5 Matching Annotations
  1. Last 7 days
    1. c.518G>A

      Case#: T.II.1, subject 48. Male. Age of Onset: 1.5 y.o. Age of evaluation: 21 y.o. Origin in UK, Caucasian.

      *DiseaseAssertion: Cytopenia, Evans syndrome

      *FamilyInfo: Father had died post autologous HSCT for non-Hodgkin lymphoma. See "supplement 1".

      CasePresentingHPOs: ORPHA:1959

      CaseHPOFreeText: Severe Psoriatic Arthritis (only patient noted to have it within the study), received a Hematopoietic stem cell transplantation and was one of nine affected mutation carriers still alive and one of three who was more than five years post-HSCT and currently well off all medication at the time of publication.

      *CaseNotHPOs: large phenotype table with unreported symptoms in table S1

      *CaseNotHPOFreeText: Patient was checked for a number of additional phenotypes but none were identified. Please see Supplementary table S1 for details.

      CasePreviousTesting: Genome-wide methods were not used (sequencing of CTLA4 was performed, but no reference made to other genes tested). Some families received whole-exome sequencing but we are unsure if this patient was included.

      GenotypingMethod: The authors imply that they sequenced the four exons of CTLA4.

      PreviouslyPublished: Yes, Slatter, et al. PMID: 27102614

      Variant: c.518G>A, p.G173E

      ClinVarID: N/A

      CAID: CA350138990

      gnomAD: Not Found

      SupplementalData: extensive data in S1

      Note: Not functionally tested using transendocytosis

    2. c.257C>T

      Case#: AAA.II.1, subject 130. Male. Age of Onset: 23y.o. Age of evaluation: 46 y.o. Origin in Switzerland, Caucasian.

      DiseaseAssertion: Gastrointestinal involvement

      FamilyInfo: None found

      CasePresentingHPOs: HP:0008207 (Addison's disease), HP:0004313 (Hypogammaglobulinemia), HP:0002720 (Low IgA), HP:0002014 (Diarrhea), HP:0002242 (Enteropathy), HP:0012410 (PRCA/Pure red cell aplasia)

      CaseHPOFreeText: Lymphoproliferation, Cytopenia, Autoimmune cytopenia, Endocrinological involvement, Kidney involvement

      Lymphocytic or granulomatous organ infiltration of the gut

      Thirty-five percent of affected mutation carriers (27/78) were under antibiotic prophylaxis. In one affected mutation carrier (the patient) treatment with vedolizumab (blocking α4β7 integrin) improved colitis, and in the same individual PRCA responded well to cyclosporine A.

      IgG levels: no values were available before IVIG or Rituximab

      CaseNotHPOs: large phenotype table with unreported symptoms in table S1

      CaseNotHPOFreeText: Patient was checked for a number of additional phenotypes but none were identified. Please see Supplementary table S1 for details.

      CasePreviousTesting: Genome-wide methods were not used (sequencing of CTLA4 was performed, but no reference made to other genes tested). Some families received whole-exome sequencing but we are unsure if this patient was included.

      GenotypingMethod: The authors imply that they sequenced the four exons of CTLA4.

      PreviouslyPublished: Yes, Navarini et al. PMID: 27908448

      Variant: NM_005214.5:c.257C>T

      ClinVarID: 661941

      CAID: CA2067080

      gnomAD: 2:204735456 C / T

      SupplementalData: extensive data in S1

      Note: Functionally tested using transendocytosis

    1. c.119T > C

      Case#: N/A. This patient is the only one studied in this paper. Female. Age of Onset: 11 y.o. Age of evaluation: 13 y.o. Origin not specified but looking at the author information, I believe it can be safely inferred that the patient is originally from Japan.

      DiseaseAssertion: Autoimmune enteropathy with CTLA4 haploinsufficiency

      FamilyInfo: Patient had no family history of autoimmune diseases, except for hypothyroidism in her mother and hyperthyroidism in her sister. The patient’s mother and sister were found to have the same heterozygous mutation, but they showed only thyroid gland dysfunction that was manageable with medication, which suggests incomplete penetrance.

      CasePresentingHPOs: HP:0002720 (low IgA), OMIM:188030 (immune thrombocytopenic purpura (ITP)), sometimes accompanied by HP:0001890 (autoimmune hemolytic anemia), HP:0001882 (leukopenia), and ORPHA:56425 (cold agglutinin disease).

      CaseHPOFreeText: Persistent watery diarrhea, immunoglobulin A (IgA) deficiency with low IgG2 and IgG4 subclass, recurrent immune thrombocytopenic purpura (ITP).

      The patient had CTLA4 haploinsufficiency and was positive for anti-AIE-75 autoantibody but was successfully treated with 6-mercaptopurine (6-MP)

      Patient was suspected of having interstitial nephritis

      The patient responded well to prednisolone (PSL; 2 mg/kg/day) that was used to treat ITP at every onset, and the treatment was successfully tapered off. However, watery diarrhea appeared during the tapering of PSL while the treatment for the fifth episode of ITP was ongoing.

      Her height was 155 cm (third to fifth percentile) and weight was 48 kg (fifth percentile)

      In our patient, clinical remission was achieved with 40 mg/day of PSL. Clinical remission was maintained on 6-MP even after cessation of PSL for 4 years.

      CaseNotHPOs: N/A.

      CaseNotHPOFreeText: After analyzing the patient’s past laboratory data, we found that following cessation of PSL, ITP relapsed in association with the normalization of IgG levels (861–1,747 mg/dL). In addition, we found that serum levels of sIL-2R were extremely elevated at the onset of AIE. There was no manifestation of AIE, ITP, or other autoimmune diseases for 4 years, while the dose of 6-MP was adjusted to keep the levels of IgG and sIL-2R below 700 mg/dL and 1,500 U/mL, respectively (Fig. 3).

      Flow cytometry analysis showed reduced frequency of CD4+ CD25+ FOXP3+ Tregs (Fig. 4) [10]. Consistent with clinical remission of AIE, an endoscopy and histological study 3 years after the achievement of remission demonstrated recovery from villous atrophy (Fig. 5). After 4 years of 6-MP administration, we tried to reduce the amount of 6-MP because we were concerning about the risk of secondary malignancies such as malignant lymphoma caused by 6-MP. Unfortunately, it led to the relapse of diarrhea and ITP along with soar up of serum level of rIL-2 receptor (Fig. 3).

      CasePreviousTesting: The patient underwent many different types of testing:

      None of the viruses, namely, adenovirus, enterovirus, cytomegalovirus, Epstein-Barr virus, norovirus, and rotavirus, were detected in the patient’s stool sample using polymerase chain reaction. In addition, no pathogenic bacteria were cultured from the stool. Besides, a toxin detection test for Clostridium difficile also yielded negative results. A computed tomography scan of her abdomen revealed a small volume of ascites.

      An esophagogastroduodenoscopy and a colonoscopy demonstrated prominent atrophy of the villus in the duodenum (Fig. 1A) and terminal ileum. Colon was intact endoscopically (Fig. 1B). Histopathological examinations of the duodenum and ileum showed severe villous atrophy. Crypt apoptosis, and infiltration of lymphoplasmacytes into the lamina propria were seen in the biopsies of duodenum, ileum, and colon (Fig. 1C-​-E).E). Immunostaining of the normal small intestine tissue with the patient’s serum showed positive staining of the brush borders of the intestinal epithelium, indicating the presence of anti-enterocyte autoantibodies in the serum of the patient (Fig. 2A and ​andB).B). Furthermore, autoantibodies against AIE-75 were detected by Western blotting, using a recombinant protein as an antigen (Fig. 2C). The patient was diagnosed with AIE and was administered an increased dose of PSL (40 mg/day) as induction therapy.

      Whole-exome sequencing demonstrated a heterozygous missense mutation in the CTLA4 gene. Flow cytometry analysis showed reduced frequency of CD4+ CD25+ FOXP3+ Tregs

      GenotypingMethod: Whole-exome sequencing demonstrated a heterozygous missense mutation in the CTLA4 gene

      PreviouslyPublished: Yes, PMID: 29729943. Schwab et al.

      Variant: NM_001037631.2:c.119T>C

      ClinVarID: None found

      CAID: CA350138103

      gnomAD: None found

      SupplementalData: N/A

      Note: Not functionally tested using transendocytosis

    1. Case#: Ye_2022_PL18, female, 1.5 yr (onset), Caucasian ancestry reported

      DiseaseAssertion: APDS

      FamilyInfo: family info unreported. Pedigree in Crank 2014 shows potential de novo occurance, but this is not confirmed or commented on.

      CasePresentingHPOs: lymphoma (HP:0002665), elevated IgG (HP:0003237), elevated IgM (HP:0003496), decreased B-cell percentage (HP:0010976), recurrent otitis media (HP:0000403), recurrent sinopulmonary infection (HP:0005425), lymphadenopathy (HP:0002716), splenomegaly (HP:0001744), lymphoproliferation (HP:0005523), immune thrombocytopenia (HP:0001973),

      CaseHPOFreeText: low CD3+ percentage, decreased CD4+ percentage, elevated NK percentage, decreased vaccine response,

      CaseNotHPOs: abnormal IgA (HP:0410240), abnormal lymphocyte count (HP:0040088), abnormal B-cell count (HP:0010975),

      CaseNotHPOFreeText: abnormal CD8+ percentage, EBV and CMV

      CasePreviousTesting:

      GenotypingMethod: Sanger sequencing in original article. These authors perform an additional WES from a blood sample. WES of tumor also performed to identify somatic variation.

      PreviouslyPublished: Crank 2014 (PMID:24610295)

      Variant: c.3061G>A, p.E1021K

      ClinVarID: 88675

      CAID:

      gnomAD: NR

      SupplementalData: S2 provides more information on the lymphoma.

  2. Feb 2026