Monday, 19 February 2018

Modern and Ayurvedic concept of skin(Tvaca)

v  Tvaca  and Dosha :
         Tvaca is one of the site of vata and pitta.                 (A.WØû.zÉÉ.12/13)
Ø  Vata - Skin has been considered as sparshanemdriya adhishthana which is function of vata.                                                      (cÉ.xÉÔ.8/10)                                                                                                                                                     
Ø  Pitta - bhrajaka pitta is located on the tvaca for giving luster and colour.                                                                       (cÉ.xÉÔ.12/12)                   
Ø  Kapha - snigdhata, shlakshnata, mruduta, sthirata, shitata, prasannata, snigdhavarnata are the attributed to kapha. For ropana karma (self healing process) kapha is responsible factor.
v  Tvaca  and Dhatu:
1.rasa -In the context of tvaka sara purusha lakshna  it has been also said as rasa sara. A 1st layer of tvaca  udakadhara also contains rasa (lymph) so it can be easily understood that there is a relation between tvaca and rasa.
2.rakta -Among its functions varna prasadana- mansa pushti  have
 been mentioned.                                        (xÉÑ.xÉÔ.15/6)
3.mansa - Twak is upadhatu of mansa.     
                                                           (cÉ.xÉÔ.15/7)
4.meda- Among its functions snehadharana, svedadharana,  drutatva has been mentioned.

5.asthi- kesha, roma, and nails are mala of asthi dhatu which are       embedded in the skin.
6)majja- Among its functions to from tvakaasneha, akthisneha.
7)shukra- It present all over in the body it gives prasannavarnatata skin and help inregeneration of skin.
v  tvaca  and mala:
1) sveda: It is mala of meda which is excreted by tvaca . sveda maintain  the luster and humidity of skin.         (cÉ.xÉÑ.15/5)        
                                  
2) Nails and Hairs: These are mala of asthi dhatu and tvakaagata         sneha is mala of majja dhatu.                  
   
MODERN REVIEW
        The skin is the first line of defense against the envioronmental agent and mirror or internal pathology.
v  Embryological  Description :
        The skin is developed from the surface ectoderm and its underlying mesenchyme (Mesodermal cells).
1)     Surface ectoderm gives rise to the kertinizing general surface epidermis and its appendages, the pilosebaceous units, sudariferous glands and nail units at about 8-10 weeks of gestation.
2)     Malacocites, nerves and specialized sensory receptors arise from the neuroectoderm.
3)     Dermis and its other elements in the skin that is langerhans cells, macrophages, mass cell, fibroblasts etc originate from the mesoderm.
v  Macroscopic structures :
        The skin is the organ of integumentory system that is covering system of the body.  It is formed by about-
v  8% of the total body mass.
v  2.2 square meter covering area.
v  16% of total body weight.
v  Thickness of the skin is different according to maturation, aging and regional specialization.  It may be 0.5 mm on the eyelid       and 4  mm on heal.  Most of the body skin is average 1-2cm thick. Skin is a fascinating orgain as it forms a self renewing and self repairing interface between the body and its
v  environment.
v  Within limit, it forms an effective barrier against microbial invasion and has properties which can protect against mechanical, chemical, cosmetic, thermal and phototic damage.
v  Microscopic  Structure :
        It is characterized by the epidermis, dermis and adenaxa.
1)     Epidermis:
        It is a compound tissue consisting mainly of the continuously self replacing keratinized stratified squamous epithelium.  It varies in thickness 0.04 mm on the eyelid and 0.16 mm on palms, 0.1 mm is average thickness.  Epidermis contains five layers (Strata).
        1)     Stratum bascal            2)     Stratum spinosum
        3)     Stratum granulosum    4)     Stratum corneum
        5)     Stratum lucidum
1)      Stratum Bascal:
        It is deepest layer of the epidermis and formed by a single row of columnar kerationcytes.  Four types of cells are germinated through these layers which are keratinocytes, melanocytes, langerhans cells and merkels cells.
2)      Stratum spinosum:
        It lies super ficial to bascal and it consists of 5 to 12 layers of polyhedral keratinocytes cells are joined tightly to other cells by bundles of intermediate filaments of the cytoskeleton.This arrangement provides both strength and flexibility.
3)      Stratum granulosum:
        It is 3 to 5 layers of flattened kerationocytes that contains darkly staining granules of proteins called karatophylin.  The lipid rich secretion produced by the lamellar granules work as a water repellent sealant that retards loss of body fluid and entry of foreign materials.
4)      Stratum lucidum:
        It is present only in the skin of fingertips, palms and soles. It consists of 3-5 layers of clear, flat, dead kerationocytes.
5)      Stratum corneum:
        This is the most superficial layer consisting of anucleated flattened confirmed 25-30 layers of dead karatinocytes. These cells are continuously shed and replaced by cells from the deeper strata.  It serves as an effective water repellant barrier and also protects against injury and microbes.
Adnexa of epidermis:
        It contains the eccrine glands, apocrine glands and the pilosebaceous apparatus.
1) Eccrine glands:
        These are distributed all over body except the venillion borders of the lips nailbeds, labia minora, glans penis etc.There density is maximum on the palms, sales and axillae.These glands initiate the sweat formation which dissipate heat by evaporation.
2) Apocrine glands:
          These are located in the axillar, areolae, periumbilical, perianal, external ear etc areas. These are small and nonfunctional till puberty, after which they enlarge.
3) Hair follicles:
          They presents all over body except sime parts like palm, sole etc and they protects scalp from injury and sunrays and decrease heat loss.
4) Sebaceous gland:
        They are lipid producing structures disturbed all over body except palms and soles.
5) Nail unit:
        The nail unit helps in the appreciation of the fine and tactile stimulation, protect the terminal phalanges from trauma. 
Dermis :

        The dermis rests upon the subcutaneous fat and is 15-40 time thicker than the epidermis. The dermis is composed mainly of noncellular connective tissue containing collagen, elastic tissue and ground substances within which are embedded the nerves, blood vessels, lymphatics, muscles, and pilosebaceous apocrine and eccrine sweat unit. Dermis can be divided into
1)    Superficial  -   Papillary region
2)    Deeper       -   Reticular region
1.   Superficial –  Papillary region 
It consists of areolar connective tissue containing fine elastic fibers. Elastic fibers play a role in maintaining the elasticity of the skin
2.   Deeper –  Reticular region
It consists of dense irregular connective tissue containing bundle of collagen and some elastic fibers. Both these provides strength elasticity to skin.
Pigmentation of skin
         Melanin, carotene and haemoglobin- these three pigmemts give skin a wide variety of colour. Melanin located in epidermis, carotene is mostly in the stratum corneum and dermis and haemoglobin is in red blood cells within capillaries in the dermis.
PHYSIOLOGY OF SKIN:
  1. Thermoregulation
  2. Protection
  3. Cutaneous Sensation
  4. Excretion and absorption
  5. Synthesis of vitaminD
  6. Immunity
  7. Blood reservoir
  8. Socio sexual communication
  9. Individual identification
   
Sr No.
Ancient term
Modern term
Parts of skin
1.
Avabhasini
Stratum corneum
Epidermis
2.
Lohita
Stratum lucidum
Epidermis
3.
Shweta
Stratum granulosum
Epidermis
4.
Tamra
Malpighian layer
Epidermis
5.
Vedini
Papillary layer
Dermis
6.
Rohini
Reticular layer
Dermis
7.
Mansadhara
Subcutaneous tissue Muscular layer
Dermis


Friday, 29 December 2017

MANEGEMENT OF AMENORRHEA ACCORDING TO AYURVED AND MODERN SCIENCE

INTRODUCTION
Amenorrhoea is the absence of a menstrual period in a woman of reproductive age. Physiological states of amenorrhoea are seen, most commonly, during pregnancy and lactation, the latter also forming the basis of a form of contraception known as the lactation amenorrhoea method. Outside of the reproductive years there is absence of menses during childhood and after menopause.
Amenorrhoea is a symptom with many potential causes. Primary amenorrhoea (menstruation cycles never starting) may be caused by developmental problems such as the congenital absence of the uterus, failure of the ovary to receive or maintain egg cells. Also, delay in pubertal development will lead to primary amenorrhoea. It is defined as an absence of secondary sexual characteristics by age 14 with no menarche or normal secondary sexual characteristics but no menarche by 16 years of age. Secondary amenorrhoea (menstruation cycles ceasing) is often caused by hormonal disturbances from the hypothalamus and the pituitary gland, from premature menopause or intrauterine scar formation. It is defined as the absence of menses for three months in a woman with previously normal menstruation or nine months for women with a history of oligomenorrhoea
Classification
There are two primary ways to classify amenorrhoea. Types of amenorrhoea are classified as primary or secondary, or based on functional "compartments". The latter classification relates to the hormonal state of the patient that hypo-, eu-, or hypergonadotropic (whereby interruption to the communication between gonads and follicle stimulating hormone (FSH) causes FSH levels to be either low, normal or high).
• Primary amenorrhoea is the absence of menstruation in a woman by the age of 16. As pubertal changes precede the first period, or menarche, women by the age of 14 who still have not reached menarche, plus having no sign of secondary sexual characteristics, such as thelarche or pubarche—thus are without evidence of initiation of puberty—are also considered as having primary amenorrhoea. Secondary amenorrhoea is where an established menstruation has ceased—for three months in a woman with a history of regular cyclic bleeding, or nine months in a woman with a history of irregular periods. This usually happens to women aged 40–55. However, adolescent athletes are more likely to experience disturbances to the menstrual cycle than athletes of any other age.[5] Amenorrhoea may cause serious pain in the back near the pelvis and spine. This pain has no cure, but can be relieved by a short course of progesterone to trigger menstrual bleeding.
•             By compartment: The reproductive axis can be viewed as having four compartments:
1. Outflow tract (uterus, cervix, and vagina),
2. Ovaries,
 3. Pituitary gland, and
 4. Hypothalamus.
Pituitary and hypothalamic causes are often grouped together Primary/Secondary          Outflow tract anomalies/obstruction  Gonadal/end-organ disorders    Pituitary and hypothalamic/central regulatory disorders
Overview            The hypothalamic-pituitary-ovarian axis is functional.     The ovary or gonad does not respond to pituitary stimulation. Gonadal dysgenesis or premature menopause are possible causes.Chromosome testing is usually indicated in younger individuals with hypergonadotropic amenorrhoea. Low oestrogen levels are seen in these patients and the hypo-oestrogenism may require treatment.   Generally, inadequate levels of FSH lead to inadequately stimulated ovaries which then fail to produce enough oestrogen to stimulate theendometrium (uterine lining), hence amenorrhoea. In general, women with hypogonadotropic amenorrhoea are potentially fertile.
FSH
Outflow tract abnormalities tend to be normogonadotropic and FSH levels are in the normal range.         Gonadal, usually ovarian, abnormalities tend to be linked to elevated FSH levels or hypergonadotropic amenorrhoea. FSH levels are typically in the menopausal range.            Both hypothalamic and pituitary disorders are linked to low FSH levels leading to hypogonadotropic amenorrhoea.
Primary
                •             Uterine: Müllerian agenesis (Second most common cause, 15% of primary amenorrhoea)
•             Vaginal: Vaginal atresia, cryptomenorrhoea, imperforate hymen.
•             Gonadal  dysgenesis, including Turner syndrome, is the most common cause.
•             Androgen insensitivity syndrome (Testicular feminization syndrome)
•             Receptor abnormalities for hormones FSH and LH
•             Specific forms of congenital adrenal hyperplasia
•             Swyer syndrome
•             Galactosaemia
•             Aromatase deficiency
•             Prader-Willi syndrome
•             Male pseudo-hermaphroditism (about 1 in every 150,000 births)
•             Müllerian agenesis/MRKH Syndrome
•             Other intersexed conditions
                •             hypothalamic: Kallmann syndrome
Secondary          
•             Intrauterine adhesions (Asherman's syndrome)
•             Pregnancy (most common cause)
•             Anovulation
•             Menopause
•             Premature menopause
•             Polycystic ovary syndrome
•             Drug-induced
•             Breastfeeding
•             Hypothalamic: Exercise amenorrhoea, related tophysical exercise, stress amenorrhoea, eating disorders and weight loss (obesity, anorexia nervosa, or bulimia)
•             Pituitary: Sheehan syndrome, hyperprolactinaemia,haemochromatosis
•             Other central regulatory: hypothyroidism, hyperthyroidism, arrhenoblastoma
Cause Low body weight
Women who perform considerable amounts of exercise on a regular basis or lose a significant amount of weight are at risk of developing hypothalamic (or 'athletic') amenorrhoea. Functional Hypothalamic Amenorrhoea (FHA) can be caused by stress, weight loss, and/or excessive exercise. Many women who diet or who exercise at a high level do not take in enough calories to expend on their exercise as well as to maintain their normal menstrual cycles. The threshold of developing amenorrhoea appears to be dependent on low energy availability rather than absolute weight because a critical minimum amount of stored, easily mobilized energy is necessary to maintain regular menstrual cycles.
Energy imbalance and weight loss can disrupt menstrual cycles through several hormonal mechanisms. Weight loss can cause elevations in the hormone ghrelin which inhibits the hypothalamic-pituitary-ovarial axis.[9] Elevated concentrations of ghrelin alter the amplitude of GnRH pulses, which causes diminished pituitary release of LH and follicle-stimulating hormone (FSH).
Secondary amenorrhea is caused by low levels of the hormone leptin in females with low body weight.  Like ghrelin, leptin signals energy balance and fat stores to the reproductive axis. Decreased levels of leptin are closely related to low levels of body fat, and correlate with a slowing of GnRH pulsing.
When a woman is experiencing amenorrhoea, an eating disorder, and osteoporosis together, this is called female athlete triad syndrome. A lack of eating causes amenorrhoea and bone loss leading to osteopenia and sometimes progressing to osteoporosis.[citation needed]
The social effects of amenorrhoea on a person vary significantly. Amenorrhoea is often associated with anorexia nervosa and other eating disorders, which have their own effects. If secondary amenorrhoea is triggered early in life, for example through excessive exercise or weight loss, menarche may not return later in life. A woman in this situation may be unable to become pregnant, even with the help of drugs. Long-term amenorrhoea leads to an estrogens deficiency which can bring about menopause at an early age. The hormone oestrogen plays a significant role in regulating calcium loss after ages 25–30. When her ovaries no longer produce oestrogen because of amenorrhoea, a woman is more likely to suffer rapid calcium loss, which in turn can lead to osteoporosis. Increased testosterone levels cause by amenorrhoea may lead to body hair growth and decreased breast size. Increased levels of androgens, especially testosterone, can also lead to ovarian cysts. Some research among amenorrhoea runners indicates that the loss of menses may be accompanied by a loss of self-esteem.
Drug-induced
Certain medications, particularly contraceptive medications, can induce amenorrhoea in a healthy woman. The lack of menstruation usually begins shortly after beginning the medication and can take up to a year to resume after stopping a medication. Hormonal contraceptives that contain only progestogen like the oral contraceptive Micronor, and especially higher-dose formulations like the injectable Depo Provera commonly induce this side-effect. Extended cycle use of combined hormonal contraceptives also allow suppression of menstruation. Patients who use and then cease using contraceptives like the combined oral contraceptive pill may experience secondary amenorrhoea as a withdrawal symptom. The link is not well understood, as studies have found no difference in hormone levels between women who develop amenorrhoea as a withdrawal symptom following the cessation of OCOP use and women who experience secondary amenorrhoea because of other reasons. New contraceptive pills, like continuous oral contraceptive pills (OCPs) which do not have the normal 7 days of placebo pills in each cycle, have been shown to increase rates of amenorrhoea in women. Studies show that women are most likely to experience amenorrhoea after 1 year of treatment with continuous OCP use.
The use of opiates (such as heroin) on a regular basis has also been known to cause amenorrhoea in longer term users.[citation needed]
Anti-psychotic drugs used to treat schizophrenia have been known to cause amenorrhoea as well. New research suggests that adding a dosage of Metformin to an anti-psychotic drug regimen can restore menstruation. Metformin decreases resistance to the hormone insulin, as well as levels of prolactin, testosterone, and lutenizing hormone (LH). Metformin also decreases the LH/FSH ratio. Results of the study on Metformin further implicate the regulation of these hormones as a main cause of secondary amenorrhoea.
Breastfeeding
Breastfeeding is a common cause of secondary amenorrhoea, and often the condition lasts for over six months.[20] Breastfeeding typically lasts longer than lactational amenorrhoea, and the duration of amenorrhoea varies depending on how often a women breastfeeds. Lactational amenorrhoea has been advocated as a method of family planning, especially in developing countries where access to other methods of contraception may be limited. Breastfeeding is said to prevent more births in the developing world than any other method of birth control or contraception. Lactational amenorrhoea is 98% percent effective as a method of preventing pregnancy in the first six months postpartum.
Physical
Amenorrhoea can also be caused by physical deformities. One example of this is Mayer–Rokitansky–Küster–Hauser syndrome, the second-most common cause of primary amenorrhoea. The syndrome is characterized by Müllerian agenesis. In MRKH Syndrome, the Müllerian ducts do not develop, which prevents menstruation. The syndrome usually develops during the first trimester of pregnancy. MRI techniques can be helpful in determining the extent of the problem. Women may recover from MRKH syndrome, but other times primary amenorrhoea, which is characteristic of the disorder, may prevent pregnancy for life.
DiagnosisPrimary amenorrhoea
Primary amenorrhoea can be diagnosed in women by age 14 if no secondary sex characteristics, such as enlarged breasts and body hair, are present In the absence of secondary sex characteristics, the most common cause of amenorrhoea is low levels of FSH and LH caused by a delay in puberty. Gonadal dysgenesis, often associated withTurner's Syndrome, or premature ovarian failure may also be to blame. If secondary sex characteristics are present, but menstruation is not, primary amenorrhoea can be diagnosed by age 16. A reason for this occurrence may be that a person phenotypically female but genetically male, a situation known as androgen insensitivity syndrome. If undescended testes are present, they are often removed after puberty (~21 years of age) due to the increased risk of testicular cancer. In the absence of undescended testes, an MRI can be used to determine whether or not a uterus is present. Müllerian agenesis causes around 15% of primary amenorrhoea cases. If a uterus is present, outflow track obstruction may be to blame for primary amenorrhoea.
Secondary amenorrhea
Secondary amenorrhea's most common and most easily diagnosable causes are pregnancy, thyroid disease, and hyperprolactinemia. A pregnancy test is a common first step for diagnosis.[Hyperprolactinemia, characterized by high levels of the hormone prolactin, is often associated with a pituitary tumor. A dopamine agonist can often help relieve symptoms. The subsiding of the causal syndrome is usually enough to restore menses after a few months. Secondary amenorrhea may also be caused by outflow tract obstruction, often related to Asherman's Syndrome. Polycystic ovary syndrome can cause secondary amenorrhea, although the link between the two is not well understood. Ovarian failure related to early onset menopause can cause secondary amenorrhea, and although the condition can usually be treated, it is not always reversible. Secondary amenorrhea is also caused by stress, extreme weight loss, and excessive exercise. Young athletes are particularly vulnerable, although normal menses usually return with healthy body weight. Causes of secondary amenorrhea can also result in primary amenorrhea, especially if present before onset of menarche.
Treatments
Treatments vary based on the underlying condition. Key issues are problems of surgical correction if appropriate and oestrogen therapy if oestrogen levels are low. For those who do not plan to have biological children, treatment may be unnecessary if the underlying cause of the amenorrhoea is not threatening to their health. However, in the case of athletic amenorrhoea, deficiencies in estrogen and leptin often simultaneously result in bone loss, potentially leading to osteoporosis.
"Athletic" amenorrhoea which is part of the female athlete triad is treated by eating more and decreasing the amount and intensity of exercise. If the underlying cause is the athlete triad then a multidisciplinary treatment including monitoring from a physician, dietitian, and mental health counselor is recommended, along with support from family, friends, and coaches. Although oral contraceptives can causes menses to return, oral contraceptives should not be the initial treatment as they can mask the underlying problem and allow other effects of the eating disorder, like osteoporosis, continue to develop. Weight recovery, or increased rest does not always catalyze the return of a menses. Recommencement of ovulation suggests a dependency on a whole network of neurotransmitters and hormones, altered in response to the initial triggers of secondary amenorrhoea. To treat drug-induced amenorrhoea, stopping the medication on the advice of a doctor is a usual course of action.
Looking at Hypothalamic amenorrhoea, studies have provided that the administration of a selective serotonin reuptake inhibitor (SSRI) might correct abnormalities of Functional Hypothalamic Amenorrhoea (FHA) related to the condition of stress-related amenorrhoea. This involves the repair of the PI3K signaling pathway, which facilitates the integration of metabolic and neural signals regulating gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH). In other words, it regulates the neuronal activity and expression of neuropeptide systems that promote GnRH release. However, SSRI therapy represents a possible hormonal solution to just one hormonal condition of hypothalamic amenorrhoea. Furthermore, because the condition involves the inter workings of many different neurotransmitters, much research is still to be done on presenting hormonal treatment that would counteract the hormonal affects.
As for physiological treatments to hypothalamic amenorrhoea, injections of metreleptin (r-metHuLeptin) have been tested as treatment to oestrogen deficiency resulting from low gonadotropins and other neuroendocrine defects such as low concentrations of thyroid and IGF-1. R-metHuLeptin has appeared effective in restoring defects in the hypothalamic-pituitary-gonadal axis and improving reproductive, thyroid, and IGF hormones, as well as bone formation, thus curing the amenorrhoea and infertility. However, it has not proved effective in restoring of cortisol and adrenocorticotropin levels, or bone resorption

Ayurvedic treatment
1-the use of bastis is beneficial.
2-fish kulattha,sour substances (kanji),tail,mamsa , wine ,urine(cow urine), butter-milk mixed with half water, curd and sukta should be used in diet and drinks
3-in all disorders  of artava use of lasuna , satpushpa and  satavari is beneficial.
4-A pessary made with powdered seed of ikswaku,danti,capala,jiggery,madanphla ,kinva and yavasuka triturated with latex of snuhi should be placed in yoni(cervix).this induces menstruation.
5-use of powdered leaves of jyotismati, swarjikasara or rajika ugra and steam bark of asana with cold water for three days induces menstruation positively
6-use of satawaryadi anuwasana basti is beneficial
AYURVEDIC FORMULATIONS 
1 Phalaghrata
2-Vrhatsatavari ghrta
3-Arogya vardhini vati
4- Rajaha pravartini vati
5-Dashmularista
6-Rkata pachak kwath
7-Rashpachak kwath


Saturday, 9 December 2017

Stevens–Johnson syndrome (SJS

Stevens–Johnson syndrome (SJS) is a type of severe skin reaction. Together with toxic epidermal necrolysis (TEN) it forms a spectrum of disease, with SJS being less severe. Early symptoms include fever and flu-like symptoms.
 A few days later the skin begins to blister and peel forming painful raw areas. Mucous membranes, such as the mouth, are also typically involved. Complications include dehydration, sepsis, pneumonia, and multiple organ failure.
The most common cause is certain medications such as 
1-lamotrigine,
2-carbamazepine,
3-allopurinol,
4-sulphonamide
 5-antibiotics,
6- nevirapine.
Other causes can include infections such as Mycoplasma pneumoniae and cytomegalovirus or the cause may remain unknown. Risk factors include HIV/AIDS and systemic lupus erythematosus. The diagnosis is based on involvement of less than 10% of the skin. It is known as TEN when more than 30% of the skin is involved and an intermediate form with 10 to 30% involvement. Erythema multiform (EM) is generally considered a separate condition.
Treatment -
v Treatment typically takes place in hospital such as in a burn unit or intensive care unit. Efforts may include stopping the cause, pain medication, antihistamines, antibiotics, intravenous immunoglobulins, or corticosteroids.
v Together with TEN it affects 1 to 2 people per million per year.
v It is twice as common in males as females. Typical onset is under the age of 30. Skin usually regrows over two to three weeks; however, complete recovery can take months.

v Signs and symptoms

v Mucosal desquamation in a person with Stevens–Johnson syndrome.
v Conjunctivitis (inflammation of eye and eyelid) in SJS
v SJS usually begins with fever, sore throat, and fatigue, which is commonly misdiagnosed and therefore treated with antibiotics. SJS and TEN are often heralded by fever, sore throat, cough, and burning eyes for 1 to 3 days. Patients with SJS and TEN frequently experience burning pain of their skin at the start of disease. Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips, but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in about 30% of children who develop SJS.[medical citation needed] A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.
Causes
SJS is thought to arise from a disorder of the immune system. The immune reaction can be triggered by drugs or infections. Genetic factors are associated with a predisposition to SJS. The cause of SJS is unknown in one-quarter to one-half of cases. SJS and TEN are considered a single disease with common causes and mechanisms.
Medication
Although SJS can be caused by viral infections and malignancies, the main cause is medications. A leading cause appears to be the use of antibiotics, particularly sulfa drugs. Between 100 and 200 different drugs may be associated with SJS. No reliable test exists to establish a link between a particular drug and SJS for an individual case. Determining what drug is the cause is based on the time interval between first use of the drug and the beginning of the skin reaction. Drugs discontinued more than 1 month prior to onset of mucocutaneous physical findings are highly unlikely to cause SJS and TEN. SJS and TEN most often begin between 4 and 28 days after culprit drug administration. A published algorithm (ALDEN) to assess drug causality gives structured assistance in identifying the responsible medication.
v SJS may be caused by adverse effects of the drugs vancomycin,
Ø allopurinol,
Ø valproate,
Ø levofloxacin,
Ø diclofenac,
Ø etravirine,
Ø isotretinoin,
Ø fluconazole,
Ø valdecoxib,
Ø sitagliptin,
Ø oseltamivir,
Ø penicillins,
Ø barbiturates,
Ø sulfonamides,
Ø phenytoin,
Ø azithromycin,
Ø oxcarbazepine,
Ø zonisamide,
Ø modafinil,
Ø lamotrigine,
Ø nevirapine,
Ø pyrimethamine,
Ø ibuprofen,
Ø carbamazepine,
Ø bupropion,
Ø telaprevir,and nystatin.
Medications that have traditionally been known to lead to SJS, erythema multiforme, and toxic epidermal necrolysis include sulfonamideantibiotics, penicillin antibiotics, cefixime (antibiotic), barbiturates (sedatives), lamotrigine, phenytoin (e.g., Dilantin) (anticonvulsants) and trimethoprim. Combining lamotrigine with sodium valproate increases the risk of SJS.
Ø Nonsteroidal anti-inflammatory drugs (NSAIDs) are a rare cause of SJS in adults; the risk is higher for older patients, women, and those initiating treatment.Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. Similar to NSAIDs, paracetamol (acetaminophen) has also caused rare cases of SJS. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.
Infections
Ø In pediatric cases, Epstein-Barr virus and enteroviruses have been associated with SJS.
Ø Recent upper respiratory tract infections have been reported by more than half of patients with SJS.
Ø Bacterial infections linked to SJS include group A beta-hemolytic streptococci, diphtheria, brucellosis, lymphogranuloma venereum, mycobacteria, Mycoplasma pneumoniae, rickettsial infections, tularemia, and typhoid.
Ø Fungal infections with coccidioidomycosis, dermatophytosis, and histoplasmosis are also considered possible causes. Malaria and trichomoniasis, protozoal infections, have also been reported as causes.


🧠 Developmental Milestones (3.5–4 years)

  🧠 Developmental Milestones (3.5–4 years) 1. 🗣️ Language & Communication Speaks in 4–6 word sentences Can tell simple stories ...