Measles is a most contagious disease in children characterized by skin rash, cough, runny nose, sore throat, red eyes caused by paramyxovirus. It is a fetal disease if not treated properly. In 2008 ,197000 children died of measles. Vaccination has significantly reduced the mortality rate in the world .

What causes the Measles?

Measles is caused by paramyxovirus (meales virus). Virus is transmitted though droplets from the nose, mouth and throat of a infected individual. When infected individual cough,sneeze and talks virus droplets into the air, where normal people can inhale them and get infected .

What are the risk factor for getting Measles?

1. Unimmunized children
2. Children less than 1 year
3. Low socioeconomic status
4. Vitamin A deficiency
5. Who received immunoglobulin during measles vaccination

What are the signs and symptoms of Measles ?  

1. High fever (104 to 105 F)
2. Red eyes
3. Cough
4. Photophobia
5. Runny nose
6. Sore throat
7. Loss of appetite
8. Rash : Appears 3-5 days of first symptoms and signs. Rash start from the head and spread other parts of the body . It is present either macules(flat,discolored) or as papules (solid, raised red) .
9. Koplik’s spots( Tiny bluish-white spots inside the check)

How is the measles diagnosed?

Diagnosis relies on patients history and physical examination . In doubt cases diagnosis is confirmed by blood test for antibody of virus (IgM) and virus culture.

What are the complications of the measles ?

1. Ear infection
2. Sinusitis
3. Bronchitis
4. Laryngitis
5. Pneumonia
6. Encephalitis

Miscarriage,premature delivery in pregnant women.

1. Bleeding( due to low platelets count)

How is Measles managed ?

There is no cure of measles,but some treatment relives symptoms which includes :

1. Acetaminophen(paracetamol) or ibuprofen to reduce fever and relief pain. Don t use the aspirin for the children because of the risk of developing Reye’s syndrome.
2. Plenty of fluid
3. Vitamin A supplement
4. Humidified air
5. Bed rest
6. Isolate the children from others children .
7. Antibiotic is used those who have the complications likes pneumonia, ear infection due to bacterial infection.

How is a measles prevented?

1. Immunization of MMR( measles-mumps-rubella ) vaccine is the the most effective way to prevent the measles . First dose of vaccine is given at 12-15 moths of age followed by second dose of immunization when the child is 4-6 years of old (vaccine is contraindicated who have egg allergies) .
2. Isolation of the patient( Measles is contagious from the four days before to fours days after rash)
3. Immune globulin is used for high-risk peoples who are exposed to measles includes HIV patients, child younger than 1 years old and pregnant women.

What the prognosis of Measles?

Most of the individual have good prognosis. 0.2% individual will die and few individual have sequels like panencephalitis and pneumonia .

References:

• http://www.emedicinehealth.com
• http://en.wikipedia.org
• http://www.mayoclinic.com
• http://www.medicinenet.com
• http://www.ncbi.nlm.nih.gov
• http://www.ehealthmd.com
• http://www.umm.edu

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It is a rare autosomal recessive disorder affecting the metabolism of bilirubin results in jaundice in children and infants(usually first day of life), due to lack or deficiency of the uridine diphosphate glycosyltransferase. Crigler-Najjar syndrome is divided into type 1 and type 2(also called as Arias’ syndrome )

What is the pathophysiology of Crigler-Najjar Syndrome?

Crigler-Najjar is caused due to the lack or absent of enzyme called uridine diphosphate glycosyltransferase(UTG) which is required for the metabolism of bilirubin results in high levels of unconjugated hyperbilirubinemia at birth.

What caused the crigler-Najjar syndrome?

This syndrome is caused by genetic mutation of the UGT1 gene located on 2q37 results of absent of reduced UTG activity, impairment of the bilirubin conjugation.

What is the signs and symptoms of crigler-Najjar syndrome?

1. Jaundice is the main symptom ,present at or soon after the birth in type 1 CNS . In type 2 crigler-Najjar syndrome jaundice may not evident until later in infancy or childhood.
2. Poor milk suckling
3. Irritable
4. Kernicterus ( degeneration of the basal ganglia due to unconjugated bilirubin)
5. Hearing problems
6. Mental Retardation
7. Bilirubin encephalopathy

What are the differential diagnosis or crigler-Najjar syndrome?

1. Sepsis, hypoglycemia, hypoxia, hypertrophic pyloric stenosis, fructosemia
2. Hemolysis
3. Defective erythropoiesis
4. Hepatitis
5. Cirrhosis
6. Breast milk jaundice
7. Gilbert syndrome
8. Lucey-Driscoll syndrome

How to diagnosed crigler-Najjar syndrome ?

Diagnosis relies on clinical findings, Laboratory findings and liver biopsy and radiological imaging .

Laboratory findings includes:

• Total serum unconjugated bilirubin is increased .(17-50 mg/dL in type 1 and 6-22mg/dL in type2 crigler-Najjar syndrome)
• Liver function is usually normal.
• Tranferase activity is increased in type 2 after phenobarbital treatment

Radiological imaging such as CT and MRI usually normal but may help to diagnosed crigler-Najjar syndrome .

What is the management of Crigler-Najjar syndrome?

1. In type2 syndrome no treatment is required or can managed with phenobarbital and blue-light photo therapy.
2. The goals of management of type 2 syndrome is to prevent kernicterus which includes;

• Plasma exchange transfusion is the emergent management to remove unconjugated hyperbilirubinemia .
• Long-term photo therapy helps to excrete bilirubin from urine.
• Oral calcium
• Gene and cell transfer technique may help in near future.
• Liver transplantation is required in end stage of this disease .

What is the prognosis of crigler-Najjar syndrome?

Prognosis of type 2 syndrome is excellent . Where prognosis of type 2 syndrome depends upon the disease severity and the management that is given in the patients.

References:

• http://www.emedicinehealth.com
• http://www.patient.co.uk
• http://www.nlm.nih.gov
• http://en.wikipedia.org
• http://www.whonamedit.com
• http://www.scincedaily.com

Related posts:

1. HELLP Syndrome
2. Meigs Syndrome

Bloom syndrome is a rare autosomal recessive inherited disorder cause by multiply break and rearrangements in chromosomes characterized by short stature, telangiectases and photosensitivity, immunodeficiency and greatly increases the risk of developing multiple cancer in the early life. In 1954 dermatologist Dr.David Bloom first describe about Bloom Syndrome.

what causes the Bloom syndrome ?

Bloom syndrome is resulting from mutations in a gene on the long arm of chromosome number 15. The BLM gene encodes for one part of a multi-enzyme Bloom’s syndrome complex (called BTB) that facilitates DNA repair, and helps ensure the integrity of the genome.  Only a child who receives two mutated copies of the BLM gene (one from each parent) will get the disease. More than 60 known mutations of the BLM gene have been documented in the bloom syndrome.

What are the symptoms of Bloom syndrome?

1. Growth delay.
2. congenital telangiectatic erythema (dilated blood vessels)
3. Facial rash that developed shortly after first exposure to sun (Rash may be butterfly-shaped patch mainly on the cheeks).
4. Pigmentation changes in skin including hyper or hypo pigmented areas.
5. Café-au-lait spots
6. High pitch voice
7. Long and narrow face, micrognathism of the mandible and prominent nose and ears.
8. Immune deficiency characterized by recurrent respiratory tract infection like pneumonia and ear infection.
9. Most patients have Type 2 diabetes mellitus.
10. About 20% patients with bloom syndrome may develop malignancies like acute leukemia, lymphoma, and gastrointestinal adenocarcinoma.

How Bloom syndrome diagnosed?

Bloom syndrome is diagnosed by patient’s history; physical examination and lab test. Bloom syndrome is only confirmed by chromosomal study.

Is there a cure of bloom syndrome?

There is no cure of bloom syndrome but some treatment available that can effectively reduce the symptoms and complication of the disease. Avoiding sun exposure or using sunscreens can reduce some the skin changes associated with photosensitivity.  Some physician used growth hormone for short stature.  Recurrent infection can be treated with antibiotics. Consultations with oncologist and endocrinologist for cancer and diabetes patients respectively.

What is the prognosis?

Increased risk of premature death in the second or third decade secondary to malignancies. Photosensitivity and erythema improves with age

Reference:

• www.emedicinehealth.com
• emedicine.medscape.com
• www.medicinenet.com
• en.wikipedia.org
• www.nlm.nih.gov
• www.google.com/health

Related posts:

1. Sweet’s syndrome

Cogan syndrome is rare autoimmune-mediated rheumatic disorder characterized by recurrent cornea inflammation, fever, weight loss and hearing loss. It can lead the patient to blindness or deafness if not treated properly. In 1945 D.G. Cogan first described this term. People of 20s, 30s and children are mostly affected by Cogan syndrome.

What causes Cogan syndrome?

The exact cause of cogan syndrome is still unknown, but thought that it is an autoimmune disorder. Patients own antibody to inner ear and eye tissue causes the eye and ear inflammation. Infection with the bacteria Chlamydia pneumoniae has been demonstrated in some patients prior to the development of Cogan’s syndrome but not proved at.

What are the symptoms of cogan syndrome?

1. Recurrent eye inflammation, including ketatitis, iritis, scleritis, conjunctivitis.
2. Vision difficulty
3. Dizziness ,tinnitus , hearing loss, vertigo, poor balance
4. Vasculitis
5. fever
6. Fatigue, weight loss
7. Nausea and vomiting
8. Photo sensitivity, rash
9. enlarged lymph nodes
10. Chest pain, arm pain, shortness of breath, night sweat.
11. aortitis, aortic valve insufficiency, pleuritis, pericardial effusion, coronary arteritis, and possibly myocardial infarction.

How is cogan syndrome diagnosed?

Felty’s syndrome is diagnosed by patient’s history, physical examination and lab tests.

Lab tests shows:

1. Increased CRP, WBC and C – reactive protein.
2. present of anemia or thrombocytopenia
3. MRI shows abnormal tissue.
4. Present of antigen in inner ear.

Cogan syndrome can occur in children, and is particularly difficult to recognize in that situation.

How to managed cogan syndrome ?

Anti-inflammatory eye and ear drops are used is mild cases. For moderate cases antibiotic drops can be used. For more severe disease, oral corticosteroids may be necessary to reduce the inflammatory response. When large amounts of steroids are required or if the disease is severe and is not responding to steroid therapy, other immunosuppressive medications like Methotrexate, cyclophosphamide, cyclosporine, and azathioprine are recommended. In some severe cases surgical repair of eye may be done .

References:

1. A Clinician’s Pearls & Myths in Rheumatology
2. Medical physiology, Lippincott Williams & Wilkins 3rd edi.
3. Harrison’s Principles of Internal Medicine, 17th edition.
4. Davidson’s Principles and Practice of Medicine, 20th Edition
5. Harrison’s Rheumatology, Second Edition

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1. Exploding head syndrome

Holt-oram syndrome (HOS) is an autosomal inherited disorder characterized by abnormalities of the upper limbs and heart. Holt and Oram first described this condition in 1960.

The disease is due to mutations in the transcription factor TBX5, which is important in the development both the heart and upper limbs.

Both sexes are equally affected but the defect tend be more severe in females and the malformation are present at birth.

What are the symptoms of Holt-oram syndrome?

Patients may present with limb malformation and/or sings of cardiac failure secondary to ASD, VSD, or cardiac conduction disease like atrial fibrillation.

• On physical examination:
  1. Unilateral or bilateral upper limb deformity
  2. Unequal arm length due to aplasia, hypoplasia, fusion or anomalous development of the radial, carpal, and thenar bones.
  3. Abnormal forearm pronation and supination.
  4. Abnormal opposition of thumb
  5. Phocomelia
  6. Bradycardia
  7. irregular pulse

If anomalies involves in ulnar bone, lower limb, kidneys, eyes, ear, craniofacial, vertebrae Holt-oram syndrome can be exclude.

How is Holt-oram syndrome  diagnosed?

Diagnosis relies on clinical findings by a specialist.  Criteria for the diagnosis of HOS requires 1) defect of the radial side of the hand and 2) septal defect(s) or conduction abnormality of the heart, within one individual or family.The bone defect and cardiac abnormalits is detected through X-ray and echocardiograph .some times testing to identify in the TBX5 gene may be offered, but is not necessary for the diagnosis of HOS.

Is there a cure of Holt-oram syndrome??

There is no cure of HOS but some treatment available that can effectively reduce the symptoms and complications the disease. Referral for genetic counseling should be considered for families in which HOS has been diagnosed. For children with heart defects, surgical repair is often necessary. This may take place shortly after birth if the heart abnormality is life threatening.

Prognosis for individual with HOS depends on the severity of associated birth defects.

Reference:

• www.emedicinehealth.com
• emedicine.medscape.com
• www.medicinenet.com
• en.wikipedia.org
• www.nlm.nih.gov
• www.google.com/health

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Kabuki syndrome is a rare congenital condition characterized by unusual facial features, skeletal abnormalities, and intellectual impairment due to genetic abnormalities.

Kabuki syndrome (also known as Niikawa-Kuroki syndrome) was first described in 1980 by Dr. N. Niikawa and Dr. Y. Kuroki of Japan.

Etiology of Kabuki syndrome is still unknown but thought to be genetic abnormalities of the X and Y chromosome or chromosome 4 in few individual, but is most cases, chromosomes are normal.

Signs and symptom of Kabuki syndrome can vary from individual to individual.There is a wide range of characteristics affecting many systems of the body, no one child will have all of the characteristics listed below.

Growth retardation, Intellectual impairment, reduced muscle tone, long palpebral fissures,  Eversion of later portion of lower eyelid, Drooping eyelids, Arched eyebrows, Strabismus, Protuberant ears, Preauricular pit, Cleft palate, Tooth abnormalities, Open mouth, Tented upper lip, Myopathic appearance, Short fifth finger, Incurved fifth finger, Short fourth  and fifth metacarpals, Short middle phalanges, Brachydactyly( short finger), Rib anomalies, Sagittal cleft of vertebral body, Hip dislocation, Scoliosis, Heart defects, Narrowing of the aorta, Bicuspid aortic valve, Mitral valve prolapse, Membranous ventricular septal defect, Pulmonary stenosis, Aortic stenosis, Mitral valve stenosis, Tetralogy of Fallot, Single ventricle with common atrium, Double outlet right ventricle, Transportation of great vessels, Joint hyperextensibility, Persistent fetal finger pad

How Kabuki syndrome is diagnosed?

The diagnosis of kabuki syndrome relies on patient’s history, physical examination, x-rays, ultrasound and genetic test. A person can be diagnosed with Kabuki syndrome if they possess characteristics consistent with the five different groups of cardinal symptoms: typical face, skin-surface abnormalities, skeletal abnormalities, mild to moderate mental retardation, and short stature.

Is there a cure of Kabuki syndrome?

There is no cure of Kabuki syndrome but there are some treatment available that can effectively reduce the symptoms and complication of this disease. For children with heart defects, surgical repair is often necessary. This may take place shortly after birth if the heart abnormality is life threatening. Those, who are facing some difficulties while swallowing a food, surgical operation in needed in which a tube is inserted in the abdomen so that a patient can swallow food without difficulties. Patient with hear loss can use hearing-aid device. Children with Kabuki syndrome should be educated and trained in behavioral and mechanical methods to adapt to any disabilities. Support groups and community organizations for people with disabilities often prove useful to the affected individuals and their families.

The prognosis of Kabuki syndrome depends on the severity of the symptoms and mode of the treatment given.

Reference:

• www.emedicinehealth.com
• emedicine.medscape.com
• www.medicinenet.com
• en.wikipedia.org
• www.nlm.nih.gov
• www.google.com/health

Related posts:

1. HELLP Syndrome

Jackson-Weiss syndrome is a rare genetic disorder caused by mutation in the FGFR2 gene on chromosome 10 characterized by foot abnormalities and the premature fusion of certain bones of the skull (craniosynostosis), which prevents further growth of the skull and affects the shape of the head and face.

The condition has been described in two large families by Jackson and Weiss and Escobar and Bixler, 1977

Jackson-Weiss syndrome’s baby has the sign and symptoms of misshapen skull, widely spaced eyes, bulging forehead, and underdeveloped middle area of the face (midface hypoplasia)  due to the craniosynostosis (premature fusion  of skull bones) and also have  wide big toes that curve inward toward each other. The large bones of the foot may be fused or abnormally shaped. Individuals with Jackson-Weiss syndrome usually have normal hands, normal intelligence.

Characteristic facial features and unusual toes obvious to diagnosed Jackson-Weiss syndrome’s but x-ray are also important. DNA testing for genetic mutation is the definite diagnosis.

There is no cure or medication for Jackson-Weiss syndrome. Multiple-stage surgery always offered to correct the most severe physical complications, like cleft palate.

Person with the Jackson-Weiss syndrome have good prognosis and normal intelligence.

The National Craniofacial Association has contact information for craniofacial medical teams and also provides financial support for nonmedical expenses of individuals traveling to a center for treatment.

Reference:

• www.emedicinehealth.com
• emedicine.medscape.com
• www.medicinenet.com
• en.wikipedia.org
• www.nlm.nih.gov
• www.google.com/health

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Alagille syndrome is a rare genetic disorder caused by mutations of the JAG1 gene on Chromosome 20, characterized by multisystem disorder involving primarily the liver, heart, eyes, face and skeleton seen in infants and young children. Alagille syndrome affects 1 in 100,000 people. 

Patients with Alagille syndrome usually suffer a progressive loss of the bile ducts within the liver over the first year of life and narrowing of bile ducts outside the liver and have symptoms of jaundice, loose stools, and poor growth within the first three months of life. Later, there is itching, fatty deposition in the skin, persistent jaundice. Other features are abnormalities in the kidney, cardiovascular system (murmurs), eyes and spine (spinal column may look like the wings of a butterfly on x-ray).

Diagnosis of Alagille syndrome usually relies on clinical findings and confirmed by biopsy and genetic analysis.

There is no known cure for Alagille’s Syndrome. Most of the treatments available are aimed at improving, increasing the bile flow from the liver, maintaining normal growth and development. Medications such as cholestyramine (Questran, Prevalite), rifampin naltrexone, or antihistamines may be prescribed to relieve pruritus. Hydrating the skin with moisturizers and keeping fingernails trimmed to prevent skin damage from scratching are important. Infants, children, and adults can benefit from a high-calorie diet, calcium, and vitamins A, D, E, and K. Liver transplantation may be consider in some liver failure patients.

Prognosis of Alagille syndrome depends on several factors including multiorgan involvement. Recent studies report that approximately 75 percent of children with Alagille syndrome live to at least 20 years of age because of improvement in therapies

Reference:

• www.emedicinehealth.com
• emedicine.medscape.com
• www.medicinenet.com
• en.wikipedia.org
• www.nlm.nih.gov
• www.google.com/health

Related posts:

1. HELLP Syndrome
2. Sweet’s syndrome

Fanconi syndrome is a disease of  kidney where  an impairment of the proximal tubular function of the kidney in which certain substances normally absorbed into the bloodstream by the kidneys are released into the urine instead.

It is named after Guido Fanconi, a Swiss pediatrician; this may be a misnomer since Fanconi himself never identified it as a syndrome; though, as in the case of Goodpasture’s syndrome, it is customary to name a syndrome after the first person to note a constellation of symptoms as occurring together. It should not be confused with Fanconi anemia, a separate disease.

This syndrome is caused by genetic defects and acquired causes like tetracycline, tenofovir, in the HIV population, antiretroviral regimen, didanosine and lead poisoning.

Fanconi syndrome is characterized by Polyuria, polydipsia and dehydration, hypophosphate Rickets (in children) and osteomalacia (in adults), Growth failure, Acidosis, Hypokalemia, Hyperchloremia, Hypophosphatemia/Phosphaturia, Glycosuria, Proteinuria/Aminoaciduria and Hyperuricosuria.

Fanconi syndrome is diagnosed by taking complete history, lab tests that document the excessive loss of substances in the urine (eg, amino acids, glucose, phosphate, bicarbonate) in the absence of high plasma concentrations, x-ray and renal biopsy.

Management of Fanconi syndrome mainly consists of the replacement of substances lost in the urine and an electrolyte disturbances .Kidney transplantation has been performed many patients with renal failure due to Fanconi syndrome.

Reference:

• www.emedicinehealth.com
• emedicine.medscape.com
• www.medicinenet.com
• en.wikipedia.org
• www.nlm.nih.gov
• www.google.com/health

Related posts:

1. Meigs Syndrome

A 6 year old boy is brought to the pediatrician by his mother because of a puffy face and lethargy. A few weeks before, he had an upper respiratory tract infection, probably caused by a virus .Body temperature is 36.8 degree centigrade, BP was 95/65 and heart rate was 90 bpm. Puffiness around the eyes, abdominal swelling and pitting edema in the legs are observed. A urine sample (dipstick) is negative for glucose but reveals 3+ protein. Microscopic examination of the urine reveals no cellular elements or casts. Plasma (Na) 140 mEq/L; BUN 10mg/dL; glucose 100mg/dL; Cr 0.8 mg/dL; serum albumin 2.3 g/dL and cholesterol 330 mg/dl. 24 hour urine sample has a volume of 1.10 L and contain 10 mEq/L Na+, 60mg/dL creatatine and 0.8 g/dL protein. Child is treated with the corticosteroid and prednisone, and the edema and proteinuria disappear in 2 weeks. Puffiness and proteinuria recur 4 months later, and a renal biopsy is performed. Glomeruli are normal by light microscopy, but effacement of podocyte foot processes and loss filtration slits are seen whit the electron microscope .No immune deposits or complement are seen after immunostaining. The biopsy indicates minimal change glomerulopathy. The podocyte cell surface and glomerular basement membrane show reduced staining with a cationic dye.

What features in this case would cause the suspension of nephrotic syndrome and what is the explanation for the proteinuria?

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Adverse neonatal and pediatric effects occur with maternal alcohol consumption during pregnancy. The diagnosis of fetal alcohol syndrome (FAS) is based on findings in the following 3 areas: (1) characteristic facial anomalies, (2) growth retardation (intrauterine growth restriction and failure to have catch-up growth), and (3) CNS involvement (cognitive impairment, learning disabilities, or behavioral abnormalities).
renatal exposure to alcohol is associated with a variable spectrum of effects referred to as fetal alcohol spectrum disorders (FASD), with fetal alcohol syndrome at the most severe end of that spectrum. Children with fetal alcohol syndrome disorder may have clinically significant CNS involvement but few or no characteristic physical features.

Pathophysiology

Alcohol crosses the placenta and rapidly reaches the fetus. Extensive studies have demonstrated equivalent fetal and maternal alcohol concentrations, suggesting an unimpeded bidirectional movement of alcohol between the 2 compartments. The fetus appears to depend on maternal hepatic detoxification because the activity of alcohol dehydrogenase (ADH) in the fetal liver is less than 10% of that observed in the adult liver. Furthermore, the amniotic fluid acts as a reservoir for alcohol, prolonging fetal exposure.

The mechanism for the spectrum of adverse effects on virtually all organ systems of the developing fetus is unknown. Ethanol and its metabolite acetaldehyde can alter fetal development by disrupting cellular differentiation and growth, disrupting DNA and protein synthesis and inhibiting cell migration. Both ethanol and acetaldehyde modify the intermediary metabolism of carbohydrates, proteins, and fats. Both also decrease the transfer of amino acids, glucose, folic acid, zinc, and other nutrients across the placental barrier, indirectly affecting fetal growth due to intrauterine nutrient deprivation. Elevated levels of erythropoietin in the cord blood of newborns exposed to alcohol are reported and suggest a state of chronic fetal hypoxia.
source:emedicine.medscape.com/article/974016-diagnosis

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Patent ductus arteriosus (PDA) is a persistence of the fetal connection (ductus arteriosus) between the aorta and pulmonary artery after birth, resulting in a left-to-right shunt. Symptoms may include failure to thrive, poor feeding, tachycardia, and tachypnea. A continuous machine-like murmur in the upper left sternal border is common. Diagnosis is by echocardiography. Administration of indomethacin with or without fluid restriction may be tried in premature infants with a significant shunt but not in term infants with PDA. If the connection persists, surgical or catheter-based correction is indicated. Endocarditis prophylaxis is recommended before and for 6 to 12 mo after correction.

can we used indomethacine in the child after 5 months with patent ductus arteriosus ?

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[1] A 6 month old infant has large, foul smelling stool and is not gaining weight. Sweat chloride level was 68 mmol/L. Appropriate nutritional recommendation include which of the following and why?

1. change to elemental formula.
2. pancreatic enzyme replacement.
3. high-fat diet.
4. low protein diet.
5. low carbohydrate diet.

[2] A 7 month old infant receives chronic TPN for short gut syndrome. On discharge, you discuss with the parents about the possible complications of this mode of nutrition. Which of the following is the typical complication of TPN and why?

1. sepsis.
2. renal failure.
3. chronic diarrhea.
4. vitamin A deficiency.
5. irreversible atrophy of the mucosa of the small intestine.

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