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Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14]
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11
IJPCR |Volume 1 | Issue 1 | Jan – Jun- 2017
www.ijpcr.net
Case Report Clinical Research
Chronic telogen effluvium: An outcome after ventricular septal defect closure
surgery: a rare case report
D. Ashok Kumar1*
, P.Alekhya1
, R.Siddarama1
, P Pallavi Priya2
, M. Purushothaman3
1
Pharm.D Intern, Department of Pharmacy Practice, P.Rami Reddy Memorial College of Pharmacy, Utukur,
Kadapa-516003
2
Assistant Professor, Department of Pharmacy Practice, P. Rami Reddy Memorial College of Pharmacy, Utukur,
Kadapa-516003.
3
Principal, Department of Pharmacy Practice, P. Rami Reddy Memorial College of Pharmacy, Utukur, Kadapa-
516003.
*
Address for correspondence: Dr. D. Ashok Kumar
E-mail: ashokakki1030@gmail.com
ABSTRACT
Telogen effluvium (TE) is the common cause of diffuse nonscarring hair loss. TE is caused by any disruption of hair cycle
resulting in increased, synchronized telogen shedding. In children, TE has been reported to be responsible for only a
minority of cases with hair loss. The functional mechanism of shedding in majority of these cases is immediate anagen
release. A male child of age seven years presented the out-patient department of DVL, RIMS Kadapa, with the history of
shedding of hair on head and eyebrows. He is a known congenital heart disease (ventricular septal defect) for which he has
undergone ventricular septal defect closure surgery. After a period of six months, shedding of hair on the head and eye
brows was noticed. After examining the patient, the dermatologist diagnosed as Telogen effluvium and prescribed
Mometasone furoate (synthetic corticosteroid with anti-inflammatory activity), betamethasone, ferrous fumarate (used to
treat anaemia not enough red blood cells in the blood) and isotretinoin. Based on the pathogenesis of TE, potential
therapeutic options include inhibition of catagen (so as to prolong anagen); induction of anagen in telogen follicles; or
inhibition of exogen (to reduce hair shaft shedding). Differentiating TE from other causes of diffuse nonscarring hair loss
can indeed be a daunting task. A number of factors have been implicated in the causation of TE, however, clear evidence in
their support is lacking. Possible treatment options for TE, especially the chronic form, are not many. Treatment for TE is
primarily reassurance and counselling.
Keywords: Anagen, Congenital heart disease, Diffuse nonscarring hair loss, Telogen effluvium, Ventricular septal defect.
INTRODUCTION
Telogen effluvium (TE) is the most common cause
of diffuse nonscarring hair loss. Hair loss or alopecia
is a very common complaint and rational, wide-
ranging classification system of various causes based
on etiopathogenetic principles is still deficient. [1]
Diffuse cyclical hair loss (DCHL) was the initial term
ISSN:2521-2206
International Journal of Pharmacology and
Clinical Research (IJPCR)
Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14]
www.ijpcr.net
12
used to describe discrete transitory episodes of
alterable, diffuse hair shedding. The word TE was first
coined by Kligman to describe increased shedding of
normal club hairs. The degree of effluvium depends on
the severity and duration of exposure, rather than on
the type of agent. TE is caused by any disruption of
hair cycle resulting in increased, synchronized telogen
shedding. [2] ATE can occur in either sex if the proper
inciting conditions occur. The effect of age is
uncertain, with elderly women more susceptible to
acute telogen effluvium (ATE) subsequent high fever,
severe hemorrhage, surgical trauma, or immense
psychological stress. In children, TE has been reported
to be responsible for only a minority of cases with hair
loss (2.7%). [3] In humans, synchronous hair growth
disappears in childhood. A usual normal scalp has
100,000 hairs, with approximately 86% being in
anagen, 1% in catagen, and 13% in telogen. With TE,
the ratio changes to 70% anagen and 30% telogen,
with regular shedding of up to 300 hairs. [4, 5]
Conversely, it must be kept in mind that the degree of
disability due to hair loss varies widely from patient to
patient and does not always accord with the objective
assessment of hair shedding.[6] The causal
mechanisms for this common endpoint of telogen
shedding may be entirely different in different cases.
The functional mechanism of shedding in majority of
these cases is immediate anagen release. [7] TG (ATE
seen 2-5 months after childbirth) is a distinctive form
allied with pregnancy and childbirth. [8, 9]
Acute telogen effluvium
 High fever
 Surgery[10]
 Hospitalization
 Hemorrhage[11]
 emotional stress[12]
 Changes in medication
 Postpartum (TG)
 Heavy metals: Arsenic,[13] thallium,[14] and
selenium[15]
ATE usually remits within few months in 95% of
cases. A small proportion of TG cases may experience
persistent, episodic shedding as some follicles may not
revert to an asynchronous growth pattern. [16]
Chronic telogen effluvium
CTE is a primary, idiopathic condition affecting
middle-aged women, which needs to be differentiated
from CDTHL secondary to organic causes and AGA.
It presents as TE lasting more than 6 months, without
any widening of central part or follicular
miniaturization.[17] The disorder appears to be
distinct from ATE because of its prolonged,
fluctuating course.[18] Although, some cases of CTE
may follow ATE with a known trigger, in most cases a
specific trigger cannot be identified.[19] Clinical
features include an insidious onset and a fluctuating
course lasting for several years.
Chronic diffuse telogen hair loss
CDTHL refers to telogen hair shedding, longer
than 6 months, secondary to a variety of organic
causes. Prominent ones include thyroid disorders,
profound iron deficiency anemia (IDA), acrodermatitis
enteropathica, and malnutrition.[20] Although many
drugs have been implicated in causing TE there are no
controlled studies examining possible causal
relationship.[21] Drugs can induce hair loss by
inducing an abrupt cessation of mitotic activity
(anagen effluvium) or by precipitating follicles into
premature rest (TE).[22] Although hair loss seems to
be a daunting disorder to evaluate, breaking down the
history, examination, and discussion into digestible
parts makes the experience easy. [23] Treatment for
TE is primarily reassurance and counselling. If
attempts at identifying a specific cause have been
fruitful, one should correct them. An expectant
management and observation are usually appropriate
as shedding is expected to cease within 3-6 months
and thereafter recovery should be complete. [24, 25]
This rare case report explains about telogen effluvium
(TE), which was observed after ventricular septal
defect closure surgery at the age of 9 months/3 days.
CASE STUDY
A male child of age seven years presented the out-
patient department of DVL, RIMS Kadapa, with the
history of shedding of hair on head and eyebrows. He
is a known history of poor weight gain and frequent
upper respiratory tract infections. He is a known
congenital heart disease (ventricular septal defect) for
which he has undergone ventricular septal defect
closure surgery. The diagnosis and surgical procedure
was shown in figure-1. Patient was ventilated in ICU
post-operatively and treated with analgesics,
antibiotics and diuretics. Patient general condition was
stable and discharged with the following medication
shown in figure-2. After a period of six months,
shedding of hair on the head and eye brows was
observed in figure-3. After examining the patient, the
dermatologist diagnosed as Telogen effluvium and
prescribed with the following medication:
Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14]
www.ijpcr.net
13
1. Tecum lotion 0.1% 10 ml
2. Salisone lotion 20 ml
3. Trichoton syrup 150 ml
4. Tab. B-complex OD
5. Tab. Multivitamin OD
6. Cap. A & D OD
7. Tab. Neotrex 2.5 mg (weekly 1 tab./4 weeks)
8. Tab. folirte 5 mg ½ tab. daily (should not
administered while taking neotrex).
DISCUSSION
TE is caused by any disruption of hair cycle
resulting in increased, synchronized telogen shedding.
TE has been reported to be responsible for only a
minority of cases with hair loss. The degree of
disability due to hair loss varies widely from patient to
patient and does not always accord with the objective
assessment of hair shedding. The functional
mechanism of shedding in majority of these cases is
immediate anagen release. TG (ATE seen 2-5 months
after childbirth) is a distinctive form associated with
pregnancy and childbirth. [26] ATE usually remits
within few months in 95% of cases. Some cases of
CTE may follow ATE with a known trigger, in most
cases a specific trigger cannot be identified.[27]
Although many drugs have been implicated in causing
TE there are no controlled studies examining possible
causal relationship. Drugs can induce hair loss by
inducing an abrupt cessation of mitotic activity (anagen
effluvium).
Anticoagulants (blood thinners), including
 Warfarin sodium
 Heparin injections
Cholesterol lowering drugs, including
 Clofibrate
 Gemfibrozil
Anticonvulsants
Antidepression drugs, including
 Clomipramine
 Amitriptyline
 Desipramine
 Nortriptyline
Diet/weight
Loss: Amphetamines
Heart/high blood pressure
Many drugs prescribed for the heart, including the
beta-blockers, which are also used to treat high blood
pressure, and include:
 Atenolol
 Metoprolol
 Nadolol
Based on the pathogenesis of TE, potential
therapeutic options include inhibition of catagen (so as
to prolong anagen); induction of anagen in telogen
follicles; or inhibition of exogen (to reduce hair shaft
shedding). Treatment for TE is primarily reassurance
and counseling. Tecum lotion contains mometasone
furoate for dermatologic use. Mometasone furoate is a
synthetic corticosteroid with anti-inflammatory
activity. The mechanism of the anti-inflammatory
activity of the topical steroids, in general, is unclear.
Apply a few drops of lotion to the affected skin areas
once daily and massage lightly. Salisone lotion
contains betamethasone used in various dermatological
disorders. Apply a few drops to the affected area of the
skin two times per day (morning and evening).
Trichoton syrup contains ferrous fumarate is used to
treat anaemia not enough red blood cells in the blood.
It is an iron containing drug and is sometimes known
as an oral iron salt. It is used to treat anaemia caused
by a deficiency of iron. Tab. Neotrex contains
isotretinoin. It induces apoptosis (cell death) in various
cells in the body. Tab. folirte 5 mg ½ tab. daily (should
not administered while taking neotrex).
CONCLUSION
Differentiating TE from other causes of diffuse
nonscarring hair loss can indeed be a daunting task. A
Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14]
www.ijpcr.net
14
number of factors have been implicated in the
causation of TE, however, clear evidence in their
support is lacking. Possible treatment options for TE,
especially the chronic form, are not many. The
outcomes have improved as we have gained more
knowledge about the factors that control hair follicle
cycling.
Abbreviations
ATE- Acute telogen effluvium; CTE- Chronic
telogen effluvium; DVL- Dermatology, venereology
and Leprology; DCHL- Diffuse cyclical hair los; IDA-
iron deficiency anemia
Acknowledgements
The authors thank the staff of DVL and pharmacy
practice department.
Conflict of interest
The authors have no conflicts of interest to disclose.
REFERENCES
[1]. Wiedemeyeer K, Schill WB, Loser C. Diseases on hair follicles leading to hair loss part I: Nonscarring alopecias.
Kinmed 3, 2004, 209-14.
[2]. De Berker D. Clinical relevance of hair microscopy in alopecia. Clin Exp Dermatol 27, 2002, 366-72.
[3]. Nnoruka EN, Obiagboso I, Maduechesi C. Hair loss in children in South-East Nigeria: Common and uncommon cases.
Int J Dermatol 46(1), 2007, 18-22.
[4]. Olsen E. Androgenetic alopecia. In: Disorders of hair growth. New York, NY: McGraw-Hill, Inc; 1994, 257-83.
[5]. Shapiro J. Diseases of the hair. In: Raykel R, editor. Conn’s current therapy. Philadelphia, Pa: WB Saunders; 1996,
739-41.
[6]. Messenger A. Hair loss. Clin Exp Dermatol 27, 2002, 357.
[7]. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol 129, 1993, 356-63.
[8]. Strumia R. Dermatologic signs in patients with eating disorders. Am J Clin Dermatol 6, 2005, 165-73.
[9]. Kligman AM. Pathologic dynamics of human hair loss. I. Telogen effuvium. Arch Dermatol 83, 1961, 175-98.
[10]. Dawber RPR, Simpson NB, Barth JH. Diffuse alopecia: Endocrine, metabolic and chemical influences on the follicular
cycle. In: Dawber RP, editor. Diseases of the Hair and Scalp. Oxford: Blackwell Science; 1997, 123-50.
[11]. Hadshiew IM, Foitzik K, Arck PC, Paus R. Burden of hair loss: Stress and the underestimated psychosocial impact of
telogen effluvium and androgenetic alopecia. J Invest Dermatol 123, 2004, 455 7.
[12]. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol 129, 1993, 356-63.
[13]. Smith AG. Drug induced disorders of hair and nails. AdverseDrug React Bull 173, 1995, 655-8.
[14]. Wirth H, Dunsing W, Gloor M. Telogen effluvium following application of selenium disulfide in the guinea pig.
Hautarzt 31, 1980, 502-4.
[15]. Center for Disease Control and Prevention (CDC). Thallium poisoning from eating contaminated cake--Iraq, 2008.
MMWR Morb Mortal Wkly Rep 57, 2008, 1015-8.
[16]. Messenger AG, de Berker DA, Sinclair RD. Disorders of Hair. In: Burns T, Breathnach S, Cox N, Griffiths C, editors.
Rook’s textbook of Dermatology. 8th ed. UK: Blackwell Publishing Ltd; 66, 2010, 27-66.
[17]. Harrison S, Sinclair R. Telogen effluvium. Clin Exp Dermatol 27, 2002, 389-5.
[18]. Dawber RPR, Simpson NB, Barth JH. Diffuse alopecia: Endocrine, metabolic and chemical influences on the follicular
cycle. In: Dawber RP, editor. Diseases of the Hair and Scalp. Oxford: Blackwell Science; 1997, 123-50.
[19]. Tosti A, Misciali C, Piraccini BM, Peluso AM, Bardazzi F. Drug induced hair loss and hair growth. Drug Saf 10, 1994,
310-7.
[20]. Hordinsky MK. Medical treatment of noncicatricial alopecia. Semin Cutan Med Surg 25, 2006, 51-5.
[21]. McMichael A. Approach to office visits for hair loss in women. Cutis 87, 2011, 8-9.
[22]. Whiting DA. Chronic telogen effluvium. Dermatol Clin 14, 1996, 723-31.
[23]. Messenger A. Hair loss. Clin Exp Dermatol 27, 2002, 357.
[24]. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol 129, 1993, 356-63.
[25]. Strumia R. Dermatologic signs in patients with eating disorders. Am J Clin Dermatol 6, 2005, 165-73.
[26]. Harrison S, Sinclair R. Telogen effluvium. Clin Exp Dermatol 27, 2002, 389-5.
[27]. Paus R, Olsen EA, Messenger AG. Hair growth disorders. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller
As, Leffell DJ, editors. Fitzpatrick’s Dermatology in General Medicine. USA; The McGraw-Hill Companies Inc.; 7,
2008, 753-77.

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Chronic telogen effluvium: An outcome after ventricular septal defect closure surgery: a rare case report

  • 1. Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14] www.ijpcr.net 11 IJPCR |Volume 1 | Issue 1 | Jan – Jun- 2017 www.ijpcr.net Case Report Clinical Research Chronic telogen effluvium: An outcome after ventricular septal defect closure surgery: a rare case report D. Ashok Kumar1* , P.Alekhya1 , R.Siddarama1 , P Pallavi Priya2 , M. Purushothaman3 1 Pharm.D Intern, Department of Pharmacy Practice, P.Rami Reddy Memorial College of Pharmacy, Utukur, Kadapa-516003 2 Assistant Professor, Department of Pharmacy Practice, P. Rami Reddy Memorial College of Pharmacy, Utukur, Kadapa-516003. 3 Principal, Department of Pharmacy Practice, P. Rami Reddy Memorial College of Pharmacy, Utukur, Kadapa- 516003. * Address for correspondence: Dr. D. Ashok Kumar E-mail: ashokakki1030@gmail.com ABSTRACT Telogen effluvium (TE) is the common cause of diffuse nonscarring hair loss. TE is caused by any disruption of hair cycle resulting in increased, synchronized telogen shedding. In children, TE has been reported to be responsible for only a minority of cases with hair loss. The functional mechanism of shedding in majority of these cases is immediate anagen release. A male child of age seven years presented the out-patient department of DVL, RIMS Kadapa, with the history of shedding of hair on head and eyebrows. He is a known congenital heart disease (ventricular septal defect) for which he has undergone ventricular septal defect closure surgery. After a period of six months, shedding of hair on the head and eye brows was noticed. After examining the patient, the dermatologist diagnosed as Telogen effluvium and prescribed Mometasone furoate (synthetic corticosteroid with anti-inflammatory activity), betamethasone, ferrous fumarate (used to treat anaemia not enough red blood cells in the blood) and isotretinoin. Based on the pathogenesis of TE, potential therapeutic options include inhibition of catagen (so as to prolong anagen); induction of anagen in telogen follicles; or inhibition of exogen (to reduce hair shaft shedding). Differentiating TE from other causes of diffuse nonscarring hair loss can indeed be a daunting task. A number of factors have been implicated in the causation of TE, however, clear evidence in their support is lacking. Possible treatment options for TE, especially the chronic form, are not many. Treatment for TE is primarily reassurance and counselling. Keywords: Anagen, Congenital heart disease, Diffuse nonscarring hair loss, Telogen effluvium, Ventricular septal defect. INTRODUCTION Telogen effluvium (TE) is the most common cause of diffuse nonscarring hair loss. Hair loss or alopecia is a very common complaint and rational, wide- ranging classification system of various causes based on etiopathogenetic principles is still deficient. [1] Diffuse cyclical hair loss (DCHL) was the initial term ISSN:2521-2206 International Journal of Pharmacology and Clinical Research (IJPCR)
  • 2. Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14] www.ijpcr.net 12 used to describe discrete transitory episodes of alterable, diffuse hair shedding. The word TE was first coined by Kligman to describe increased shedding of normal club hairs. The degree of effluvium depends on the severity and duration of exposure, rather than on the type of agent. TE is caused by any disruption of hair cycle resulting in increased, synchronized telogen shedding. [2] ATE can occur in either sex if the proper inciting conditions occur. The effect of age is uncertain, with elderly women more susceptible to acute telogen effluvium (ATE) subsequent high fever, severe hemorrhage, surgical trauma, or immense psychological stress. In children, TE has been reported to be responsible for only a minority of cases with hair loss (2.7%). [3] In humans, synchronous hair growth disappears in childhood. A usual normal scalp has 100,000 hairs, with approximately 86% being in anagen, 1% in catagen, and 13% in telogen. With TE, the ratio changes to 70% anagen and 30% telogen, with regular shedding of up to 300 hairs. [4, 5] Conversely, it must be kept in mind that the degree of disability due to hair loss varies widely from patient to patient and does not always accord with the objective assessment of hair shedding.[6] The causal mechanisms for this common endpoint of telogen shedding may be entirely different in different cases. The functional mechanism of shedding in majority of these cases is immediate anagen release. [7] TG (ATE seen 2-5 months after childbirth) is a distinctive form allied with pregnancy and childbirth. [8, 9] Acute telogen effluvium  High fever  Surgery[10]  Hospitalization  Hemorrhage[11]  emotional stress[12]  Changes in medication  Postpartum (TG)  Heavy metals: Arsenic,[13] thallium,[14] and selenium[15] ATE usually remits within few months in 95% of cases. A small proportion of TG cases may experience persistent, episodic shedding as some follicles may not revert to an asynchronous growth pattern. [16] Chronic telogen effluvium CTE is a primary, idiopathic condition affecting middle-aged women, which needs to be differentiated from CDTHL secondary to organic causes and AGA. It presents as TE lasting more than 6 months, without any widening of central part or follicular miniaturization.[17] The disorder appears to be distinct from ATE because of its prolonged, fluctuating course.[18] Although, some cases of CTE may follow ATE with a known trigger, in most cases a specific trigger cannot be identified.[19] Clinical features include an insidious onset and a fluctuating course lasting for several years. Chronic diffuse telogen hair loss CDTHL refers to telogen hair shedding, longer than 6 months, secondary to a variety of organic causes. Prominent ones include thyroid disorders, profound iron deficiency anemia (IDA), acrodermatitis enteropathica, and malnutrition.[20] Although many drugs have been implicated in causing TE there are no controlled studies examining possible causal relationship.[21] Drugs can induce hair loss by inducing an abrupt cessation of mitotic activity (anagen effluvium) or by precipitating follicles into premature rest (TE).[22] Although hair loss seems to be a daunting disorder to evaluate, breaking down the history, examination, and discussion into digestible parts makes the experience easy. [23] Treatment for TE is primarily reassurance and counselling. If attempts at identifying a specific cause have been fruitful, one should correct them. An expectant management and observation are usually appropriate as shedding is expected to cease within 3-6 months and thereafter recovery should be complete. [24, 25] This rare case report explains about telogen effluvium (TE), which was observed after ventricular septal defect closure surgery at the age of 9 months/3 days. CASE STUDY A male child of age seven years presented the out- patient department of DVL, RIMS Kadapa, with the history of shedding of hair on head and eyebrows. He is a known history of poor weight gain and frequent upper respiratory tract infections. He is a known congenital heart disease (ventricular septal defect) for which he has undergone ventricular septal defect closure surgery. The diagnosis and surgical procedure was shown in figure-1. Patient was ventilated in ICU post-operatively and treated with analgesics, antibiotics and diuretics. Patient general condition was stable and discharged with the following medication shown in figure-2. After a period of six months, shedding of hair on the head and eye brows was observed in figure-3. After examining the patient, the dermatologist diagnosed as Telogen effluvium and prescribed with the following medication:
  • 3. Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14] www.ijpcr.net 13 1. Tecum lotion 0.1% 10 ml 2. Salisone lotion 20 ml 3. Trichoton syrup 150 ml 4. Tab. B-complex OD 5. Tab. Multivitamin OD 6. Cap. A & D OD 7. Tab. Neotrex 2.5 mg (weekly 1 tab./4 weeks) 8. Tab. folirte 5 mg ½ tab. daily (should not administered while taking neotrex). DISCUSSION TE is caused by any disruption of hair cycle resulting in increased, synchronized telogen shedding. TE has been reported to be responsible for only a minority of cases with hair loss. The degree of disability due to hair loss varies widely from patient to patient and does not always accord with the objective assessment of hair shedding. The functional mechanism of shedding in majority of these cases is immediate anagen release. TG (ATE seen 2-5 months after childbirth) is a distinctive form associated with pregnancy and childbirth. [26] ATE usually remits within few months in 95% of cases. Some cases of CTE may follow ATE with a known trigger, in most cases a specific trigger cannot be identified.[27] Although many drugs have been implicated in causing TE there are no controlled studies examining possible causal relationship. Drugs can induce hair loss by inducing an abrupt cessation of mitotic activity (anagen effluvium). Anticoagulants (blood thinners), including  Warfarin sodium  Heparin injections Cholesterol lowering drugs, including  Clofibrate  Gemfibrozil Anticonvulsants Antidepression drugs, including  Clomipramine  Amitriptyline  Desipramine  Nortriptyline Diet/weight Loss: Amphetamines Heart/high blood pressure Many drugs prescribed for the heart, including the beta-blockers, which are also used to treat high blood pressure, and include:  Atenolol  Metoprolol  Nadolol Based on the pathogenesis of TE, potential therapeutic options include inhibition of catagen (so as to prolong anagen); induction of anagen in telogen follicles; or inhibition of exogen (to reduce hair shaft shedding). Treatment for TE is primarily reassurance and counseling. Tecum lotion contains mometasone furoate for dermatologic use. Mometasone furoate is a synthetic corticosteroid with anti-inflammatory activity. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. Apply a few drops of lotion to the affected skin areas once daily and massage lightly. Salisone lotion contains betamethasone used in various dermatological disorders. Apply a few drops to the affected area of the skin two times per day (morning and evening). Trichoton syrup contains ferrous fumarate is used to treat anaemia not enough red blood cells in the blood. It is an iron containing drug and is sometimes known as an oral iron salt. It is used to treat anaemia caused by a deficiency of iron. Tab. Neotrex contains isotretinoin. It induces apoptosis (cell death) in various cells in the body. Tab. folirte 5 mg ½ tab. daily (should not administered while taking neotrex). CONCLUSION Differentiating TE from other causes of diffuse nonscarring hair loss can indeed be a daunting task. A
  • 4. Ashok K D et al / Int. J. of Pharmacology and Clin. Res. Vol-1(1) 2017 [11-14] www.ijpcr.net 14 number of factors have been implicated in the causation of TE, however, clear evidence in their support is lacking. Possible treatment options for TE, especially the chronic form, are not many. The outcomes have improved as we have gained more knowledge about the factors that control hair follicle cycling. Abbreviations ATE- Acute telogen effluvium; CTE- Chronic telogen effluvium; DVL- Dermatology, venereology and Leprology; DCHL- Diffuse cyclical hair los; IDA- iron deficiency anemia Acknowledgements The authors thank the staff of DVL and pharmacy practice department. Conflict of interest The authors have no conflicts of interest to disclose. REFERENCES [1]. Wiedemeyeer K, Schill WB, Loser C. Diseases on hair follicles leading to hair loss part I: Nonscarring alopecias. Kinmed 3, 2004, 209-14. [2]. De Berker D. Clinical relevance of hair microscopy in alopecia. Clin Exp Dermatol 27, 2002, 366-72. [3]. Nnoruka EN, Obiagboso I, Maduechesi C. Hair loss in children in South-East Nigeria: Common and uncommon cases. Int J Dermatol 46(1), 2007, 18-22. [4]. Olsen E. Androgenetic alopecia. In: Disorders of hair growth. New York, NY: McGraw-Hill, Inc; 1994, 257-83. [5]. Shapiro J. Diseases of the hair. In: Raykel R, editor. Conn’s current therapy. Philadelphia, Pa: WB Saunders; 1996, 739-41. [6]. Messenger A. Hair loss. Clin Exp Dermatol 27, 2002, 357. [7]. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol 129, 1993, 356-63. [8]. Strumia R. Dermatologic signs in patients with eating disorders. Am J Clin Dermatol 6, 2005, 165-73. [9]. Kligman AM. Pathologic dynamics of human hair loss. I. Telogen effuvium. Arch Dermatol 83, 1961, 175-98. [10]. Dawber RPR, Simpson NB, Barth JH. Diffuse alopecia: Endocrine, metabolic and chemical influences on the follicular cycle. In: Dawber RP, editor. Diseases of the Hair and Scalp. Oxford: Blackwell Science; 1997, 123-50. [11]. Hadshiew IM, Foitzik K, Arck PC, Paus R. Burden of hair loss: Stress and the underestimated psychosocial impact of telogen effluvium and androgenetic alopecia. J Invest Dermatol 123, 2004, 455 7. [12]. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol 129, 1993, 356-63. [13]. Smith AG. Drug induced disorders of hair and nails. AdverseDrug React Bull 173, 1995, 655-8. [14]. Wirth H, Dunsing W, Gloor M. Telogen effluvium following application of selenium disulfide in the guinea pig. Hautarzt 31, 1980, 502-4. [15]. Center for Disease Control and Prevention (CDC). Thallium poisoning from eating contaminated cake--Iraq, 2008. MMWR Morb Mortal Wkly Rep 57, 2008, 1015-8. [16]. Messenger AG, de Berker DA, Sinclair RD. Disorders of Hair. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook’s textbook of Dermatology. 8th ed. UK: Blackwell Publishing Ltd; 66, 2010, 27-66. [17]. Harrison S, Sinclair R. Telogen effluvium. Clin Exp Dermatol 27, 2002, 389-5. [18]. Dawber RPR, Simpson NB, Barth JH. Diffuse alopecia: Endocrine, metabolic and chemical influences on the follicular cycle. In: Dawber RP, editor. Diseases of the Hair and Scalp. Oxford: Blackwell Science; 1997, 123-50. [19]. Tosti A, Misciali C, Piraccini BM, Peluso AM, Bardazzi F. Drug induced hair loss and hair growth. Drug Saf 10, 1994, 310-7. [20]. Hordinsky MK. Medical treatment of noncicatricial alopecia. Semin Cutan Med Surg 25, 2006, 51-5. [21]. McMichael A. Approach to office visits for hair loss in women. Cutis 87, 2011, 8-9. [22]. Whiting DA. Chronic telogen effluvium. Dermatol Clin 14, 1996, 723-31. [23]. Messenger A. Hair loss. Clin Exp Dermatol 27, 2002, 357. [24]. Headington JT. Telogen effluvium. New concepts and review. Arch Dermatol 129, 1993, 356-63. [25]. Strumia R. Dermatologic signs in patients with eating disorders. Am J Clin Dermatol 6, 2005, 165-73. [26]. Harrison S, Sinclair R. Telogen effluvium. Clin Exp Dermatol 27, 2002, 389-5. [27]. Paus R, Olsen EA, Messenger AG. Hair growth disorders. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller As, Leffell DJ, editors. Fitzpatrick’s Dermatology in General Medicine. USA; The McGraw-Hill Companies Inc.; 7, 2008, 753-77.