeably impaired bonemarrow-dependent (B cell) system and intact thymus-dependent (T cell) system. No evidence of humoral or cellular hypersensitivity to homologous lung determinants was found.
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3/30. common variable immunodeficiency with mosaic trisomy 8: report of one case.

    This case study reported a 17-year-old female of common variable immunodeficiency (CVID) associated with bronchiectasis, pernicious anemia and mosaic trisomy 8. Clinically this patient presented with recurrent sinopulmonary infections, intractable diarrhea, macrocytic anemia, and primary amenorrhea. Immunological tests showed pan-hypogammaglobulinemia and a decrease of peripheral blood B cells (4%) and CD4 cells (25%). Lymphoproliferative responses to mitogen (PHA) and specific antigen (BCG) were profoundly impaired in the patient in comparison to those in control. Production of interleukin 4 (IL-4) and gamma interferon (IFN-gamma) in the in vitro lymphoproliferation was also profoundly depressed. Pernicious anemia demonstrated by larger MCV (112.9 fl) and hyper-segmental granulocytes on peripheral blood smear responded to parental administration of vitamin B12. Interestingly, she had a mosaic trisomy 8 in peripheral blood mononuclear cells but normal 46XX karyotype in the bone marrow cells. To our knowledge, this is the first case of CVID associated with mosaic trisomy 8 reported in the literature. As the case exemplifies, CVID should be considered when the physicians evaluate the patient presenting with recurrent sinopulmonary infections, diarrhea, malnutrition, and pernicious anemia. It requires further study to explore whether the genes in the chromosome 8 are linked to CVID.
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4/30. Development of rheumatoid arthritis in a patient with pernicious anemia: case report.

    Very few cases of rheumatoid arthritis combined with pernicious anemia have been reported in the world literature and none in the Chinese literature. A 62-year-old female initially presented with anemia. Pernicious anemia was diagnosed by characteristic blood and bone marrow morphology. Laboratory data showed a deficiency of vitamin B12 and positive anti-gastric parietal cell antibodies. Her anemia improved after vitamin B12 therapy. Painful swelling of multiple joints developed 6 years later. The clinical presentation supported a diagnosis of rheumatoid arthritis. We report herein a rare case of rheumatoid arthritis and pernicious anemia in the same ethnic Chinese patient. We also review the literature and discuss a possible association between a non-organ-specific autoimmune disease, rheumatoid arthritis, and an organ-specific autoimmune disease, pernicious anemia.
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5/30. A female with asymptomatic primary biliary cirrhosis associated with pernicious anemia.

    We experienced a female case with asymptomatic primary biliary cirrhosis that was associated with pernicious anemia after 16 years from the onset. She was 52 years old when she first visited a clinic in 1981 for liver dysfunction treatment. Antimitochondrial antibody was negative and antipyruvate dehydrogenase complex antibody was positive in a low titer in its immunoglobulin (Ig)M type. Histological examination of her liver revealed a presence of definite chronic non-suppurative destructive cholangitis with numerous epithelioid cell granuloma. She had been given 600 mg of the oral daily dose of ursodeoxycholic acid since 1992. Macrocytic anemia incidiously appeared in September 1999. An immunological examination detected negative antiparietal cell antibodies and positive anti-intrinsic factor antibodies. Her bone marrow smear showed numerous megaloblasts and serum vitamin B12 in her blood was low at 99 pg/mL. Severe reversed atrophic-type gastritis (type A gastritis) was demonstrated by the use of dye-endoscopy with congo red. Her macrocytic anemia dramatically improved after intramuscular administration of vitamin B12. In conclusion, attention should be given to the association of pernicious anemia during the follow up of primary biliary cirrhosis.
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6/30. Pernicious anemia: presentations mimicking acute leukemia.

    Vitamin B12 deficiency can cause profound alterations in the bone marrow. These alterations can mimic the more serious diagnosis of acute leukemia. The two patients described in this report were originally suspected of having acute leukemia or myelodysplasia on the basis of the bone marrow smear, and induction chemotherapy was considered. However, after further studies, they were both found to have vitamin B12 deficiency, and parenteral vitamin B12 administration resulted in normalization of the bone marrow.
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7/30. Slowly progressive type 1 diabetes mellitus associated with vitiligo vulgaris, chronic thyroiditis, and pernicious anemia.

    A 81-year-old woman was diagnosed as having diabetes mellitus (DM) at 58 years of age. She started insulin therapy the following year, but her blood sugar levels were poorly controlled. At the age of 75, she tested positive for the anti-GAD antibody (7.8 U/ml) and was diagnosed as having slowly progressive type 1 DM (SPIDDM), as well as vitiligo vulgaris. At 78 years of age, chronic thyroiditis was diagnosed after positive tests for anti-thyroid peroxidase antibody and anti-thyroglobulin antibody. At the age of 81, general fatigue and jaundice appeared concomitantly with severe anemia, with Hb levels at 5.2 g/dl. Low serum vitamin B12 levels and the finding of erythroblastic hyperplasia with megaloblasts in bone marrow led to the diagnosis of pernicious anemia. anemia was alleviated by intramuscular injections of vitamin B12. The patient developed chronic thyroiditis, vitiligo vulgaris, and pernicious anemia concomitantly with SPIDDM, and was diagnosed as having polyglandular autoimmune syndrome type III. attention should be paid to these potentially associated autoimmune diseases in daily practice during the follow-up of SPIDDM patients.
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8/30. Pernicious anemia and widespread absence of gastrointestinal endocrine cells in a patient with autoimmune polyglandular syndrome type I and malabsorption.

    CONTEXT: Autoimmune polyglandular syndrome type I (APS I) is characterized by multiple endocrine gland failures, with other manifestations such as gastrointestinal (GI) symptoms. OBJECTIVE: The objective of the study was to study the histopathological and immunological findings in the GI mucosa of a patient with typical features of APS I, malabsorption, and pernicious anemia. DESIGN AND PATIENT: Biopsies from the GI tract of a patient with APS I were immunostained with chromogranin for GI endocrine cells (GIECs). Blinded slides were graded for numbers of endocrine cells. Normal gastric mucosa was exposed to the patient's serum to test for circulating anti-GIEC and antiparietal cell antibodies using indirect immunofluorescence. SETTING: The study was conducted at the Departments of pediatrics and Medical gastroenterology in an academic medical center. RESULTS: The patient's GI mucosa demonstrated absence of GIECs throughout, including gastric gastrin-secreting cells, and her laboratory tests for serum gastrin levels were low normal. Both GIECs and parietal cells were absent in her gastric corpus. The patient's serum contained anti-GIEC antibody but no antiparietal cell antibody. CONCLUSIONS: These observations suggest that GIECs in APS I are subject to an autoimmune destruction that can cause widespread GIEC loss. This could explain the GI dysfunctions that are often noted in the syndrome including malabsorption and atrophic gastric changes with pernicious anemia. We also hypothesize that absence of gastric parietal cells may result mainly from hypogastrinemia that is mainly the loss of gastrin-secreting cells rather than from immune-mediated destruction of parietal cells like that seen in the atrophic gastritis associated with adult-onset pernicious anemia.
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9/30. Pure red cell aplasia following pernicious anemia.

    A rare case of pure red cell aplasia (PRCA) in association with pernicious anemia is reported. A 40-year-old man presented with typical clinical and laboratory features of pernicious anemia and received intramuscular injections of vitamin B12, with satisfactory response. anemia recurred 6 months later despite continued therapy, and the patient was noted to have PRCA, which was treated successfully with two courses of high-dose bolus methylprednisolone therapy. His peripheral mononuclear cells before the therapy suppressed colony formation of early erythroid precursors (BFU-E) from normal bone marrow; such a suppressive effect was not found after recovery from anemia.
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10/30. Platelet peroxidase-like activity detected in mature erythroblasts from a patient with pernicious anemia.

    We report a case of pernicious anemia in which the possession of platelet peroxidase (PPO)-like activity was proved in its erythroblasts. PPO-positive cells were found in a distinct minor population of hemoglobinized (as a mean of differentiated) erythroid cells in the bone marrow before treatment, but these cells disappeared following therapy with vitamin B12. The present report is considered to be the first case to identify PPO-like activity in mature erythroblasts from the nonmalignant clone. The existence of PPO in erythroid lineage in cases with pernicious anemia is discussed.
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