Hepatomegaly, and Encephalitis

Diseases related with Hepatomegaly and Encephalitis

In the following list you will find some of the most common rare diseases related to Hepatomegaly and Encephalitis that can help you solving undiagnosed cases.


Top matches:

High match X-LINKED LYMPHOPROLIFERATIVE DISEASE


X-linked lymphoproliferative disease is a hereditary immunodeficiency characterized, in the majority of cases, by an inadequate immune response to infection with the Epstein-Barr virus (EBV).

X-LINKED LYMPHOPROLIFERATIVE DISEASE Is also known as xlpd|duncan disease|xlp|immunodeficiency 5|infectious mononucleosis, severe, susceptibility to|purtilo syndrome|imd5|ebvs|lymphoproliferative disease, x-linked|epstein-barr virus infection, familial fatal|lyp|ebv infection, severe, susceptibility to|immun

Related symptoms:

  • Seizures
  • Neoplasm
  • Anemia
  • Hepatomegaly
  • Fever


SOURCES: ORPHANET OMIM MENDELIAN

More info about X-LINKED LYMPHOPROLIFERATIVE DISEASE

High match HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS, FAMILIAL, 2; FHL2


Familial hemophagocytic lymphohistiocytosis-2 (FHL2) is an autosomal recessive disorder of immune dysregulation with onset in infancy or early childhood. It is characterized clinically by fever, edema, hepatosplenomegaly, and liver dysfunction. Neurologic impairment, seizures, and ataxia are frequent. Laboratory studies show pancytopenia, coagulation abnormalities, hypofibrinogenemia, and hypertriglyceridemia. There is increased production of cytokines, such as gamma-interferon (IFNG ) and TNF-alpha (OMIM ), by hyperactivation and proliferation of T cells and macrophages. Activity of cytotoxic T cells and NK cells is reduced, consistent with a defect in cellular cytotoxicity. Bone marrow, lymph nodes, spleen, and liver show features of hemophagocytosis. Chemotherapy and/or immunosuppressant therapy may result in symptomatic remission, but the disorder is fatal without bone marrow transplantation (summary by Dufourcq-Lagelouse et al., 1999, Stepp et al., 1999, and Molleran Lee et al., 2004).For a general phenotypic description and a discussion of genetic heterogeneity of FHL, see {267700}.

HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS, FAMILIAL, 2; FHL2 Is also known as hplh2|hlh2

Related symptoms:

  • Seizures
  • Global developmental delay
  • Generalized hypotonia
  • Ataxia
  • Failure to thrive


SOURCES: OMIM MENDELIAN

More info about HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS, FAMILIAL, 2; FHL2

High match IMMUNODEFICIENCY WITH HYPER-IGM, TYPE 1; HIGM1


HIGM is a rare immunodeficiency characterized by normal or elevated serum IgM levels associated with markedly decreased IgG, IgA, and IgE, resulting in a profound susceptibility to bacterial infections and an increased susceptibility to opportunistic infections. Patients with X-linked HIGM also tend to have neutropenia, as well as a high rate of gastrointestinal and central nervous system infections, often resulting in severe liver disease and/or neurodegeneration (summary by Levy et al., 1997). Genetic Heterogeneity of Immunodeficiency with Hyper-IgMOther forms of HIGM include HIGM2 (OMIM ), which results from mutation in the AICDA gene (OMIM ), HIGM3 (OMIM ), which results from mutation in the CD40 gene (OMIM ), and HIGM5 (OMIM ), which results from mutation in the UNG gene (OMIM ). See also HIGM4 (OMIM ).

IMMUNODEFICIENCY WITH HYPER-IGM, TYPE 1; HIGM1 Is also known as hyper-igm immunodeficiency, x-linked|hyper-igm syndrome 1|ihis|hyper-igm syndrome|xhim|imd3|higm|immunodeficiency 3

Related symptoms:

  • Seizures
  • Global developmental delay
  • Failure to thrive
  • Cognitive impairment
  • Anemia


SOURCES: OMIM MENDELIAN

More info about IMMUNODEFICIENCY WITH HYPER-IGM, TYPE 1; HIGM1

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Other less relevant matches:

High match REYNOLDS SYNDROME


Reynolds syndrome (RS) is an autoimmune disorder characterized by the association of primary biliary cirrhosis (PBC) with limited cutaneous systemic sclerosis (lcSSc) (see these terms).

REYNOLDS SYNDROME Is also known as primary biliary cirrhosis and systemic scleroderma|primary biliary cirrhosis, scleroderma, raynaud disease, and telangiectasia

Related symptoms:

  • Pain
  • Hepatomegaly
  • Fever
  • Fatigue
  • Dysphagia


SOURCES: OMIM ORPHANET MENDELIAN

More info about REYNOLDS SYNDROME

High match HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS, FAMILIAL, 1; FHL1


Zur Stadt et al. (2005) summarized the clinical features of hemophagocytic lymphohistiocytosis (HLH), a rare autosomal recessive disorder characterized by massive infiltration of several organs by activated lymphocytes and macrophages. The clinical features of the disease include fever, hepatosplenomegaly, cytopenia, and less frequently central nervous system involvement. In FHL, the familial form of the disease, first episodes occur mostly during infancy, with a rapidly fatal outcome if untreated. Diagnostic criteria also include low fibrinogen and high triglyceride and ferritin levels. Chemoimmunotherapy based on corticosteroids, epipodophyllotoxins, and cyclosporin succeeds in controlling the disease in the majority of patients, although remission is rarely obtained (Henter et al., 2002). Most patients suffer an early death unless they are treated by hematopoietic stem cell transplantation (Durken et al., 1999). Genetic Heterogeneity of Familial Hemophagocytic LymphohistiocytosisFamilial hemophagocytic lymphohistiocytosis exhibits genetic heterogeneity. In some families, familial hemophagocytic lymphohistiocytosis has been found to be linked to chromosome 9q (HPLH1, FHL1). FHL2 (OMIM ) is caused by mutation in the PRF1 gene (OMIM ) on chromosome 10q22; FHL3 (OMIM ) is caused by mutation in the UNC13D gene (OMIM ) on chromosome 17q25; FHL4 (OMIM ) is caused by mutation in the syntaxin-11 gene (STX11 ) on chromosome 6q24; and FHL5 (OMIM ) is caused by mutation in the syntaxin-binding protein-2 (STXBP2 ), which is an interaction partner of STX11, on chromosome 19p13.Furthermore, before the identification of mutations in the RAG1 (OMIM ) and RAG2 (OMIM ) genes, both of which map to 11p, Omenn syndrome (familial reticuloendotheliosis with eosinophilia; {603554}) was not thought to be clearly distinct from other reported cases of hemophagocytic lymphohistiocytosis.

HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS, FAMILIAL, 1; FHL1 Is also known as hemophagocytic reticulosis, familial|hlh1|hemophagocytic lymphohistiocytosis, familial|erythrophagocytic lymphohistiocytosis, familial|reticulosis, familial histiocytic|hplh1|fhl|fhlh|hplh|fel

Related symptoms:

  • Seizures
  • Global developmental delay
  • Generalized hypotonia
  • Ataxia
  • Neoplasm


SOURCES: OMIM MENDELIAN

More info about HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS, FAMILIAL, 1; FHL1

High match AICARDI-GOUTIERES SYNDROME 1; AGS1


Aicardi-Goutieres syndrome is a genetically heterogeneous encephalopathy characterized in its most severe form by cerebral atrophy, leukodystrophy, intracranial calcifications, chronic cerebrospinal fluid (CSF) lymphocytosis, increased CSF alpha-interferon (IFNA1 ), and negative serologic investigations for common prenatal infections (Ali et al., 2006). AGS is phenotypically similar to in utero viral infection. Severe neurologic dysfunction becomes clinically apparent in infancy, and manifests as progressive microcephaly, spasticity, dystonic posturing, profound psychomotor retardation, and often death in early childhood. Outside the nervous system, thrombocytopenia, hepatosplenomegaly, and elevated hepatic transaminases along with intermittent fever may also erroneously suggest an infective process (Crow et al., 2006).In a review of AGS, Stephenson (2008) noted that an expanded phenotypic spectrum has been recognized and that most of the original criteria for diagnosis no longer apply: affected individuals may show later onset and may not have severe or progressive neurologic dysfunction, calcification of the basal ganglia, or CSF lymphocytosis. The appearance of chilblains is an important clinical sign for correct diagnosis. The most severe neonatal form of AGS is typically due to mutation in the TREX1 gene.Cree encephalitis was originally considered a separate disorder, but genetic evidence has shown that it is the same as AGS1. See also pseudo-TORCH syndrome (OMIM ), which shows phenotypic overlap and may in some cases represent AGS (Crow et al., 2000; Crow et al., 2003). AGS is distinct from the similarly named Aicardi syndrome (OMIM ), which is characterized by agenesis of the corpus callosum, spinal skeletal abnormalities, and chorioretinal abnormalities. Genetic Heterogeneity of Aicardi-Goutieres SyndromeSee also AGS2 (OMIM ), caused by mutation in the gene encoding subunit B of ribonuclease H2 (RNASEH2B ) on chromosome 13q; AGS3 (OMIM ), caused by mutation in the RNASEH2C gene (OMIM ) on chromosome 11q13.2; AGS4 (OMIM ), caused by mutation in the RNASEH2A gene (OMIM ) on chromosome 19p13.13; AGS5 (OMIM ), caused by mutation in the SAMHD1 gene (OMIM ) on chromosome 20; AGS6 (OMIM ), caused by mutation in the ADAR1 gene (OMIM ) on chromosome 1q21; and AGS7 (OMIM ), caused by mutation in the IFIH1 gene (OMIM ) on chromosome 2q24.

AICARDI-GOUTIERES SYNDROME 1; AGS1 Is also known as cree encephalitis|encephalopathy, familial infantile, with intracranial calcification and chronic cerebrospinal fluid lymphocytosis|ags|pseudotoxoplasmosis syndrome

Related symptoms:

  • Seizures
  • Global developmental delay
  • Generalized hypotonia
  • Microcephaly
  • Nystagmus


SOURCES: OMIM MENDELIAN

More info about AICARDI-GOUTIERES SYNDROME 1; AGS1

High match ALPERS-HUTTENLOCHER SYNDROME


Alpers Huttenlocher syndrome (AHS) is a cerebrohepatopathy and a rare and severe form of mitochondrial DNA (mtDNA) depletion syndrome characterized by the triad of progressive developmental regression, intractable seizures, and hepatic failure.

ALPERS-HUTTENLOCHER SYNDROME Is also known as alpers syndrome|alpers-huttenlocher syndrome|pndc|alpers progressive infantile poliodystrophy|progressive neuronal degeneration of childhood with liver disease|neuronal degeneration of childhood with liver disease, progressive|alpers diffuse degeneration

Related symptoms:

  • Intellectual disability
  • Seizures
  • Global developmental delay
  • Short stature
  • Generalized hypotonia


SOURCES: OMIM ORPHANET MENDELIAN

More info about ALPERS-HUTTENLOCHER SYNDROME

High match TMEM70-RELATED MITOCHONDRIAL ENCEPHALO-CARDIO-MYOPATHY


Mitochondrial encephalo-cardio-myopathy due to TMEM70 mutation is characterized by early neonatal onset of hypotonia, hypetrophic cardiomyopathy and apneic spells within hours after birth accompanied by lactic acidosis, hyperammonemia and 3-methylglutaconic aciduria.

TMEM70-RELATED MITOCHONDRIAL ENCEPHALO-CARDIO-MYOPATHY Is also known as encephalocardiomyopathy, mitochondrial, neonatal, due to atp synthase deficiency|mitochondrial encephalo-cardio-myopathy due to f1fo atpase deficiency|mitochondrial encephalo-cardio-myopathy due to isolated mitochondrial respiratory chain complex v defici

Related symptoms:

  • Seizures
  • Global developmental delay
  • Generalized hypotonia
  • Microcephaly
  • Ataxia


SOURCES: MESH ORPHANET OMIM MENDELIAN

More info about TMEM70-RELATED MITOCHONDRIAL ENCEPHALO-CARDIO-MYOPATHY

High match GLUTARYL-COA DEHYDROGENASE DEFICIENCY


Glutaryl-CoA dehydrogenase (GCDH) deficiency (GDD) is an autosomal recessive neurometabolic disorder clinically characterized by encephalopathic crises resulting in striatal injury and a severe dystonic dyskinetic movement disorder.

GLUTARYL-COA DEHYDROGENASE DEFICIENCY Is also known as ga i|glutaric aciduria i|gcdhd|ga1|glutaryl-coenzyme a dehydrogenase deficiency|glutaric aciduria type 1|glutaric acidemia type 1|glutaryl-coa dehydrogenase deficiency

Related symptoms:

  • Seizures
  • Global developmental delay
  • Generalized hypotonia
  • Ataxia
  • Failure to thrive


SOURCES: ORPHANET MESH OMIM MENDELIAN

More info about GLUTARYL-COA DEHYDROGENASE DEFICIENCY

High match GM1-GANGLIOSIDOSIS, TYPE I


GM1-Gangliosidosis is an autosomal recessive lysosomal storage disease characterized by accumulation of ganglioside substrates in lysosomes. Clinically, patients show variable degrees of neurodegeneration and skeletal abnormalities. There are 3 main clinical variants categorized by severity and variable residual beta-galactosidase activity. Type I, or infantile form, shows rapid psychomotor deterioration beginning within 6 months of birth, generalized central nervous system involvement, hepatosplenomegaly, facial dysmorphism, macular cherry-red spots, skeletal dysplasia, and early death. Type II, or late-infantile/juvenile form (OMIM ), has onset between 7 months and 3 years, shows generalized central nervous system involvement with psychomotor deterioration, seizures, localized skeletal involvement, and survival into childhood. Hepatosplenomegaly and cherry-red spots are usually not present. Type III, or adult/chronic form (OMIM ), shows onset from 3 to 30 years and is characterized by localized skeletal involvement and localized central nervous system involvement, such as dystonia or gait or speech disturbance. There is an inverse correlation between disease severity and residual enzyme activity (Suzuki et al., 2001).See also Morquio B disease (OMIM ), an allelic disorder with skeletal anomalies and no neurologic involvement.The GM2-gangliosidoses include Tay-Sachs disease (OMIM ) and Sandhoff disease (OMIM ).

GM1-GANGLIOSIDOSIS, TYPE I Is also known as gangliosidosis, generalized gm1, type 1|gangliosidosis, generalized gm1, type i|glb1 deficiency|gangliosidosis, generalized gm1, infantile form|beta-galactosidase-1 deficiency

Related symptoms:

  • Intellectual disability
  • Seizures
  • Global developmental delay
  • Short stature
  • Scoliosis


SOURCES: ORPHANET OMIM MENDELIAN

More info about GM1-GANGLIOSIDOSIS, TYPE I

Top 5 symptoms//phenotypes associated to Hepatomegaly and Encephalitis

Symptoms // Phenotype % cases
Seizures Very Common - Between 80% and 100% cases
Global developmental delay Common - Between 50% and 80% cases
Fever Common - Between 50% and 80% cases
Splenomegaly Common - Between 50% and 80% cases
Failure to thrive Common - Between 50% and 80% cases
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Other less frequent symptoms

Patients with Hepatomegaly and Encephalitis. may also develop some of the following symptoms:

Common Symptoms - More than 50% cases


Ataxia

Uncommon Symptoms - Between 30% and 50% cases


Generalized hypotonia Muscular hypotonia Encephalopathy Thrombocytopenia Hepatosplenomegaly Elevated hepatic transaminase Abnormality of the liver Coma Irritability Jaundice Spasticity Leukoencephalopathy Anemia Abnormality of movement Increased CSF protein Aciduria Vomiting Hypertonia Meningitis Lymphadenopathy Respiratory failure Tetraplegia Dystonia Hemiplegia Cerebellar atrophy Feeding difficulties Choreoathetosis Pneumonia Microcephaly Gliosis CSF pleocytosis Dilatation Immunodeficiency Recurrent infections Skin rash Neurodegeneration Dysphagia Pancytopenia Hepatic failure Tremor Abnormal facial shape Spastic diplegia Developmental regression Dementia Acidosis Cardiomyopathy

Rare Symptoms - Less than 30% cases


Hypertrophic cardiomyopathy Optic atrophy Episodic fever Peripheral demyelination Blindness Cerebral degeneration Generalized dystonia Retrognathia Strabismus Abnormality of the retinal vasculature Cholestasis Rigidity Cirrhosis Lactic acidosis Respiratory insufficiency Paralysis Chronic hepatitis Nystagmus Growth delay Intrauterine growth retardation Neuronal loss in central nervous system Neoplasm Increased serum lactate 3-Methylglutaconic aciduria Abnormality of extrapyramidal motor function Inguinal hernia Progressive encephalopathy Hepatitis Long philtrum Congestive heart failure Motor delay Brain atrophy Abnormality of the cerebral white matter Feeding difficulties in infancy Cerebral cortical atrophy Cerebral atrophy Intellectual disability Short stature Abnormality of the skeletal system Camptodactyly of finger Cerebral palsy Hyperbilirubinemia Clumsiness Increased total bilirubin Immune dysregulation Cellular immunodeficiency Lymphocytosis Histiocytosis Weight loss Hypoproteinemia Increased IgM level Dysgammaglobulinemia Cognitive impairment Hypofibrinogenemia Edema Agammaglobulinemia Headache Hemophagocytosis Hypertriglyceridemia Decreased liver function Leukopenia Increased intracranial pressure Hypoalbuminemia Hyponatremia Increased serum ferritin Prolonged prothrombin time Hemolytic anemia Generalized edema IgG deficiency Sepsis Hemiparesis Memory impairment Increased antibody level in blood Decreased antibody level in blood Lymphoma Microvesicular hepatic steatosis Abnormality of the urinary system Generalized hirsutism Intellectual disability, moderate Abnormality of the kidney Wide mouth Gingival overgrowth Short philtrum Bile duct proliferation Decreased beta-galactosidase activity Small for gestational age Abnormality of epiphysis morphology Flat face Astrocytosis Premature birth Gastrointestinal dysmotility Oligohydramnios Interphalangeal joint contracture of finger Tics Fetal akinesia sequence Severe failure to thrive Abnormal form of the vertebral bodies Abnormality of visual evoked potentials Celiac disease Bundle branch block Neonatal hypotonia Abnormal heart valve morphology Cataract Phonic tics Epilepsia partialis continua Multifocal seizures Hypoplastic vertebral bodies Vacuolated lymphocytes Rough bone trabeculation Ethylmalonic aciduria Exaggerated startle response Cerebral cortical neurodegeneration Cherry red spot of the macula Gastric ulcer Psychomotor deterioration Angiokeratoma corporis diffusum Cryptorchidism Umbilical hernia Low-set ears Abnormality of the scrotum Hypertension Wide nasal bridge Abnormal diaphysis morphology Anteverted nares Aplasia/Hypoplasia of the abdominal wall musculature Micronodular cirrhosis Thickened ribs Dysostosis multiplex Hypospadias Arrhythmia Beaking of vertebral bodies Flexion contracture Intention tremor Abnormality of the metaphysis Abnormality of the skin Subdural hemorrhage Ketonemia Macroglossia Symmetrical progressive peripheral demyelination Macrocephaly at birth Glutaric acidemia Glutaric aciduria Retinal hemorrhage Hypertelorism Infantile encephalopathy Cardiomegaly Acute encephalopathy Fasting hypoglycemia Akinesia Decreased plasma carnitine Dilation of lateral ventricles Scoliosis Muscle weakness Ketonuria Macrotia Corneal opacity Joint stiffness Abdominal distention Hyperlordosis Arthralgia Coarse facial features Skeletal dysplasia Mandibular prognathia Depressed nasal bridge Severe short stature Broad nasal tip Recurrent respiratory infections Kyphosis Short neck Frontal bossing Skeletal muscle atrophy Hyperreflexia Cerebral ischemia Depressed nasal ridge Pulmonary arterial hypertension Gastroparesis Hypoglycemia Hyperhidrosis Prominent forehead Myopathy Gait disturbance Macrocephaly Abnormal pulmonary valve morphology Hyperalaninemia Stroke Moderate global developmental delay Abnormal aortic valve morphology Flat occiput Hyperammonemia Aplasia/Hypoplasia of the corpus callosum Microretrognathia Dilated cardiomyopathy Respiratory tract infection Neurological speech impairment Malignant hyperthermia Large fontanelles Bulbar palsy Opisthotonus Malnutrition Intracranial hemorrhage Hyperkinesis Joint dislocation Exercise intolerance Dehydration Abnormality of eye movement Migraine Delayed myelination Abnormal cerebellum morphology Metabolic acidosis Dyskinesia Hypertrichosis Inability to walk Vertigo Progressive spasticity Systemic lupus erythematosus Slurred speech IgE deficiency Arthritis Myalgia Gastroesophageal reflux Fatigue Pain Impaired memory B cell generation Opportunistic infection Ascites Agranulocytosis Enlarged tonsils Absence of lymph node germinal center Impaired Ig class switch recombination Decreased T cell activation Cholangiocarcinoma Sclerosing cholangitis Pruritus Gastrointestinal hemorrhage Stomatitis Xerostomia Lichenification Biliary cirrhosis Esophageal varix Calcinosis Antinuclear antibody positivity Raynaud phenomenon Irregular hyperpigmentation Telangiectasia Keratoconjunctivitis sicca Scleroderma Telangiectasia of the skin Elevated erythrocyte sedimentation rate Steatorrhea Elevated alkaline phosphatase Skin ulcer IgM deficiency Cholangitis Mucosal telangiectasiae Recurrent pharyngitis Burkitt lymphoma Hepatic necrosis Pure red cell aplasia Chorioretinitis Granulomatosis Hepatic encephalopathy Aplastic anemia Pharyngitis B-cell lymphoma Hodgkin lymphoma Sarcoma Bone marrow hypocellularity Vasculitis Bronchiectasis Falls Non-Hodgkin lymphoma Reduced natural killer cell activity Gingivitis Otitis media Recurrent lower respiratory tract infections Hepatocellular carcinoma IgA deficiency Recurrent bacterial infections Chronic diarrhea Involuntary movements Recurrent otitis media Neutropenia Fulminant hepatitis Autoimmunity Carcinoma Diarrhea Dysarthria Papilledema Abnormality of coagulation Diplopia Abnormality of the gastric mucosa Sclerodactyly Abnormality of vision Multiple gastric polyps Hearing impairment Increased CSF interferon alpha Deep white matter hypodensities Chronic CSF lymphocytosis Chilblains CSF lymphocytic pleiocytosis Autoamputation Peripheral neuropathy Vegetative state Morphological abnormality of the pyramidal tract Diffuse cerebral atrophy Acrocyanosis Atrophy/Degeneration affecting the brainstem Basal ganglia calcification Prolonged neonatal jaundice Micrognathia Visual loss Petechiae Status epilepticus Intellectual disability, progressive Spastic paraparesis Paraparesis Cerebral visual impairment Hepatic fibrosis Progressive neurologic deterioration Generalized-onset seizure Areflexia Epileptic encephalopathy Focal-onset seizure Peripheral axonal neuropathy Generalized tonic-clonic seizures Abnormality of the eye Hyperactivity Myoclonus Congenital glaucoma Poor head control Lip telangiectasia Eosinophilia Acute leukemia Pulmonary infiltrates Severe combined immunodeficiency Combined immunodeficiency Abnormality of the coagulation cascade Albinism Purpura Decreased HDL cholesterol concentration Aspiration Confusion Leukemia Abnormality of the nervous system Generalized abnormality of skin Calcinosis cutis Palmar telangiectasia Prolonged partial thromboplastin time Increased LDL cholesterol concentration Leukodystrophy Glaucoma Progressive microcephaly Postnatal microcephaly Intellectual disability, profound Spastic tetraplegia Cerebral calcification Severe global developmental delay Muscular hypotonia of the trunk Agenesis of corpus callosum Partial albinism Abnormal natural killer cell physiology Lipogranulomatosis Plasmacytosis Polyneuritis Increased VLDL cholesterol concentration T-cell lymphoma Granulocytopenia Abnormality of ganglioside metabolism



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