Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histoplasma meningitis (HM) has been reported to occur primarily in association with disseminated histoplasmosis (DH). We report a case of histoplasma meningitis occurring in a patient with common variable hypogammaglobulinemia (CVH) in which no manifestations of DH were observed. L. L., a 66-year-old Caucasian male, clerical worker, developed occasional episodes of dizziness and tinnitus in mid-1971. During 1972, increasing frequency of these episodes and gradually progressive confusion were noted. In January 1973, vomiting, forther confusion, obnubilation, and a left central facial paresis developed and he was hospitalized. Physical examination revealed no pulmonary abnormalities, lymphadenopathy or hepatosplenomegaly. Over the ensuing 6-week evaluation, there was occasional fever to 38.5 degrees C. Chest roentgenogram was normal. Cerebral angiography suggested a mass in the left cerebellar hemisphere. EEG was diffusely slow. Multiple CSF examinations revealed: Glucose 7-18 mg/with a normal blood glucose, protein 109-256 mg/and cells 66-140 (95 + % mononuclear). Histoplasma capsulatum was cultured from CSF but not from sputum, urine, blood or bone marrow. Skin tests for PPD, histoplasmosis, coccidiodomycosis, blastomycosis, mumps, dinitrochlorobenzene and streptokinase-streptodornase were negative then and 6 months later. Histoplasma serum antibody was absent. Immunoglobulin analysis revealed IgG 430 mg %, IgA 46 mg %, and IgM 35 mg %, which with the history and skin test results suggested CVH. Treatment with 2.51 gm of amphotericin B given intravenously over a 3-month period resulted in complete reversal of all neurologic signs and clearing of the confusion. The remission has been maintained for two years. This case represents a primary infection of the CNS by histoplasma. The relationship between the HM and the CVH will be discussed.
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PMID:Histoplasma meningitis with common variable hypogammaglobulinemia. 61 43

A case of polyarteritis nodosa (PN) in childhood involving various organs such as the gastrointestinal tract, skin, CNS, kidneys and liver with hypogammaglobulinemia is reported. This 6 month old girl was admitted to our hospital with vomiting, diarrhea, bloody stools with mucous and weight loss. For the past 5 months she had these abdominal symptoms. She was diagnosed as having PN of the Kussmaul-Maier variety on the grounds of the biopsy of skin lesion where a necrotizing vasculitis was found. Prednisolone and methylprednisolone pulse treatment were not effective in suppressing the progress of the disease. At the age of 1 year 7 month a combination therapy of prednisolone and immunosuppressants (cyclophosphamide) was started and this was found to be effective. She was discharged when she was 2 year and 2 month. The dosage of prednisolone was tapered as the activity of the PN decreased and she did well with a maintainance dosage of 9.5 mg/day. At 3 year 6 month of age she suddenly developed hypertension (the plasma renin activity was found to be 16.6 ng/m/hr. and the aldosterone 220 ng/dl). CNS involvement such as spinal cord dysfunction, left sided convulsions, cerebral hemorrhage developed 5 months later. Methylprednisolone pulse therapy was performed 3 times and 2 mg/kg/day of prednisolone was administered. In spite of this therapy she passed away with a massive cerebral hemorrhage at the age of 4 year 8 month. Unfortunately an autopsy was not performed. Results of the immunological tests proved that the hypogammaglobulinemia was a common variable immunodeficiency (CVI). It has been reported that primary immuno-deficiency syndrome is often associated with collagen disease and auto-immune disease. This lack of the defense mechanism against the virus or extra antigen could be related to the onset of collagen and auto-immune disease. As the correlation between CVI and PN has not been clarified this case is of interest as concerns the cause of PN.
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PMID:[A case of hypogammaglobulinemia associated with polyarteritis nodosa presenting a variety of symptoms in childhood]. 197 16

A boy aged 6 months who presented with poor weight gain, diarrhoea, and infection with Pneumocystis carinii was found to have congenital hypogammaglobulinaemia, which did not improve despite monthly treatment with intravenous gammaglobulin. At the age of 3 years and 2 months he developed severe vomiting and diarrhoea due to cryptosporidiosis, which failed to respond to conventional treatment. Infusion of hyperimmune bovine colostrum produced against parasite antigen, given by nasogastric tube, was started after symptoms had persisted for three weeks. His vomiting and diarrhoea resolved within five days of treatment, and oocysts were no longer seen in the stools after eight days. Later, however, he developed a rare complication, and oocysts were found in the common bile duct. Hyperimmune bovine colostrum may be useful in the treatment of many patients with immunodeficiency disorders.
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PMID:Remission of diarrhoea due to cryptosporidiosis in an immunodeficient child treated with hyperimmune bovine colostrum. 309 62

Male patients with the X-linked lymphoproliferative syndrome (XLP) have an inherited immune deficiency to Epstein-Barr virus (EBV) infection that results in fatal infectious mononucleosis (IM), acquired hypogammaglobulinemia- or agammaglobulinemia, virus-associated hemophagocytic syndrome, and non-Hodgkin's malignant lymphoma (ML). A clinicopathologic analysis of 17 patients with XLP who developed ML was performed. The median age of the patients at the time of diagnosis was 4.0 years (range, 2-19 years). The median overall survival was 12 months (range, 1-216 months). Eight patients had maternally related male relatives with ML. Other phenotypes of XLP were documented in male relatives of the remaining nine patients. Common presenting symptoms were fever, nausea, vomiting, and abdominal pain. Nine patients had "B" symptoms. All ML occurred at extranodal sites. The intestines, most commonly ileocecal, were involved in 76.5% of the cases. Thirteen patients had localized disease (Stages I and II) and four patients had advanced disease (Stages III and IV). A diffuse histologic pattern of growth was observed in all cases. The distribution of histologic subtypes included small noncleaved (41.2%), large noncleaved (17.6%), immunoblastic (17.6%), small cleaved or mixed cell (11.8%), and unclassifiable (5.9%) ML. Surgical resection, radiation therapy, and chemotherapy resulted in disease-free survivals of up to 192 months in eight patients (median 114 months; range, 12-192 months). Eight of 17 patients (47%) are still alive. A median survival of only 6.0 months (range, 1-12 months) was observed in the nine patients who died. No residual ML was found at autopsy. The small noncleaved subtype had an adverse prognosis (seven of nine deaths versus one of eight survivors; P less than 0.05). Bacterial infection was the major cause of death (seven of nine patients). Characteristics that distinguish ML in XLP from other ML include a maternal family history of XLP, early age of onset, acquired hypogammaglobulinemia, post-EBV infection, and ileocecal involvement.
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PMID:Malignant lymphoma in the X-linked lymphoproliferative syndrome. 381 12

Giardia lamblia is the first protozoan to be identified and recognized as an important pathogen in human disease. We studied 8 pediatric patients with giardiasis in order to examine the clinical spectrum, the structural changes of the small intestinal mucosa and mainly the protozoan's ultrastructural features. The most common clinical manifestations were diarrhea, abdominal pain, anorexia, vomiting, failure to thrive. Infection was confirmed by excreted cysts in the stools in one patient, by the presence of trophozoites in duodenal aspirate and on jejunal mucosa. Giardiasis was not associated with hypogammaglobulinemia in our patients and no or only slight mucosal abnormalities were present in jejunal biopsies, except one which showed a flat mucosa. Specimens for transmissions and scanning electron microscopy were taken. We could establish the protozoan's features, its normal distribution, its relationship to intestinal mucosa and structural indications of the normal reaction of intestine with the use of ultrastructural techniques. The trophozoites colonized the proximal intestine, adhered to microvilli of columnar cells near the bases of villi, wedged or lodged in mucus. The sticky mucus producing an effective diffusion barrier to nutrients could explain malabsorption phenomena. Numerous intraluminal lymphocytes were seen, suggesting an immune response. These observations indicate that in giardiasis the clinical spectrum and structural changes of the small intestinal mucosa vary widely, suggesting a different reaction of immune system and/or a different degree of infection.
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PMID:[Giardiasis in children. Ultrastructural study of the parasite]. 664 80

A boy born healthy, developed gastrointestinal symptoms (diarrhea, vomiting, ulcerative stomatitis) and megaloblastic anaemia with thrombocytopenia and neutropenia at the age of five weeks. Serum levels of folate and cobalamin were normal, but there was cobalamin-mal absorption. In his serum apo-TC2 was not detectable and immunoreactive total TC2 was very low (10% of normal values). Cultured skin fibroblasts failed to secrete functioning TC2. Pharmacological amounts of parenteral Cyanocobalamin, administered regularly, led to hematological remission and normal development. Interruption of therapy was followed by relapse within a few weeks. A coexisting hypogammaglobulinemia did not respond to cobalamin therapy at the selected dose level. A family investigation of serum TC2 concentrations and the genetic TC2 variants in 7 persons of three generations yielded evidence of autosomal-recessive inheritance of a silent TC2 allele (TC2 QLFL SEA-like). Three persons with heterozygous deficiency were asymptomatic.
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PMID:[Inherited transcobalamin-II-deficiency: clinical, genetic studies and diagnosis using cultured fibroblasts]. 666 2

We describe a familial form of recurrent acute, life-threatening secretory diarrhea associated with distinctive jejunal histologic changes and IgG2 subclass deficiency. Symptoms begin abruptly with anorexia and vomiting, and progress within hours to massive secretory diarrhea and shock with profound neutropenia and hypoproteinemia, including hypoalbuminemia and hypogammaglobulinemia. Affected survivors recover quickly and thereafter grow and develop normally. Biopsy specimens obtained during remission from 3 adults and 11 children show club-shaped jejunal villi broadened by edema and histiocytes with imbibed fluid; the overlying intestinal epithelium and brush border appear normal, but the basement membrane is interrupted in some areas. No characteristic microorganisms have been identified in association with the syndrome. Clinical manifestations cease in the second decade, but the abnormal jejunal histologic pattern persists into adult life. Female and male patients are equally affected, although all fatal cases have been in female subjects. Inheritance appears dominant with variable penetrance: one family member without a history of diarrhea has characteristic biopsy findings and another appears to be an obligate carrier with normal biopsy findings. Affected individuals have a reduced serum concentration of IgG2. We believe that this familial enteropathy is a unique entity, not previously described.
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PMID:Familial enteropathy with villous edema and immunoglobulin G2 subclass deficiency. 862 57

Protein-losing enteropathy (PLE), the manifestation of a diverse set of disorders, is characterized by excessive loss of plasma proteins into the affected portions of the gastrointestinal tract, and this results in hypoalbuminemia. A 5-month-old breastfed boy presented severe PLE with hypogammaglobulinemia, hypocalcemia, and hypomagnesemia induced by an egg allergy. He developed hypocalcemic convulsions. The diagnosis of PLE was confirmed by elevated fecal alpha1-antitrypsin clearance and a positive finding on a protein-losing scintigram. His allergy to egg delivered through maternal milk was confirmed as the cause of PLE, since the mother's elimination of egg from her diet improved his condition and maternal egg challenge provoked symptoms of diarrhea, vomiting, and elevated alpha1-antitrypsin clearance. At the time of writing, he is 22 months old and has experienced no further episodes after the elimination of egg-containing food.
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PMID:Protein-losing enteropathy associated with egg allergy in a 5-month-old boy. 1836 Nov 5

A 64-year-old woman with a progressive marginal zone lymphoma for which she had received induction therapy with six courses of rituximab and fludarabine presented with fever while receiving maintenance therapy with rituximab. In addition to the fever she complained of nausea, vomiting, weight loss and fatigue. After an extensive diagnostic procedure no cause was found for the fever. Finally, additional testing showed a positive polymerase chain reaction (PCR) for enterovirus in the cerebrospinal fluid and faeces. Because the immunoglobulin G level of our patient was 4.06 g/l (normal values 5.2 to 16 g/l), she was treated with intravenous immunoglobulins (IVI g) weekly with the goal to maintain an IgG level above 10 g/l. This resulted in a significant rise in anti-enteroviral antibodies from 10 IE /ml to 106 IE /ml. One month after treatment with IVI g, while withholding the rituximab, the PCR for enterovirus on faeces was negative and antibodies to the enterovirus in the serum had returned to normal levels. Rituximab can cause a prolonged B-cell deficiency resulting in hypogammaglobulinaemia. We believe that treatment with ritxumab may have played a significant role in the development of this rare central nervous system infection.
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PMID:Enteroviral encephalitis in a patient with a marginal zone lymphomatreated with rituximab. 2050 71

Carbamazepine is used to control seizures. Its common side effects are sleep disorders, anorexia, nausea, vomiting, polydipsia, irritability, ataxia, and diplopia. Involvement of the immune system is rare, and few cases of decreased immunoglobulin levels have been reported. We describe a patient with low immunoglobulin levels due to carbamazepine use who presented with recurrent urinary tract infection. Intravenous immunoglobulin was administered, and immunoglobulin levels increased to safer levels after discontinuation of carbamazepine. Previous reports describe severe infection after carbamazepine-induced hypogammaglobulinemia. Therefore, in patients using antiepileptics, particularly carbamazepine, serum immunoglobulin levels should be checked in those with recurrent infections.
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PMID:Carbamazepine-induced hypogammaglobulinemia. 2225 25


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