Hepatitis A: Symptoms, treatment and prevention

Hepatitis A is the inflammation of the liver caused by the hepatitis A virus.

Hepatitis A Symptoms

Hepatitis A infection may or may not have any symptoms. Sometime symptoms are mild that they are not noticed first. Older people are more likely to have severe symptoms associated with hepatitis A infection.

Symptoms usually appear between 2 to 6 weeks after infection. Most common symptoms associated with the infection are

• Nausea and vomiting
• Diarrhoea
• Mild, moderate or high fever
• Abdominal discomfort and loss of appetite.
• Skin rashes, itching
• tiredness, fatigue,
• jaundice, yellowish pigmentation of eyes, nail beds and skin.
• darkish brown urine, and or
• pain in area of liver.

Mode of transmission of virus

Hepatitis is transmitted through faecal-oral route. Contaminated water and food can cause the disease. Close personal contact and having sex with a person who is infected also can transmit the disease.

Treatment

Specific medication to control the infection is not available. Proper rest is very important to avoid any complications. Alcohol consumption and use of medications that are toxic to liver should be avoided. Vitamin B supplementation may be necessary. Fluid intake is another important factor in proper cure from the disease. Drink more purified water and if patient has uncontrolled vomiting or diarrhoea, an IV infusion may be necessary.

Prevention

Vaccination is available against Hepatitis A virus. Good hygienic practices will keep you safe from getting this disease. Hand washing, proper waste disposal, drinking boiled or purified water and avoiding unhygienic foods are some important things that will prevent the disease.

What is Haemophilia

Haemophilia is a group of inherited bleeding disorder resulting in an abnormal bleeding tendency and poor blood clotting. Patient will develop abnormalities related to high bleeding tendency. Haemophilia is an X-linked recessive genetic pattern and is more common in males than females. There are mainly two types of Haemophilia, they are Haemophilia A and Haemophilia B. Rarely there is another type of haemophilia known as haemophilia C.

What is haemophilia A, B and C?

Haemophilia A is caused by the deficiency of clotting factor VIII, B type is caused by the deficiency of clotting factor IX (Christmas Factor) and haemophilia C is caused by the deficiency of clotting factor XI. In all the above cases, patient will have abnormal bleeding tendency.

Incidence

Haemophilia A : 1: 5000 males. It is four times more common than Type B.
Haemophilia B: 1: 34,000 Males.
Haemophilia in girls is very rare condition. This condition develops in girls only when both the X genes are defective. If a girl has one defective X gene and a normal X gene, she is not affected but her male children have 50% chance of getting the disease.

Causes

Genetic mutation is the primary cause of the disease. As a result of defect in the genetic code that is responsible for formation of proteins that are essential for clotting mechanism, there will be an abnormality in the clotting factors. Symptoms of abnormal bleeding occurs as a result of this condition.

Blood clotting mechanism involves complex processes and 13 chemically different proteins are necessary for this mechanism to be effective. If any of these 13 factors are deficient, there will be abnormalities in clotting mechanism. As in type A, there will be a deficiency in clotting factor VIII, deficiency of clotting factor IX in type B and deficiency of factor XI in Type C.

Signs and symptoms

Signs and symptoms of Haemophilia varies according to the severity of the disease. Signs are same for all types of haemophilia. According to the factor activity, Haemophilia can be categorized as mild, moderate and severe.

When the factor activity is more than 5%, it said to be mild haemophilia. Bleeding occurs in response to injury or trauma. If the factor activity is 1 per cent to 5 per cent, it is moderate haemophilia and bleeding occurs in response to mild injuries and the onset is late. Severe haemophilia occurs when the factor activity is less than 1%. Spontaneous bleeding occurs anywhere in the body and the onset is early.

Common symptoms associated with this condition are

1. Hemarthrosis: It is the bleeding into the joints. Ankles and knee joints are mostly affected. This caused intense pain on the joints, distension of joint space and eventually destruction of the joints occurs.
2. Bleeding into muscles: This causes formation of hematoma and compartment syndrome. 
3. Mouth and nose bleeds 
4. Bleeding in gastro-intestinal tract (presence of blood in stools) 
5. Blood in urine caused by bleeding in the urinary tract 
6. Bleeding into brain and skull can cause mild to severe complications 
7. Uncontrolled bleeding after surgery, invasive procedure or trauma.

Diagnosis

History collection is done to find out any family history of Haemophilia. If the patient is not having any family history, spontaneous genetic mutation of the gene will be the cause.

Platelet count, Prothrombin time, activated partial prothrombin time and specific tests for identifying the deficiency of clotting factor will confirm the diagnosis.

Genetic testing also can be done to find out the specific gene mutation responsible for haemophilia. This can be done in female to know if she is a carrier of the mutated gene.

Treatments

The primary treatment of haemophilia is the replacement therapy. The clotting factor must be replaced as needed to prevent or control the episodes of bleeding. This clotting factor may be purified concentrates from human donor blood or made in laboratory. With proper training, patient can perform replacement therapy in home as needed.

Drug Desmopressin is sometimes prescribed for patients with mild haemophilia which can be administered slowly through intra-venous route or as nasal preparation. This drug stimulates release of more clotting factor.

When pain is present, pain relievers are prescribed. Pain relievers such as Aspirin and non-steroidal anti-inflammatory drugs will further inhibits the clotting mechanism and must not be used in pain control. Acetaminophen is usually the drug of choice for Haemophilic patients for pain control.

Complications

Major complication of replacement therapy is the formation of antibodies against the infused clotting factors. These inhibitors will destroy the infused concentrates of clotting factor and the replacement therapy will be ineffective. Immune tolerance therapy may be necessary in cases of severe haemophilia with formation of inhibitors.

Atopic dermatitis

Atopic dermatitis is a chronic inflammatory pruritic skin disorder which is non-contagious. Other names of this disease are "prurigo Besnier," "neurodermitis," "endogenous eczema," "flexural eczema," "infantile eczema," and "prurigo diathésique".

Signs and symptoms

Signs and symptoms of atopic dermatitis varies with age. Skin is hypersensitive to allergens, irritants and some foods and become itchy, flaky and red. This irritability causes more vulnerability to infections by some bacteria.

Atopic symptoms like hay fever and asthma may also be present with dermatitis.

Psoriasis like dermatitis occurs in adults and older children.

Symptoms are more on areas like hands, feet, ankles, wrists, face, neck and upper chest. Symptoms varies with age and from person to person.

Incidence

It affects 10–20% of children and 1–3% of adults in industrialized countries. It is affected in both men and women. Usually atopic dermatitis begins in childhood and persists throughout.

Causes

Epidermal Barrier Dysfunction

Some changes on genetic factors responsible for some structural proteins may cause dysfunction of epidermal barrier making skin more vulnerable to irritants and allergens.

Allergy

Symptoms occurs only when the skin is exposed to allergens.

Microwave radiation

Studies have shown that microwaves like radiation from a cell phone may increase chances of dermatitis and worsen an existing allergic condition.

Food allergy

Some food may cause allergic reaction in susceptible individuals.

Histamine intolerance

Affected patients may have intolerance to exogenous histamine. Exogenous histamine means histamine from outside the body. In this case, body will have some difficulty in degrading histamines received from external sources. Histamine free diet is recommended for such individuals.

Biological

There is a strong genetic predisposition in atopic dermatitis.

Prevention

Diet should be monitored to avoid foods that may cause allergic reaction.
Environment must be free of dust and allergens. Skin should be cared to prevent exposure to allergens drying.

Treatment

Maintaining the skin barrier

All measures are to be taken to prevent exposure to allergens. A moisturizer may be used to prevent dryness of skin. It must be selected after consulting with your doctor.

Ceramide based creams may be used to prevent ceramide deficiency. It is one of the three lipids that comprise skin barrier.

The primary treatment involves prevention, includes avoiding or minimizing contact with (or intake of) known allergens. Once that has been established, topical treatments can be used Topical treatments focus on reducing both the dryness and inflammation of the skin.

To improve skin dryness, lotions containing sodium hyaluronate may be used.

An aqueous cream may be used instead of normal soap to maintain a healthy skin.
Prescription drugs

Topical corticosteroids, or injections are used to minimize allergic reactions. In severe cases, prednisone or cortisone may be necessary to control the allergic reaction.

Infections of skin, if present are treated with appropriate antibiotics as recommended by the physician.

Light (UV) therapy

Exposure to broad or narrow band UV light is found to be effective to decrease the severity and frequency of flares.

Atopy

Atopy is a hereditary condition in which patient is susceptible towards developing allergic hypersensitivity reactions when the patient is in contact with an allergen. The term "atopy" was coined by Coca and Cooke in 1923.

Presentation

Atopy is a condition of being hyper allergic. Atopy patients are presented with the following symptoms:
Eczema, rhinitis, conjunctivitis and/or asthma.

Causes

Atopy has a strong hereditary component and environmental factors.

It is hypothesised that extreme cleanliness in an infant’s environment may decrease the number of encounter with infectious stimuli and this will impair the proper development of child’s immune system causing development of Atopy.

Maternal diets like some antioxidants, lipids and Mediterranean diet also may increases the chance of getting this disease.

Excess use of antibodies and antipyretics are also a cause.

Signs and symptoms

Eczema, hay fever, allergic asthma and food allergies.

Presence of cracks on skin and under earlobes

The symptoms occurs only when the individual is exposed to certain allergens like pollen, dust mites or some chemicals.

When the patient is having an allergic reaction, there will be elevated levels of IgE in serum.

Treatment

Corticosteroids are used to treat allergic reactions. Ingestion and topical application of corticosteroids are practiced based on symptoms.

Immune modulators like Pimecrolimus and tacrolimus creams are used which interferes with T cells.

Patients with Atopy often have dry skin. Creams and others measures should be taken to prevent drying of skin.

Most importantly, Patients should avoid any expose to allergens and irritants.

Antiphospholipid syndrome-signs treatment and prevention

Antiphospholipid syndrome is an autoimmune disorder caused by the production of antibodies against a cell membrane substance, phospholipids. This antiphospholipids causes coagulation in arteries and veins causing problems associated with blood clots. Anti-phospholipids syndrome may occur in conjunction with other autoimmune diseases.

Anti-phospholipids syndrome causes blood clots in arteries and veins resulting in related health problems and pregnancy related complications like miscarriage, stillbirth, severe pre-ecclampsia and pre-term delivery. This disease is also called as Hughes syndrome which is named after Dr. Graham R. V. Hughes, a famous rheumatologist in London.

Incidence

As in many other autoimmune disorders, women are more affected than men. This disease can occur at any age group. This disease can have a genetic predisposition.

Signs and symptoms

Complications associated with clots in veins and arteries like deep vein thrombosis and stroke.

Pregnancy related complications like miscarriage, stillbirth, severe pre-ecclampsia and pre-term delivery. Miscarriage occurs before 20th weeks of gestation and pre-ecclampsia after that.

Mental and physical developmental problems occurs in newborn of affected mothers.
Other complications are thrombocytopenia (Low platelet count), headaches, Migraine, heart valve disease and livedo reticularis (a skin condition)

Diagnosis

Laboratory tests include liquid coagulation assays and ELISA assays for anti-cardiolipin antibodies.

Differential diagnosis is done by Factor V Leiden variant test, Factor VIII levels, Prothrombin mutation test and C-reactive protein for differentiating it from Genetic thrombocytopenia.

Pathogenesis

It is an autoimmune disease, caused by formation of antibodies against phospholipids. These antibodies react against proteins of plasma membrane. The exact cause for the formation of antibodies is not known. But this reaction causes activation of coagulation system. This leads to conditions associated with clot formation.

Treatment

Aspirin or warfarin is given to treat this disease. Aspirin and warfarin are anticoagulants which prevents the formation of blood clots. These medications are given only when the patient is presented with symptoms associated with clot formation.

During pregnancy, warfarin is not recommended because of its teratogenic effects. Low molecular weight heparin and low dose aspirin are used in pregnancy. These medications should be started immediately after missing first menstrual cycle.

Ankylosing spondylitis

Ankylosing spondylitis is a chronic inflammatory arthritis and autoimmune disease which mainly affects the joints in spine, pelvis and sacroiliac joints which leads to fusion of the spine and joints.

Epidemiology

Men are more affected than women. Male female ratio is 3:1. Ankylosing spondylitis has a strong genetic pre-disposition. Onset of the disease is usually at the age of 20 to 40 years.

Signs and symptoms

• Initial symptoms include chronic pain and stiffness in middle part of the spine.
• Pain usually radiates to buttock or back of thigh from sacroiliac joint.
• Inflammation of the eye causing redness, itching, pain, photophobia and loss of vision.
• Fatigue and nausea
• Aortitis, lung fibrosis and ectasia
• Pain and swelling of ankles and feet.
• Pain is severe at rest and improves with physical activity

Development and progression

Ankylosing spondylitis affects the entire body. Specific genotype or antibodies affetcts the CD8 T cells which causes inflammation of the joints and spine. Disease progresses and the symptoms worsens. Eventually fusion of the joints and spine occurs.

Diagnosis

• MRI of sacroiliac joints
• X-ray shows Banboo spine
• CT scan showing Bamboo spine in ankylosing spondylitis
• The Schober's test for clinical measure of flexion of the lumbar
• Blood test may show increase in C-reactive protein and increase in ESR

Treatment

• There is no complete cure for the disease, only supportive treatments are available.
• Exercise and physical therapy are performed along with medications to reduce inflammation and pain. This will help control pain and stiffness.
• Use of supportive aids for walking and performing daily activities may be necessary in advanced stages of the disease.

Medication

• Drugs to relieve pain and inflammation like NSAIDs (Ibuprofen, Diclofenac, Naproxen etc.)
• Drugs to reduce immune system reaction like cyclosporine, methotrexate and corticosteroids
• Rituximab may be used as antibody against CD 20

Surgery

In severe cases, surgery is performed for joint repair or replacement.

Physical therapy

Massages and mild exercise can benefit the patient in reducing inflammation and pain. Physical therapy must be aimed at improving movements of affected joints.

Prognosis

The disease is not curable but with adequate supportive therapies patient can lead a quality life. Surgery can help retain the movements of joints.

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis is a degenerative motor neuron disorder caused by the degenerative changes occurs on the neurons at the ventral horn of the spinal cord as well as on the cortical neurons. This condition is also known as Lou Gehrig’s disease as this was first observed in a famous baseball player named Lou Gehrig.
This is a progressive degenerative disorder characterised by rapidly progressing muscle weakness, atrophy, spasticity, dysarthria, dysphagia and finally respiratory compromise. Patients with Amyotrophic lateral sclerosis dye of respiratory compromise and pneumonia within 2 to 3 years.

Epidemiology

Amyotrophic lateral sclerosis is the most common neuromuscular disease and people with all races and ethnic backgrounds are affected. Two in one lack people are affected every year worldwide. People with 40 to 60 years of age are mostly affected.

Signs and symptoms

Muscle weakness and atrophy of muscles that is progressive in nature.

Loss of control of all voluntary muscles except bladder and bowel sphincter muscles and muscles responsible for eye movement.

Initial symptoms

• Muscle weakness and atrophy
• Muscle twitching, cramping and stiffness
• Slurred and nasal speech
• Initially limbs are affected causing tripping or stumbling or dropped foot.
• When arms are affected, it causes inability in simple tasks like buttoning a shirt, writing etc.
• When other systems are affected, symptoms like difficulty in speech and swallowing are noticed. Loss of mobility of tongue also occurs.

Progression of the disease

As the disease progresses symptoms worsens. Patients will not be able to walk and move hands. They become bed ridden. There will be risk of choking and aspiration of foods as the disease progresses. Weight loss and nutritional deficiency occurs as the patient is not able to take food by mouth. A small percent of people develop dementia as a result of fronto- temporal involvement. Cognitive abilities are not affected in most of the patients.

As the muscles of diaphragm and ribs that are essential for breathing are involved, breathing will become difficult and patient may develop pneumonia. Usually death is due to breathing difficulty and pneumonia.

Cause

In 95 per cent of the cases the cause is unknown and there will be no family history of the disease. In patients with a family history of Amyotrophic lateral sclerosis, the cause is due to any genetic disorder. In 20 per cent of patients with family history of amyotrophic lateral sclerosis, there will be a defect in chromosome 21 that causes the disease.

There are several risk factors identified and are:

1. Exposure to dietary neuro toxin called BMAA which is produced by Cyanobacteria.
2. Use of pesticides that are neurotoxin.
3. Some performance enhancing drugs used by athletes may cause amyotrophic lateral sclerosis

Diagnosis

Disease is usually diagnosed based on the presentation (signs) of the disease and based on the neurologic examination.

Magnetic Resonance Imaging may reveal increased T2 signal within posterior part of internal capsule.

Electromyography is performed to inspect the electrical activity in muscles.
Nerve conduction velocity test is done to rule out possible peripheral neuropathy or myopathy.

Treatment

Slowing disease progression

Riluzole is the only drug of choice used to reduce the damage of motor nurons. This drug also offers some neuro-protective effects.

Symptomatic Treatment

Medications to control increased salivation are prescribed if needed. Pain , constipation, sleep disturbances and depression are managed with appropriate drugs. Physical therapies are performed to delay muscle atrophy and loss of muscle strength. Support for speech and language are also given. As respiratory compromise occurs, respiratory support with tracheotomy may be done.

Prognosis

Most of the patients will die on respiratory failure within 2 to 3 years and 10 to 20 per cent patients may survive longer than 10 years.

Alopecia areata or spot baldness

Alopecia areata, also known as spot baldness is a medical condition characterized by loss of hair from areas of body especially from the scalp. This baldness can range from a spot on the scalp to the whole area of scalp or entire dermis (skin).

Classification

1. Hair loss from whole scalp more diffusely is known as diffuse alopecia areata.
2. Baldness only in one spot on scalp or dermis is known as alopecia areata monolocularis.
3. Multiple areas of baldness on scalp or dermis is known as alopecia areata multilocularis.
4. Alopecia areata barbae is a condition in which baldness is only seen on the beard.
5. Total loss of hair from the scalp is known as alopecia areata totalis
6. Loss of hair from whole body is alopecia areata universalis which is very rare.

Epidemiology

0.1 to 0.2 percent of the population is affected by alopecia areata. It can occur in both male and female. Initial presentation may occur in late teen ages and progress as the age advances. Persons with immune system disorders like asthma and allergies are affected more than persons who have normal immune system.

Signs and symptoms

• Rapid loss of hair from a particular area of body or from whole body.
• Round or oval shaped area or areas of baldness.
• Normal looking skin under the areas of baldness, but may be slightly painful.
• “Exclamation point appearance” due to hairs becoming narrower close to the base.
• Pitting nails

Diagnosis

Alopecia areata is usually diagnosed based on clinical features.
On inspection using Trichoscopy, area of baldness shows yellow dots or black dots due to hyper-pigmentation.
Biopsy is rarely required for differential diagnosis and may reveal lymphocytic infiltration.

Causes

The exact cause of the disease is still not known. Studies have found a link between the genetic factors and alopecia areata. Persons with one or more family members affected with this disease are more likely to have alopecia areata.
Alopecia areata is thought to be an autoimmune disease. T-cells are found to be accumulated in areas of baldness that probably attacks the hair follicles causing hair fall and prevents re-growth.

It is also associated with emotional distress and pathogens in some cases. It is also found that this disease is associated with the colour of hair. Gray coloured hairs are more affected than black hair.

Treatment

Corticosteroids can control the disease to some extent. However there are no effective treatment to control alopecia areata.

Some medications used to treat alopecia areata are minoxidill, elocon ointment and topical immunotherapy. Topical tacrolomus ointments are also used to suppress hair loss.

Diphenylcyclopropenone may be used to increase the regrowth of hair from areas of baldness.

Prognosis

In some cases hair re-growth occurs in areas of baldness and may become normal within few months to years. These patches may also increase overtime and lead to alopecia totalis or universalis. Effect of this disease is psychological and proper adaptive mechanism is essential in coping with the effects of this disease.

Addisons disease (Chronic adrenal insufficiency, hypocortisolism, Hypocorticism)

Addison’s disease is a chronic rare condition in which the adrenal glands are not capable to produce sufficient steroid hormones needed for the body. The hormones produced by adrenal gland is glucocorticoids and mineralocorticoids. Addison’s disease is an endocrinal disorder which require lifelong steroid replacement therapy.

Addison’s disease is named after a British physician Thomas Addison who described the condition for the first time.

Epidemiology

Around one in 100,000 population is affected with Addison’s disease. Addison’s disease affects any age group, ethnicity or gender. It is seen mostly in adults between 30 to 50 years of age.

Signs and symptoms

Signs of Addison’s disease

The signs of Addison’s disease are insidious in nature which may take long time to recognize the disease. Most common signs are fatigue and weakness, light headedness on standing position, fever, headache, diarrhoea, mood changes, muscle pain and weakness and weight loss.

Clinical signs include low blood pressure, calcification of pinna of the ear, hyperpigmentation of the skin and medical conditions like thyroid disease, Diabetes mellitus (Type I), and vitiligo may occur together with Addison’s disease.

Signs of Addisonian crisis

Addisonian crisis occur when the adrenal insufficiency is severe enough to affect the normal body mechanism. It is a medical emergency and a life-threatening condition requiring immediate medical attention.

Signs of Addisonian crisis (Adrenal crisis) include Severe pain on legs, abdomen and back which is sudden in onset, Vomiting, diarrhoea and dehydration, loss of consciousness and inability to stand up, low blood pressure, Low blood sugar, Psychological problems, low sodium levels, increase in blood level of potassium, elevated calcium levels, fever and convulsions.

Causes

The main causes of Addison’s disease are

1. Developmental problem of the adrenal gland (Adrenal dysgenesis).

Adrenal dysgenesis is a developmental problem and is genetic. This is a very rare condition and include mutations of SFI transcription factor, DAX-I gene mutation etc.

2. Biochemical problems of the gland leading to inability to produce the cortisol

Adrenal glands require cholesterol to produce cortisol and any condition resulting in impairment in availability of cholesterol leads to this condition.

3. Disease of the adrenal gland resulting in destruction of the gland

The most common cause of adrenal gland destruction is the auto immune adrenalitis caused by the immune reaction against the enzyme 21-hydroxylase. Cancer, Haemorrhage and infections are also the causes of adrenal destruction.

Diagnosis

Blood test: reveals Hypercalcemia (Increase in calcium levels in blood), low blood sugar, low sodium levels, high potassium levels, Eosinophilia (increased number of white blood cells), increased acidity of blood (metabolic acidosis) etc.

ACTH stimulation test: In this test a manual stimulation to the adrenal glands is given and in presence of Addison’s disease, adrenal hormones will be below normal even with the stimulation of the gland.

Other tests: Estimation of rennin and adrenocorticotropic hormone levels and imaging techniques like MRI will reveal the cause of hypoadrenalism.

Treatment

Replacement

Hormone replacement is an important treatment in Addison’s disease. Cortisol must be replaced according to the body requirements. Hydrocortisone tablets are used to supply cortisol required by the body. Sometimes prednisolone may be used instead of hydrocortisone to mimic the effect of it on the body.

Crisis management:

When the body does not have adequate supply of cortisol Adrenal crisis occurs. This is managed by administering large doses of saline solution with glucose and glucocorticoids. As the condition of the patient improves, dose of glucocorticoid is decreased gradually.

Recovery

With proper treatment a patient with Addison’s disease can lead a normal life. It is important to carry an identification card stating that the person has the disease will help to provide immediate medical attention at the time of Adrenal crisis. Patient should carry the medication while travelling. With all these precautions, patient can lead a quality life.

Acute disseminated encephalomyelitis (ADEM)

Acute disseminated encephalomyelitis (ADEM) is an immune mediated disease involving the nervous system in which there is de-myelination of the nerves. It usually occurs after an infection of viral, bacterial or parasitic in origin or vaccination or sometimes spontaneously.

                                                            MRI differances in ADEM


The autoimmune response produce inflammatory lesions in the brain and spinal cord and is somewhat similar to multiple sclerosis. The areas involved are usually, in the white matter of the brain and spinal cord.

Incidence

Acute disseminated encephalomyelitis (ADEM) affects 8 per 1,000,000 people per year. Children and adolescents are more affected. There is a 5% mortality rate and in 50 to 75% cases there is complete recovery from the disease. Recovery is complete within 6 months of treatment.

Causes

Viral infections: enterovirus, measles, rubella, influenza virus, mumps, varicella zoster, cytomegalovirus, herpes simplex virus, coxsackievirus and hepatitis A

Bacterial infections: Mycoplasma pneumonia, leptospira, borrelia burgdorferi and beta haemolytic streptococci.

Vaccination: Semple form of rabies, Hepatitis B vaccine, Pertussis vaccine, diphtheria vaccine and rubella vaccine.

Other causes: Organ transplantation

Signs and symptoms

Usually Acute disseminated encephalomyelitis (ADEM) has an abrupt onset. After 1 to 3 weeks of infection the signs and symptoms begins which includes fever, head ache, seizure, drowsiness and coma. Symptoms usually worsens after two or three days and if untreated leads to hemoparesis and nerve damage which is irreversible.

Treatment

The first line treatment for Acute disseminated encephalomyelitis (ADEM) is aimed at reducing the inflammatory response of the patient. For this purpose high doses of corticosteroids like methylprednisolone or dexamethosone are used. After a 3 to 6 weeks of treatment with high dose corticosteroids the doses can gradually be decreased.

Intravenous immunoglobulin, mitoxantrone and cyclophosphamide are considered as alternatives in case the patient cannot be treated with corticosteroids or the treatment with corticosteroids show poor outcomes.

If both the above treatment modalities fails to control the disease, a combination of both that is corticosteroids with immunoglobulin is administered to control the immune reaction.

Prognosis

Complete recovery in 50% to 70% with adequate treatment and 70 to 90 per cent recovery with minor disorders. There is a 5 per cent mortality rate even with adequate treatment.

Complications

1. Motor deficiencies: about 8 to 30 per cent cases residual motor deficiencies are seen.
2. Neuro cognitive impairment
3. Acute disseminated encephalomyelitis (ADEM) with multiple sclerosis
4. Acute hemorrhagic leuko encephalitis.

Celiac disease

Celiac disease is a condition in which the lining of the small intestine (Villi) is destroyed due to reaction to eating gluten resulting in loss of ability to absorb certain nutrients and resultant malnutrition.

Gluten is found in wheat, barley, rye and oats. Some individual develop immune reaction towards gluten and when they eat food containing gluten, their villi present in the small intestine are damaged due to this immune reaction.


Incidence, cause and risk factors

• Exact cause is unknown.
• People with celiac disease develop an auto immune reaction towards gluten which destroys the lining of the small intestine resulting in loss of its ability to absorb nutrients.
• The person becomes malnourished as a result of this and signs and symptoms of malnutrition occurs.


This disease can occur at any stages of life. An individual with a family history of celiac disease are more vulnerable to developing this disease. Caucasians and persons of European ancestry are at greater risk of developing celiac disease. Women are more prone to get this disease than men.

Associated disorders

Celiac disease can cause diseases like – Rheumatoid arthritis, Addison’s disease, Down syndrome, Sjogren syndrome, Systemic lupus erythematous, Some types of intestinal cancer, lymphoma, diabetes mellitus, lactose intolerance and thyroid disease.

Signs of celiac disease

• Abdominal pain, gas and indigestion
• Constipation or diarrhoea
• Appetite changes (Increased or decreased)
• Nausea and vomiting
• Foul smelling, fatty stools
• Weight loss
• Signs of malnutrition

Diagnosis

Serum Albumin test show below normal levels of albumin.

Alkaline phosphatise may be increased significantly because of loss of bone.

Abnormalities of blood clotting mechanism.

Blood test reveals signs of anaemia

Low cholesterol levels

Blood tests for specific antibodies-
• Anti-tissue transglutaminase antibodies
• Anti-endomysium antibodies

If the above tests are positive for celiac disease, an upper endoscopy is performed to take the biopsy of the small intestine which may show abnormalities of villi.

To find out who are at risk of developing celiac disease genetic testing can be done for the presence of genetic factors associated with this condition.

Treatment

There are no treatment modalities that can cure the disease completely. The person is instructed to avoid diet containing gluten. He has to avoid eating foods containing wheat, barley, rye and oats. Make sure that you read the label of any food items to find out the presence of gluten. Once you started a gluten free diet, villi that is present on your intestine starts to grow slowly and the signs gradually disappear. Time taken for this changes varies with the age and general health status of the person. For children, it takes 3 to 4 months for complete cure and growth of villi but in adults it is few years for complete cure and growth.

During the treatment, physician may order certain minerals and vitamins to compensate your daily requirements. These vitamins and minerals are administered intravenously because your intestine is not able to absorb them if taken in oral route.

Sometimes corticosteroids are prescribed (e.g.: Prednisone) to suppress the immune reaction.

Prognosis

Symptoms usually subsides gradually as the lining of the small intestine is healed with the gluten-free diet. Additional treatments may be necessary to cure associated disorders.

Complications

If not treated celiac disease may lead to complications or even a life-threatening condition.

• Immune system disorders
• Diseases of bone
• Cancer
• Retarded growth and development for children
• Infertility
• Systemic diseases

Graves Disease

Graves disease is caused by the over activity of thyroid gland. It is a type of hyperthyroidism caused by an autoimmune disorder. The over activity of the thyroid glands results in over production of thyroid hormones – Thyroxin (T4) and Tri-iodothyronine (T3). These hormones control the metabolism in the body. Imbalance of these hormones causes a serious metabolic condition known as thyrotoxicosis. This condition is caused by thyroid auto antibodies resulting in excessive secretion of thyroid hormones and an enlargement of thyroid glands known as Goitre.

Onset of the disease

Graves disease is most common among women and the age at the onset of this disease is 20 years. It is the commonest form of hyperthyroidism.

Symptoms

Common symptoms of Graves disease includes -
psychological problems like anxiety, concentration problems, insomnia, nervousness and tremor

Physical Problems Like Breast enlargement in Men, Double vision, Exophthalmia (Protrusion of eye ball), tearing and eye irritation, Generalised weakness, increased bowel movements, enlarged thyroid (Goitre), increased appetite, sweating, Heart problems, menstrual irregularity, restlessness, Breathing difficulty and weight loss.




Diagnosis

Physical examination-Reveals Symptoms related to hyperthyroidism
Blood Tests – Increased TSH, T3 and T4 Levels
Radioactive iodine Uptake
Screening for thyroid auto antibodies

Treatment
The main aim of the treatment is to control the over activity of the thyroid gland.

1. Propranolol: Used to treat symptoms of increased heart rate, anxiety and sweating.
2. Prednisone: used to suppress the immune system and prevent eye irritation and tearing.
3. Anti-thyroid medications: Used to depress thyroid gland and is used to treat hyperthyroidism.
4. Radioactive iodine: Used to destroy thyroid cells and thereby controlling hyperthyroidism.
5. Surgery: Performed to remove the thyroid gland. If thyroid is removed, you will need to take thyroid hormones for the rest of your life.

Treatment Outcome (prognosis)

In most of the cases, surgery may be necessary to control the disease. Surgery or radioactive iodine therapy cures the disease completely but you will need to take thyroid hormone replacement for the life time because, otherwise it will lead to hypothyroidism which is caused by deficiency of thyroid hormones.

Complications

Complications of thyroidectomy (removal of thyroid gland) include voice problems due to nerve damage (Glosso-pharyngeal nerve), Low calcium levels as a result of damage of parathyroid glands which is often temporary, Scar on the surgical site (Neck).

Complications resulting from the disease include heart problems, eye problems and damage of the eye, Thyroid crisis- a life threatening condition due to over activity of the thyroid gland and osteoporosis- a condition resulting from calcium deficiency causing less strength of bones.

Lyme disease - Symptoms,Treatment and Prevention

Lyme disease is an inflammatory disease caused by Borrelia burgdorferi (B. burgdorferi) bacteria. These bacteria are carried by certain ticks. When these ticks bites infected mice or deer, the bacteria enters the ticks and transmitted to human being when they bite a human.

It is called Lyme disease because it was first reported in United States in the town of Old Lyme, Connecticut, in 1975. It is reported mostly in United States. Incidence is higher during late spring, summer and early fall.



Stages

Stage 1-also called as primary Lyme disease
Stage 2 - early disseminated Lyme disease.
Stage 3 - chronic persistent Lyme disease.

Risk Factors

Activities with increased risk of exposure to ticks
Presence of a pet at home that carry ticks.

Symptoms

To be infected, the ticks must be on our body for up to 48 hours and if present more up to this time, the bacteria enters in to our body. The primary Lyme disease is characterized by flu-like symptoms.
• Itching
• General weakness
• Head ache and fainting
• Increased body temperature
• Muscle pain
• Stiff neck

As the infection advances there may be a ‘bulls eye’ rash on the site of tick bite and will be 1 – 3 inch wide. If untreated Lyme disease advances in to chronic persistent Lyme disease. It may affect brain, heart and joints.

Symptoms during this stage include –
• Abnormal muscle movements and weakness
• Joint pain and swelling
• Numbness and tingling
• Unusual behaviour
• Speech disturbances

Diagnosis

A blood test may reveal the presence of antibodies formed against the bacteria. Elisa test for Lyme disease is done to confirm the antibodies and Western Blot test is carried out to confirm the Elisa test.
In late stage Lyme disease, additional tests are carried out to find the condition of heart and brain.
 ECG
 Echo cardiogram
 Lumbar puncture
 MRI scan

Treatment

If a person is suspected to have an insect bite with a tick that carries the bacteria is identified and the bacteria was present on the body for more than 36 hours, then the person has to start a prophylactic antibiotic provided the patient is over 8 years old and is not pregnant or breast feeding.
If the patient is already infected with Lyme disease, a full course of antibiotic is necessary. If the patient is not treated at an early stage, this can lead to a chronic Lyme disease.

Prognosis

If treated early, Lyme disease subsides without any complications. Very rarely, it may lead to chronic persistent symptoms even with adequate treatment.
If the patient is not treated, Lyme disease advances into a chronic late stage Lyme disease affecting heart, brain and joint leading to a life threatening condition.

Complications

If the Lyme disease is not treated adequately, it will lead to late stage Lyme disease with the following permanent disabilities.
• Decreased concentration
• Memory disorders
• Nerve damage
• Numbness
• Pain
• Facial muscle paralysis
• Sleep disorders
• Vision problems

Prevention

When you are at risk of exposure to ticks, wear full sleeve shirt and rubber boots to prevent insect bites.

If an insect bite occurred, spray an insect repellent over the site of bite and also on clothes. Do not spray on face or over an open wound and spray only in outdoors.
Wear light coloured dress on areas where there is a risk of insect bite. This will help to identify the ticks easily.

Seek medical help if you-

Have a Bull’s eye-like rash on the skin or after a tick bite if you develop numbness, weakness, or tingling, or heart problems or any Symptoms of Lyme disease, especially if you may have been exposed to ticks.

Chocolate craving and depression

People crave for chocolate when they feel board or depressed. Dr. Beatrice Golomb and her colleagues at the University of California conducted a study to find out any possible link between depression and chocolate craving.

In the study, more than 900 people are surveyed about their weekly chocolate consumption and overall diet. They also screened the participants for depression.

It was found that depressed people ate more than 55% chocolate than people without depression. They also found that, with increasing depression, an individual is tend to eat more and more chocolates.

They also concluded that this behaviour may be actually a form of self medication or may be an actual cause of depression. They are even considering the possibility that chocolate may act as alcohol, giving temporary mood changes in individual.

Hand Sanitizers may cause Outbreaks of NoroVirus

In health care setting, hand sanitizers are really important. Most of the staff of a health care setting give preference to hand sanitizer than soap and water. This saves their time and provides more satisfaction because we think hand sanitizers are more effective in its germicidal action.

A new research found that, use of hand sanitizer may increase the chances of outbreaks of Norovirus. Norovirus is a virus causing gastro-enteritis. The research was conducted in American College of Preventative Medicine and found that in 53% of the hospital setting, where alcohol based hand sanitizers are used, there is an outbreak of noro virus. It is significantly less in hospitals were soap and water is used to clean hands.

It is hypothesized that the same mechanism where bacteria and virus gets resistant to anti-microbial agents with persistent use is acting here. With the use of alcohol based hand sanitizers, norovirus may get resistant to it and cause the outbreak of gastro-enteritis.

According to experts, more detailed research is necessary to find out exactly what is causing this. Scientists could not prove any direct link between the norovirus outbreak and resistance developed as a result of use of hand sanitizers. Scientists also have to find out the role of alcohol in this phenomena.

According to the author of the study, Dr. David Blaney of the Epidemic Intelligence Service at the US Centers for Disease Control and Prevention (CDC), what they found shows that hand sanitizers could be "suboptimal in controlling the spread of noroviruses". And that any casual link is non-existent due to the survey's retrospective design.

He also said that more reports from hopitals using hand sanitizers about the outbreaks of norovirus may be because they may have a more efficient system for identifying hospital based infections..

New epidemiological model for HIV treatment

Scientists have proposed a new epidemiologic model for HIV treatment using a virus like particle that will subdue the infection and can spread from individual to individual in the same way the HIV virus spread. The new treatment modality will help decrease the death rate by spreading it to high-risk population who are unreachable for the health care system.

The engineered particle is called as ‘therapeutic interfering particle’ or TIP. TIP, with the support of anti-retroviral therapy will decrease the death rate considerably. These are molecular parasites that can spread from one individual to another in the same way, like unprotected sex, sharing of needles etc. TIP s have the same molecular structure as an HIV virus but lack the structures needed for HIV infection. These particles can infect additional cells by replication and can transmit to others. These particles remains in blood stream for years and thus increases the chance of spread to others.

Once TIP enters the body of an individual infected with HIV, it will be packed with genes that disrupts the normal functioning of the HIV virus and thus helps in control of viral load and the life expectancy increases. In an individual without HIV infection, TIP remains inactive or dormant until he is infected with the HIV virus.

TIP cannot replace other treatment modalities for HIV infection, but is expected to decrease HIV deaths considerably by infecting high-risk population and population that the health care industry cannot reach. TIP should be used with other treatments like anti-retroviral therapy and it can enhance the therapeutic effects of such drugs when used in conjunction with ART or vaccines. Use of TIP in a high risk population is expected to lower the number of HIV infection to one thirtieth the current level within 30 years.

Effective Gene Therapy against Leukemia Developed

Researchers from Pennsylvania's Abramson Cancer Centre have developed an effective way to control Leukaemia in about three weeks! They have developed a ‘serial killer’ cell that selectively destroys the tumour in patient’s body. It is a US engineered therapy involving treatment against cancer cells using their own T cells. According to the researcher, this treatment is highly effective in blowing away the tumour cells within a month. It has fewer side effects as compared with the Chemotherapy, because unlike chemotherapy, the new therapy is aimed at destroying only the affected cells and not the normal cells of body.

The T cells of the patient is removed first from the body and re-program it to identify the cancer cells by binding with protein expressed by the cancer cells. Previous therapeutic agents against cancer cells were unable to distinguish between the normal cells and the cancer cells. But with the new technology, the Modified T cells are able to distinguish between the normal cells and the cancer cells enabling them to selectively destroy them without affecting the normal cells in the body. A protein called Chimeric Antigen Receptor (CAR) is used to re-program the T cells.

During the research, Scientists found that the modified T cells are capable of fusion with other T cells inside the body, resulting in formation of more and more number of modified T cells and this helps in a rapid destroying of the Cancer cells. They have found this phenomenon in all the patients underwent treatment.

The researchers are now preparing to test this treatment in children with Leukaemia and also try this method for other types of cancers. Dr. David Porter who was one of the researcher said that they are planning to test this treatment in children with no other options to control the Leukaemia.




The study was published in the Journal of Medicine and science. It is reported that the new treatment modality has only minimal side effects compared to chemotherapy as this treatment can selectively destroy the affected cells only, unlike chemotherapy. This treatment can manage Leukaemia but can be cured only by bone marrow transplantation followed by the therapy. This poses a risk of dying with a 50/50 chances.