Anemia, and Limb-girdle muscular dystrophy

Diseases related with Anemia and Limb-girdle muscular dystrophy

In the following list you will find some of the most common rare diseases related to Anemia and Limb-girdle muscular dystrophy that can help you solving undiagnosed cases.


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Medium match DEHYDRATED HEREDITARY STOMATOCYTOSIS 1 WITH OR WITHOUT PSEUDOHYPERKALEMIA AND/OR PERINATAL EDEMA; DHS1


Dehydrated hereditary stomatocytosis (DHS), also known as hereditary xerocytosis, is an autosomal dominant hemolytic anemia characterized by primary erythrocyte dehydration. DHS erythrocytes exhibit decreased total cation and potassium content that are not accompanied by a proportional net gain of sodium and water. DHS patients typically exhibit mild to moderate compensated hemolytic anemia, with an increased erythrocyte mean corpuscular hemoglobin concentration and a decreased osmotic fragility, both of which reflect cellular dehydration (summary by Zarychanski et al., 2012). Patients may also show perinatal edema and pseudohyperkalemia due to loss of K+ from red cells stored at room temperature. A minor proportion of red cells appear as stomatocytes on blood films. Complications such as splenomegaly and cholelithiasis, resulting from increased red cell trapping in the spleen and elevated bilirubin levels, respectively, may occur. The course of DHS is frequently associated with iron overload, which may lead to hepatosiderosis (summary by Albuisson et al., 2013).Dehydrated red blood cells, including those from hereditary xerocytosis patients, show delayed infection rates to Plasmodium in vitro, suggesting a potential protective mechanism against malaria (Tiffert et al., 2005). A polymorphism in PIEZO1 that is enriched in populations of African descent and results in xerocytosis conferred resistance to Plasmodium infection in vitro (see {611184.0016}).The 'leaky red blood cells' in familial pseudohyperkalemia show a temperature-dependent loss of potassium when stored at room temperature, manifesting as apparent hyperkalemia. The red blood cells show a reduced life span in vivo, but there is no frank hemolysis. Studies of cation content and transport show a marginal increase in permeability at 37 degrees C and a degree of cellular dehydration, qualitatively similar to the changes seen in dehydrated hereditary stomatocytosis. Physiologic studies show that the passive leak of potassium has an abnormal temperature dependence, such that the leak is less sensitive to temperature than that in normal cells (summary by Iolascon et al., 1999).Carella et al. (2004) noted that 3 clinical forms of pseudohyperkalemia unassociated with hematologic manifestations, based predominantly on the leak-temperature dependence curve, had been reported: (1) pseudohyperkalemia Edinburgh, in which the curve has a shallow slope; (2) pseudohyperkalemia Chiswick or Falkirk (see {609153}), in which the curve is shouldered; and (3) pseudohyperkalemia Cardiff (see {609153}), in which the temperature dependence of the leak shows a 'U-shaped' profile with a minimum at 23 degrees C. Gore et al. (2004) stated that potassium-flux temperature profiles are consistent both from year to year in an individual as well as consistent within affected members of a pedigree. Genetic Heterogeneity of Hereditary StomatocytosisDehydrated hereditary stomatocytosis-2 (DHS2 ) is caused by mutation in the KCNN4 gene (OMIM ) on chromosome 19q13. Another form of stomatocytosis, involving familial pseudohyperkalemia with minimal hematologic abnormalities (PSHK2 ), is caused by mutation in the ABCB6 gene (OMIM ) on chromosome 2q35. Cryohydrocytosis (CHC ) is caused by mutation in the SLC4A1 gene (OMIM ) on chromosome 17q21, and stomatin-deficient cryohydrocytosis with neurologic defects (SDCHCN ) is caused by mutation in the SLC2A1 gene (OMIM ) on chromosome 1p34. An overhydrated form of hereditary stomatocytosis (OHST ) is caused by mutation in the RHAG gene (OMIM ) on chromosome 6p12.See {137280} for a discussion of the association of familial stomatocytosis and hypertrophic gastritis in the dog, an autosomal recessive syndrome. ReviewsDelaunay (2004) reviewed genetic disorders of red cell membrane permeability to monovalent cations, noting 'inevitable' overlap between entities based on clinical phenotype.Bruce (2009) provided a review of hereditary stomatocytosis and cation-leaky red cells, stating that consistent features include hemolytic anemia, a monovalent cation leak, and changes in red cell morphology that appear to follow a continuum, from normal discocyte to stomatocyte to echinocyte in DHS, and from discocyte to stomatocyte to spherocyte to fragmentation in OHST. Bruce (2009) suggested that the underlying pathologic mechanism might involve misfolded mutant proteins that escape the quality control system of the cell and reach the red cell membrane, where they disrupt the red cell membrane structure and cause a cation leak that alters the hydration of the red cell, thereby changing the morphology and viability of the cell.King and Zanella (2013) provided an overview of 2 groups of nonimmune hereditary red cell membrane disorders caused by defects in membrane proteins located in distinct layers of the red cell membrane: red cell cytoskeleton disorders, including hereditary spherocytosis (see {182900}), hereditary elliptocytosis (see {611804}), and hereditary pyropoikilocytosis (OMIM ); and cation permeability disorders of the red cell membrane, or hereditary stomatocytoses, including DHS, OHST, CHC, and PSHK. The authors noted that because there is no specific screening test for the hereditary stomatocytoses, a preliminary diagnosis is based on the presence of a compensated hemolytic anemia, macrocytosis, and a temperature- or time-dependent pseudohyperkalemia in some patients. King et al. (2015) reported the International Council for Standardization in Haematology (ICSH) guidelines for laboratory diagnosis of nonimmune hereditary red cell membrane disorders.

DEHYDRATED HEREDITARY STOMATOCYTOSIS 1 WITH OR WITHOUT PSEUDOHYPERKALEMIA AND/OR PERINATAL EDEMA; DHS1 Is also known as pseudohyperkalemia, familial, 1, due to red cell leak|pshk1|dhs|dehydrated hereditary stomatocytosis|xerocytosis, hereditary|desiccytosis, hereditary|pseudohyperkalemia edinburgh

Related symptoms:

  • Anemia
  • Hepatomegaly
  • Fever
  • Fatigue
  • Edema


SOURCES: OMIM MENDELIAN

More info about DEHYDRATED HEREDITARY STOMATOCYTOSIS 1 WITH OR WITHOUT PSEUDOHYPERKALEMIA AND/OR PERINATAL EDEMA; DHS1

Low match MCLEOD SYNDROME; MCLDS


Hematologically, McLeod syndrome is characterized by the absence of red blood cell Kx antigen, weak expression of Kell red blood cell antigens, acanthocytosis, and compensated hemolysis. Most carriers of this McLeod blood group phenotype have acanthocytosis and elevated serum creatine kinase levels and are prone to develop a severe neurologic disorder resembling Huntington disease (OMIM ). Onset of neurologic symptoms ranges between 25 and 60 years (mean onset 30-40 years), and penetrance appears to be high. Additional symptoms include generalized seizures, neuromuscular symptoms leading to weakness and atrophy, and cardiomyopathy mainly manifesting with atrial fibrillation, malignant arrhythmias, and dilated cardiomyopathy (summary by Jung et al., 2007).The cooccurrence of McLeod syndrome and chronic granulomatous disease (CGD ) results from a contiguous gene deletion (Francke et al., 1985).

MCLEOD SYNDROME; MCLDS Is also known as mcleod phenotype|neuroacanthocytosis, mcleod type

Related symptoms:

  • Seizures
  • Muscle weakness
  • Cognitive impairment
  • Anemia
  • Peripheral neuropathy


SOURCES: MESH OMIM MENDELIAN

More info about MCLEOD SYNDROME; MCLDS

Low match HEMOPHILIA A; HEMA


Hemophilia A is an X-linked recessive bleeding disorder caused by a deficiency in the activity of coagulation factor VIII. The disorder is clinically heterogeneous with variable severity, depending on the plasma levels of coagulation factor VIII: mild, with levels 6 to 30% of normal; moderate, with levels 2 to 5% of normal; and severe, with levels less than 1% of normal. Patients with mild hemophilia usually bleed excessively only after trauma or surgery, whereas those with severe hemophilia have an annual average of 20 to 30 episodes of spontaneous or excessive bleeding after minor trauma, particularly into joints and muscles. These symptoms differ substantially from those of bleeding disorders due to platelet defects or von Willebrand disease (OMIM ), in which mucosal bleeding predominates (review by Mannucci and Tuddenham, 2001).

HEMOPHILIA A; HEMA Is also known as hemophilia, classic

Related symptoms:

  • Pain
  • Anemia
  • Flexion contracture
  • Peripheral neuropathy
  • Blindness


SOURCES: ORPHANET OMIM MENDELIAN

More info about HEMOPHILIA A; HEMA

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Other less relevant matches:

Low match PHOSPHOGLYCERATE KINASE 1 DEFICIENCY


Phosphoglycerate kinase-1 deficiency is an X-linked recessive condition with a highly variable clinical phenotype that includes hemolytic anemia, myopathy, and neurologic involvement. Patients can express 1, 2, or all 3 of these manifestations (Shirakawa et al., 2006).

PHOSPHOGLYCERATE KINASE 1 DEFICIENCY Is also known as pgk1 deficiency

Related symptoms:

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


SOURCES: MESH OMIM MENDELIAN

More info about PHOSPHOGLYCERATE KINASE 1 DEFICIENCY

Low match EPIDERMOLYSIS BULLOSA SIMPLEX WITH MUSCULAR DYSTROPHY


Epidermolysis bullosa simplex with muscular dystrophy (EBS-MD) is a basal subtype of epidermolysis bullosa simplex (EBS, see this term) characterized by generalized blistering associated with muscular dystrophy.

EPIDERMOLYSIS BULLOSA SIMPLEX WITH MUSCULAR DYSTROPHY Is also known as epidermolysis bullosa simplex and limb-girdle muscular dystrophy|md-ebs|ebs-md|mdebs|limb-girdle muscular dystrophy with epidermolysis bullosa simplex

Related symptoms:

  • Short stature
  • Growth delay
  • Muscle weakness
  • Ptosis
  • Anemia


SOURCES: ORPHANET OMIM MESH MENDELIAN

More info about EPIDERMOLYSIS BULLOSA SIMPLEX WITH MUSCULAR DYSTROPHY

Low match MITOCHONDRIAL NEUROGASTROINTESTINAL ENCEPHALOMYOPATHY


Mitochondrial NeuroGastroIntestinal Encephalomyopathy (MNGIE) syndrome is characterized by the association of gastrointestinal dysmotility, peripheral neuropathy, chronic progressive external ophthalmoplegia and leukoencephalopathy.

MITOCHONDRIAL NEUROGASTROINTESTINAL ENCEPHALOMYOPATHY Is also known as myoneurogastrointestinal encephalopathy syndrome|polip syndrome|mitochondrial neurogastrointestinal encephalopathy syndrome, tymp-related|polyneuropathy, ophthalmoplegia, leukoencephalopathy, and intestinal pseudoobstruction|mngie|mngie, tymp-related

Related symptoms:

  • Intellectual disability
  • Hearing impairment
  • Ataxia
  • Sensorineural hearing impairment
  • Muscle weakness


SOURCES: OMIM ORPHANET MENDELIAN

More info about MITOCHONDRIAL NEUROGASTROINTESTINAL ENCEPHALOMYOPATHY

Low match KEARNS-SAYRE SYNDROME


Kearns-Sayre syndrome (KSS) is a mitochondrial disease characterized by progressive external ophthalmoplegia (PEO), pigmentary retinitis and an onset before the age of 20 years. Common additional features include deafness, cerebellar ataxia and heart block.

KEARNS-SAYRE SYNDROME Is also known as ophthalmoplegia, pigmentary degeneration of retina, and cardiomyopathy|cpeo with myopathy|oculocraniosomatic syndrome|ophthalmoplegia, progressive external, with ragged-red fibers|cpeo with ragged-red fibers|chronic progressive external ophthalmoplegia wi

Related symptoms:

  • Seizures
  • Short stature
  • Generalized hypotonia
  • Hearing impairment
  • Microcephaly


SOURCES: OMIM MESH ORPHANET MENDELIAN

More info about KEARNS-SAYRE SYNDROME

Low match CAMURATI-ENGELMANN DISEASE


Camurati-Englemann disease (CED) is a rare, clinically variable bone dysplasia syndrome characterized by hyperostosis of the long bones, skull, spine and pelvis, associated with severe pain in the extremities, a wide-based waddling gait, joint contractures, muscle weakness and easy fatigability. Camurati-Englemann disease (CED) is a rare, clinically variable bone dysplasia syndrome characterized by hyperostosis of the long bones, skull, spine and pelvis, associated with severe pain in the extremities, a wide-based waddling gait, joint contractures, muscle weakness and easy fatigability.

CAMURATI-ENGELMANN DISEASE Is also known as diaphyseal dysplasia 1, progressive|engelmann disease|progressive diaphyseal dysplasia|dpd1|ced|pdd

Related symptoms:

  • Hearing impairment
  • Scoliosis
  • Ataxia
  • Muscle weakness
  • Abnormal facial shape


SOURCES: OMIM ORPHANET MENDELIAN

More info about CAMURATI-ENGELMANN DISEASE

Low match GLYCOGEN STORAGE DISEASE DUE TO MUSCLE PHOSPHOFRUCTOKINASE DEFICIENCY


Muscle phosphofructokinase (PFK) deficiency (Tarui's disease), or glycogen storage disease type 7 (GSD7), is a rare form of glycogen storage disease characterized by exertional fatigue and muscular exercise intolerance. It occurs in childhood.

GLYCOGEN STORAGE DISEASE DUE TO MUSCLE PHOSPHOFRUCTOKINASE DEFICIENCY Is also known as tarui disease|glycogen storage disease type 7|glycogen storage disease type vii|gsd type 7|glycogenosis type 7|glycogenosis due to muscle phosphofructokinase deficiency|gsd type vii|glycogenosis type vii|gsd due to muscle phosphofructokinase deficiency

Related symptoms:

  • Muscle weakness
  • Anemia
  • Skeletal muscle atrophy
  • Myotonia
  • Hyperuricemia


SOURCES: ORPHANET MENDELIAN

More info about GLYCOGEN STORAGE DISEASE DUE TO MUSCLE PHOSPHOFRUCTOKINASE DEFICIENCY

Low match AUTOSOMAL RECESSIVE LIMB-GIRDLE MUSCULAR DYSTROPHY TYPE 2J


Autosomal recessive limb-girdle muscular dystrophy type 2J (LGMD2J) is a form of limb-girdle muscular dystrophy that usually has a childhood onset (but can range from the first to third decade of life) of severe progressive proximal weakness, eventually involving the distal muscles. Some patients may remain ambulatory but most are wheelchair dependant 20 years after onset.

AUTOSOMAL RECESSIVE LIMB-GIRDLE MUSCULAR DYSTROPHY TYPE 2J Is also known as lgmd2j|muscular dystrophy, limb-girdle, type 2j

Related symptoms:

  • Cardiomyopathy
  • Myopathy
  • Elevated serum creatine phosphokinase
  • Proximal muscle weakness
  • Distal muscle weakness


SOURCES: OMIM MESH ORPHANET MENDELIAN

More info about AUTOSOMAL RECESSIVE LIMB-GIRDLE MUSCULAR DYSTROPHY TYPE 2J

Top 5 symptoms//phenotypes associated to Anemia and Limb-girdle muscular dystrophy

Symptoms // Phenotype % cases
Muscular dystrophy Very Common - Between 80% and 100% cases
Myopathy Common - Between 50% and 80% cases
Muscle weakness Common - Between 50% and 80% cases
Pain Uncommon - Between 30% and 50% cases
Fatigue Uncommon - Between 30% and 50% cases
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Other less frequent symptoms

Patients with Anemia and Limb-girdle muscular dystrophy. may also develop some of the following symptoms:

Uncommon Symptoms - Between 30% and 50% cases


Skeletal muscle atrophy Ataxia Elevated serum creatine phosphokinase Cardiomyopathy Peripheral neuropathy Splenomegaly Ophthalmoparesis Hepatosplenomegaly Paralysis Ptosis Hearing impairment Dilated cardiomyopathy Short stature Proximal muscle weakness Hepatomegaly Seizures Abnormality of mitochondrial metabolism Ophthalmoplegia

Rare Symptoms - Less than 30% cases


Carious teeth Myoclonus Pneumonia Encephalopathy Areflexia Arrhythmia Dementia Depressivity Sensorineural hearing impairment Cardiomegaly Bilateral ptosis Hypogonadism Vertigo Sensory neuropathy Optic atrophy Blindness Flexion contracture Left ventricular hypertrophy Dysphagia Ventricular hypertrophy Intellectual disability Aphasia Rhabdomyolysis EMG abnormality Acidosis Hemolytic anemia Easy fatigability Cachexia Abnormality of the mitochondrion Ragged-red muscle fibers Leukoencephalopathy External ophthalmoplegia Hyperbilirubinemia Poor appetite Mitochondrial myopathy Progressive external ophthalmoplegia Thromboembolism Reticulocytosis Increased CSF protein Jaundice Facial palsy Slender build Muscle cramps Rod-cone dystrophy Elevated hepatic transaminase Dysarthria Lactic acidosis Cognitive impairment Limb muscle weakness Distal muscle weakness Retinopathy Nyctalopia Hypothyroidism Basal ganglia calcification Syncope Growth hormone deficiency Ventricular arrhythmia Abnormality of retinal pigmentation Memory impairment Atrioventricular block Bundle branch block Pigmentary retinopathy Incoordination Adrenal insufficiency Cerebral calcification Hemiplegia/hemiparesis Nasal speech Reduced tendon reflexes Subsarcolemmal accumulations of abnormally shaped mitochondria Reduced visual acuity Decreased number of large peripheral myelinated nerve fibers Macrovesicular hepatic steatosis Cytochrome C oxidase-negative muscle fibers Gastroparesis Intermittent diarrhea Hyperalaninemia Intestinal pseudo-obstruction Skeletal myopathy Diffuse leukoencephalopathy Gastrointestinal dysmotility Demyelinating peripheral neuropathy Absent Achilles reflex Abnormality of the gastrointestinal tract Abnormality of the vasculature Scleroderma Axonal degeneration Decreased sensory nerve conduction velocity Multiple mitochondrial DNA deletions Diabetes mellitus Nystagmus Severe short stature Cerebellar hypoplasia Delayed skeletal maturation Hyporeflexia Congestive heart failure Muscular hypotonia Microcephaly Primary adrenal insufficiency Generalized hypotonia Small intestinal dysmotility Abnormality of the extraocular muscles Abnormal cell morphology Atrophic muscularis propria Hypointensity of cerebral white matter on MRI Intestinal perforation Renal tubular acidosis Adrenocorticotropin deficient adrenal insufficiency Exocrine pancreatic insufficiency Abnormality of the vertebral column Abnormality of femur morphology Abnormality of tibia morphology Facial paralysis Abnormality of the ulna Raynaud phenomenon Gangrene Abnormality of the skull Aplasia/Hypoplasia of the radius Metaphyseal dysplasia Otosclerosis Elevated erythrocyte sedimentation rate Reduced subcutaneous adipose tissue Hyperostosis Abnormality of pelvic girdle bone morphology Tinnitus Increased intracranial pressure Leukopenia Coxa valga Vasculitis Extramedullary hematopoiesis Abnormality of the humerus Increased bone mineral density Craniofacial osteosclerosis EMG: myopathic abnormalities Increased muscle glycogen content Hyperuricemia Myotonia Elevated aldolase level Abnormal subcutaneous fat tissue distribution Cortical thickening of long bone diaphyses Cortical sclerosis Optic nerve compression Urinary retention Diaphyseal dysplasia Diaphyseal sclerosis Cranial nerve compression Abnormality of the radius Limb pain Cranial hyperostosis Sclerosis of skull base Lower limb pain Abnormal diaphysis morphology Bone marrow hypocellularity Bone pain Hypoparathyroidism First degree atrioventricular block Scoliosis Low CSF 5-methyltetrahydrofolate Progressive intervertebral space narrowing Second degree atrioventricular block Third degree atrioventricular block Decreased muscle mass Folate deficiency Renal Fanconi syndrome Sideroblastic anemia Gait disturbance Muscle fiber atrophy Titubation Anterior hypopituitarism Stroke-like episode Gait imbalance Severe lactic acidosis Hypomagnesemia Hyperaldosteronism Heart block Abnormal facial shape Frontal bossing Diplopia Feeding difficulties in infancy Anorexia Lumbar hyperlordosis Waddling gait Limitation of joint mobility Delayed eruption of teeth Genu valgum Delayed puberty Neurological speech impairment Hyperlordosis Hypertrophic cardiomyopathy Kyphosis Abnormality of the nervous system Difficulty walking Pes planus Skeletal dysplasia Mandibular prognathia Proptosis Glaucoma Hyperactivity Headache Difficulty climbing stairs Gastroesophageal reflux Malnutrition Phonic tics Osteoarthritis Gastrointestinal hemorrhage Hematuria Bruising susceptibility Stroke Arthritis Arthralgia Abetalipoproteinemia Arthropathy Personality disorder Tics Acanthocytosis Motor axonal neuropathy Aspiration pneumonia Abnormality of the musculature Obsessive-compulsive behavior Intracranial hemorrhage Joint swelling Atrial fibrillation Intramuscular hematoma Brachydactyly Delayed speech and language development High palate Global developmental delay Splenic rupture Bleeding with minor or no trauma Oral cavity bleeding Persistent bleeding after trauma Abnormality of the elbow Intraventricular hemorrhage Reduced factor VIII activity Spontaneous hematomas Joint hemorrhage Stomatitis Prolonged partial thromboplastin time Dyschromatopsia Aspiration Generalized-onset seizure Visual loss Cholelithiasis Elliptocytosis Spherocytosis Generalized edema Esophageal varix Increased serum ferritin Pericardial effusion Hyperkalemia Hepatitis Intermittent jaundice Dehydration Ascites Abnormality of the liver Pallor Respiratory failure Edema Fever Gastritis Stomatocytosis Chorea Increased intracellular sodium Dyskinesia Ichthyosis Anxiety Dystonia Behavioral abnormality Increased red cell hemolysis by shear stress Exercise-induced hemolysis Increased mean corpuscular hemoglobin concentration Hemoglobinuria Recurrent thromboembolism Pyropoikilocytosis Schistocytosis Compensated hemolytic anemia Portal vein thrombosis Chronic hemolytic anemia Antiphospholipid antibody positivity Renal insufficiency Myalgia Decreased motor nerve conduction velocity Urethral stricture Weight loss Abdominal pain Constipation Diarrhea Vomiting Punctate keratitis Decreased miniature endplate potentials Muscle flaccidity Malabsorption Hyperconvex fingernails Scarring alopecia of scalp Oculomotor nerve palsy Increased connective tissue Hypoplastic fingernail Echolalia Nemaline bodies Abnormality of the cerebral white matter Abnormality of eye movement Lipoma Chronic diarrhea Abnormality of the hand Polycystic ovaries Hypogonadotrophic hypogonadism Hypergonadotropic hypogonadism Foot dorsiflexor weakness Sensorimotor neuropathy Leukodystrophy Peripheral demyelination Paresthesia Abdominal distention Polyneuropathy Distal sensory impairment Distal amyotrophy Cirrhosis Nausea Peripheral axonal neuropathy Severe postnatal growth retardation Fatigable weakness Mental deterioration Acute kidney injury Exercise-induced myoglobinuria Exercise-induced muscle cramps Recurrent myoglobinuria Increased muscle fatiguability Decreased mean corpuscular volume Myoglobinuria Progressive encephalopathy Emotional lability Alopecia Hemiplegia Spastic tetraparesis Purpura Exercise intolerance Tetraparesis Migraine Retinal dystrophy Growth delay Scarring Aplasia/Hypoplasia of the skin Mutism Skin vesicle Milia Dysphasia Keratitis Neonatal respiratory distress Dermal atrophy Palmoplantar hyperkeratosis Ventricular tachycardia Papule Abnormality of dental enamel Progressive muscle weakness Hypoplasia of dental enamel Abnormal blistering of the skin Nail dysplasia Tachycardia Hypotrichosis Nail dystrophy Transient myeloproliferative syndrome



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