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Recurrent tonsillitis

MedGen UID:
1781351
Concept ID:
C0740402
Disease or Syndrome
Synonym: Tonsillitis
 
HPO: HP:0011110
Monarch Initiative: MONDO:0001039

Definition

Inflammation of the tonsils that has occurred repeatedly. The definition of recurrent may vary somewhat, but the criteria used recently as a measure of severity were five or more episodes of true tonsillitis per year, symptoms recurring for at least a year, and episodes that are disabling and that prevent normal functioning. In some cases recurrent tonsillitis may be related to immunosusceptibility. Evidence exists for a genetic predisposition for recurrent tonsillitis. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVRecurrent tonsillitis

Conditions with this feature

Griscelli syndrome type 1
MedGen UID:
347092
Concept ID:
C1859194
Disease or Syndrome
Griscelli syndrome type 1 (GS1) is a rare autosomal recessive disorder that results in pigmentary dilution of the skin and hair, the presence of large clumps of pigment in hair shafts, and an accumulation of melanosomes in melanocytes. In addition to the characteristic silvery-gray appearance of hair and pigmentary defects of skin, GS1 is characterized by primary neurologic deficits that usually are apparent in early infancy and include hypotonia, developmental delay, intellectual disability, and seizures. Immune impairment is not present (summary by Abd Elmaksoud et al., 2020). Bahadoran et al. (2003) characterized GS1 as comprising hypomelanosis and severe central nervous system dysfunction, corresponding to the 'dilute' phenotype in the mouse, and GS2 as comprising hypomelanosis and lymphohistiocytic hemophagocytosis, corresponding to the 'ashen' phenotype in mouse. Anikster et al. (2002), Menasche et al. (2002), Huizing et al. (2002), and Bahadoran et al. (2003, 2003) suggested that Elejalde neuroectodermal melanolysosomal syndrome (256710) in some patients and GS1 represent the same entity. Genetic Heterogeneity of Griscelli Syndrome Griscelli syndrome type 2 (GS2; 607624), characterized by hypomelanosis with immunologic impairment, is caused by mutation in the RAB27A gene (603868). Griscelli syndrome type 3 (GS3; 609227), characterized by hypomelanosis with no immunologic or neurologic manifestations, is caused by mutation in the melanophilin (MLPH; 606526) gene.
Complement component 3 deficiency
MedGen UID:
462421
Concept ID:
C3151071
Disease or Syndrome
C3 glomerulopathy (C3G) is a complex ultra-rare complement-mediated renal disease caused by uncontrolled activation of the complement alternative pathway (AP) in the fluid phase (as opposed to cell surface) that is rarely inherited in a simple mendelian fashion. C3G affects individuals of all ages, with a median age at diagnosis of 23 years. Individuals with C3G typically present with hematuria, proteinuria, hematuria and proteinuria, acute nephritic syndrome or nephrotic syndrome, and low levels of the complement component C3. Spontaneous remission of C3G is uncommon, and about half of affected individuals develop end-stage renal disease (ESRD) within ten years of diagnosis, occasionally developing the late comorbidity of impaired visual acuity.
Autoinflammation with episodic fever and lymphadenopathy
MedGen UID:
1719052
Concept ID:
C5394286
Disease or Syndrome
Autoinflammation with episodic fever and lymphadenopathy (AIEFL) is an autosomal dominant immunologic disorder characterized by onset of recurrent episodes of unexplained fever beginning in early infancy. The episodes occur in a cyclic pattern with a frequency of every week or every few weeks and a duration of several days. Patients have accompanying lymphadenopathy, and some may have hepatosplenomegaly. Rash and genital ulcers are not observed. Patient serum shows increased levels of inflammatory cytokines and chemokines, including IL6 (147620) and TNF (191160), consistent with abnormal activation of the innate inflammatory system. Treatment with anti-IL6R (147880) antibodies may result in clinical improvement (summary by Lalaoui et al., 2020).
Granulomatous disease, chronic, autosomal recessive, 5
MedGen UID:
1710326
Concept ID:
C5394542
Disease or Syndrome
Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder of phagocytes (neutrophils, monocytes, macrophages, and eosinophils) resulting from impaired killing of bacteria and fungi. CGD is characterized by severe recurrent bacterial and fungal infections and dysregulated inflammatory responses resulting in granuloma formation and other inflammatory disorders such as colitis. Infections typically involve the lung (pneumonia), lymph nodes (lymphadenitis), liver (abscess), bone (osteomyelitis), and skin (abscesses or cellulitis). Granulomas typically involve the genitourinary system (bladder) and gastrointestinal tract (often the pylorus initially, and later the esophagus, jejunum, ileum, cecum, rectum, and perirectal area). Some males with X-linked CGD have McLeod neuroacanthocytosis syndrome as the result of a contiguous gene deletion. While CGD may present anytime from infancy to late adulthood, the vast majority of affected individuals are diagnosed before age five years. Use of antimicrobial prophylaxis and therapy has greatly improved overall survival.
Immunodeficiency 77
MedGen UID:
1788976
Concept ID:
C5543173
Disease or Syndrome
Immunodeficiency-77 (IMD77) is an immunologic disorder characterized by recurrent and persistent polymicrobial infections with multiple unusual organisms. Skin and pulmonary infections are the most common, consistent with increased susceptibility to epithelial cell infections. The age at onset is highly variable: some patients have recurrent infections from childhood, whereas others present in late adulthood. The limited number of reported patients are all female, suggesting incomplete penetrance or a possible sex-influenced trait. Patient cells, mainly macrophages, show impaired killing of intracellular bacteria and organisms, including nontubercular mycobacteria, although there is also impaired killing of other organisms, such as Pseudomonas, Candida, and Aspergillus. Treatment with gamma-IFN (IFNG; 147570) may be a therapeutic option (summary by McCormack et al., 2017 and Merselis et al., 2020).

Professional guidelines

PubMed

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Bar-Yishay M, Yehoshua I, Bilitzky A, Press Y
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Recent clinical studies

Etiology

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Eur Arch Otorhinolaryngol 2015 Apr;272(4):949-969. Epub 2014 Apr 3 doi: 10.1007/s00405-014-3010-x. PMID: 24695941

Diagnosis

Smith KL, Hughes R, Myrex P
Am Fam Physician 2023 Jan;107(1):35-41. PMID: 36689967
Nakano S, Kondo E, Iwasaki H, Akizuki H, Matsuda K, Azuma T, Sato G, Kitamura Y, Abe K, Takeda N
J Med Invest 2021;68(1.2):38-41. doi: 10.2152/jmi.68.38. PMID: 33994477
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Zautner AE
Recent Pat Inflamm Allergy Drug Discov 2012 May;6(2):121-9. doi: 10.2174/187221312800166877. PMID: 22452646
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South Med J 1986 Sep;79(9):1126-8. doi: 10.1097/00007611-198609000-00021. PMID: 3749999

Therapy

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Ramos SD, Mukerji S, Pine HS
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Zautner AE
Recent Pat Inflamm Allergy Drug Discov 2012 May;6(2):121-9. doi: 10.2174/187221312800166877. PMID: 22452646
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Prognosis

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McKerrow WS
Am Fam Physician 2002 Nov 1;66(9):1735-6. PMID: 12449272

Clinical prediction guides

Smith KL, Hughes R, Myrex P
Am Fam Physician 2023 Jan;107(1):35-41. PMID: 36689967
Hulse K, Lindsay E, Rogers A, Young D, Kunanandam T, Douglas CM
Arch Dis Child 2022 Dec;107(12):1106-1110. Epub 2022 Aug 5 doi: 10.1136/archdischild-2022-323910. PMID: 36396170
Sizer B, Deveci E, Demir S, Yorgancilar AE
Eur Rev Med Pharmacol Sci 2022 Oct;26(20):7443-7453. doi: 10.26355/eurrev_202210_30013. PMID: 36314314
Chen S, Wang WW, Wang Y, Li YQ, Zhu LX
Int J Pediatr Otorhinolaryngol 2020 Jun;133:110004. Epub 2020 Mar 14 doi: 10.1016/j.ijporl.2020.110004. PMID: 32200310
Chung JH, Lee YC, Shin SY, Eun YG
J Laryngol Otol 2014 Dec;128(12):1084-8. Epub 2014 Nov 17 doi: 10.1017/S002221511400259X. PMID: 25399610

Recent systematic reviews

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