06/28/08

Permalink 08:23:07 am, Categories: Medicine  

Clinical Medicine Cases

Dr. Anwar Nabeel Jaffri Chief Resident Internal Medicine in AKUH, Pakistan. He has written many articles on Abdominal Tuberculosis, Tuberculosis and Hyponatremia, for more Clinical Medicine Cases Visit www.ezinevalley.com

Clinical Medicine Cases

Case 1:
? 50 year old man presented with generalized weakness, dizziness, lethargy for 10 days. He was also having loose stools for the past 15 days. On examination was pale and thin lean emaciated man. His blood pressure was 70/40 mm of mercury, with pulse of 130 beats / minute. He had bilateral decrease air entry on chest, epigastric tenderness and pedal edema on examination. Neurological exam was non focal. He had some history of undocumented weight loss, but no history of fever. His past history was significant for episodes of loose stools, which would resolve on taking antibiotics


? Hemoglobin: 8 mg/dl Abumin: 1.5

? MCV: 68 Total Bilirubin: 8.1

? WBC: 14 cmm Direct Bilurubin: 5.5

? Platelet: 176 GGT: 304

? SGPT:71

? RBS: 106 AP: 359

? BUN: 15

? Cr.:1 mg/dl ESR: 53

? Na: 126 meq Stool DR: Normal

? K: 4.6 meq Calcium: 7.3

? Cl: 111 Phos:1.6

? HCO: 18

? PT: 17.8
? INR: 1.7
? APTT: 35.7

Case 1:
? What is the most likely diagnosis?
? How would you investigate this patient, suggest 2 investigations
? How would you treat this patient?
? What other diseases are associated with this condition


Case 2:
? 32 yr old woman presents to the medicine clinic with generalized bodyaches, hairloss, undocumented weight loss. On examination she is thin and lean. She was tachcycardic , but the rest of the examination was unremarkable. She had recently delivered a baby girl 3 months back. There was nothing significant in her past history.

Case 2:
? What is the most likely diagnosis?
? What is the differential Diagnosis?
? How would you further investigate?
? How would you treat this patient?
The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 9 4042-4047


? Postpartum thyroiditis is a common thyroid disorder that presents during the first postpartum year. It is the occurrence of either transient hyperthyroidism, transient hypothyroidism, or transient hyperthyroidism followed by transient hypothyroidism
? Beta-blockers are given to alleviate palpitations, irritability, and nervousness.
? Antithyroid medicines (thioureas) are not a potential treatment alternative, because the hyperthyroidism is caused by a destructive thyroiditis resulting in release of preformed thyroid hormone.

Case 3:
? A 36 year-old man is referred to you with increasing problems with concentration. He also complains of irregular jerky movements of his extremities and fingers. He consumes approximately 20 units of alcohol a week. His father was diagnosed with dementia at the age of 40. Apart from generalised choreiform movements, his neurological and systemic examination was normal.


Case 3:
What is the most likely diagnosis?
? Alcoholic cerebral degeneration
? Early onset Alzheimer"s disease
? Hemiballismus
? Huntington"s disease
? Parkinson"s disease


Huntington"s disease:
? Huntington"s disease is an autosomally inherited condition due to an expanded CAG trinucleotide repeat on the short arm of chromosome 4.
? It is characterised by progressive dementia and worsening choreiform movements.
? Symptoms typically appear between 30 and 50 years of age.
? Genetic testing now provides an accurate method of establishing the diagnosis.
? Average life span after clinical onset is about 15 years.

Case 4:
? 65 year woman, presented with drowsiness, lethargy for a week. She also had associated history of productive cough with weight loss and intermeittent fever. On examination, she was dehydrated,drowsy but arousable, had right sided crackles on chest examination. On neurological examination, she was drowsy, but arousable and was nonfocal.

Case 4:
? What is the complete diagnosis?
? How will you treat the hyponatrenmia?
Cerebral Salt Wasting Syndrome in a Patient withTuberculous Meningitis
JAPI ? VOL. 54 ? MAY 2006

Case 5:
? A 60 year-old man presents with a 2 month history of progressive confusion, gait disturbance, and urinary incontinence. Examination reveals mild global cognitive dysfunction and gait ataxia. CT brain shows enlarged ventricles with no evidence of obstruction to CSF outflow. Lumbar puncture reveals normal CSF pressure and constituents.

Case 5:
Which one of the following management?s steps is likely to be most helpful?
? CSF drainage via repeated lumbar puncture
? EEG
? Intracranial pressure monitoring
? MRI brainstem
? Serum B12 and folate levels


Normal Pressure Hydrocephalus:
? Normal pressure hydrocephalus presents with the triad of dementia, gait disturbance and incontinence.
? It is associated with episodes of increased pressure related to impaired CSF absorption and therefore may benefit from CSF shunting.
? Although the ventricular enlargement described in this case may derive from global atrophy and need not represent hydrocephalus the other features of the case strongly point to the diagnosis.
? In equivocal cases therapeutic CSF drainage via lumbar puncture is performed to identify the patients likely to benefit from permanent drainage.
? Intracranial pressure monitoring to demonstrate the episodes of increased pressure is a more invasive alternative.

Case 6:
? In the post operative period after an abdominal surgery, a58 year old man gets sudden acute pain in the right knee joint. He gives history of previous episodes of acute pain involving the left knee, wrist joints. He takes glibenclamide 5 mg daily for control of diabetes and has been given disprin tablets for pain by his doctor
? Examination reveals pulse of 90/in, temperature 98.8 F, right knee joint swollen and tender with mild effusion, movements restricted and painful
? Laboratory test reveal CBC normal,2 hrs post prandial blood sugar 190mg%, uric acid: 7mg/dl

Case 6:
? What is the most likely diagnosis?
? Suggest 2 investigations with expected findings?
? Enumerate 4 steps in his treatment?

Acute Psuedogout:
? Most common cause of acute monoartritis in elderly
? Due to CPPD crystal deposition in hyaline and fibrocartilage of joints
? Triggering factors include direct trauma,intercurrent illness or surgery
? Commonly involved joint, followed by the wrist, shoulder,ankle, and elbow.
? Develops rapidly with severe pain, stiffness and swelling maximal within 24 hrs
? Synovial fluid aspiration,xrays,metabolic profile
? Treatment is aspiration which relieves pain, steroid injection,NSAID and colchinine

Case 7:
? A 51 year old woman , who is diabetic, hypertensive and has family history of heart disease and is 170 cm tall and weighs 90 kg. She leads a sedentary life. During a screening clinic visit she was positive for microalbuminuria. Her periods have become variable over the past few months. She was smoking till last month but says that she has given up. She is a corporate lawyer in a multinational company and complains of stress at work. She takes about 7 to 8 cups of balck coffee.

Case 7:
? Identify her coronary artery disease risk factors?
? What is the role of smoking and coffee in the causation of hypertension?
? She wants to know what effect her changing menstrual cycle will have on the risk of coronary artery disease?
? What risk factor control and lifestyle modification advice would you give her?

Case 8:
? A 40 year old woman presented with 4 months history of progressive dyspnea. She gives history of chest pain precipitated by exercise for last 2 months with poor response to nitrates, beta blocker and calcium antagonists.
? She developed ankle edema for the last one month for which she was started on frusemide. Type 2 Diabetes was discovered 2 yrs ago and managed by diet alone. She had been taking some tablets for weight reduction for the last one year.
? Her investigations are: Hb: 13g/dl, hematocrit 50%, MCV 102 fl,WBC 7.4, platelets:190, Na: 138 mmol/L, K:4.6 mmol/L,urea 6.2 mmol/L, serum creatinine 132 umol/L, bilirubin 32 umol/L, AST 24u/L, ALT 20u/L, albumin 40gm/L, globulin: 28gm/L

Case 8:
? What is the most likely diagnosis?
? What other investigations are required
? What are the treatment options?

Pulmonary Hypertension:
Chest, Mar 2002; 121: 54S - 56S.

? Usually sporadic,or due to weight reducing drugs, HIV infection, connective tissue disorders (SS), familial due to TGF-ß;BMPR2
? Hypertrophy of media and intima, marked narrowing of vessel lumen, thrombosis,increased PVR
? Pulmonary hypertension is defined as mild if mean PAP >20 mm,moderate if >30mm and severe if > 45mm
? Workup of hypercoaguable state, CT chest, ECG, Echo, PFT
? Treat the cause, anticoagulation, oxygen, diuretics, Epoprostenol, Sidenafil, transplant


Case 9:
? A 72 year old male diabetic presents with weakness and lethargy. He was diagnosed with type 2 diabetes mellitus 12 years ago and remains on gliclazide and metformin therapy and takes atenolol for hypertension.
? There is little to find on examination with a blood pressure of 164/88 mmHg lying and standing. He has loss of pin prick and vibration sensation to the ankle in both legs and a background diabetic retinopathy.

Case 9:
What is the likely cause for these electrolyte abnormalities?
? Acute renal failure
? Addison"s disease
? Hyporeninaemic hypoaldosteronism
? Liddle"s syndrome
? Proximal renal tubular acidosis

Hyporeninaemic hypoaldosteronism:
? The electrolyte abnormalities show a highish sodium concentration and raised potassium. In conjunction with the renal impairment this would suggest a diagnosis of Hyporeninaemic hypoaldosteronism (Type IV renal tubular acidosis).
? Treatment is usually successful with conservative measures such as stopping provocatory agents, a low potassium diet. Small doses of fludrocortisone could be considered for refractory cases.

Case 10:
? A 60 year old man presents with gradually increasing weakness in the lower limbs, deafness and bone pains. He is a nondiabetic and normotensive.
? His examination reveals bowing of lower legs and scoliosis with crepitus in both knee joints. Examination of CNS showed grade 4/5 power in proximal muscles with down going planters. Early signs of CCF were present.
? Xray spine and pelvis showed marked sclerosis of the bones.

Case 10:
? What is your diagnosis and differential diagnosis in this patient?
? What investigation will you do to confirm your diagnosis?
? How would you manage this patient?

Paget`s Disease:
? Characterised by increased , disorganized bone remodeling on a focal and motional basis at various sites in the skeleton
? Due to increased osteoclastic activity, marrow fibrosis, increased vascularity and osteoblastic activity
? Raised ALPhos, radiograph, isostope bone scan
? Bisphosphonates are the treatment of choice, calcitonin

Case 11:
? A 54-year-old man was referred to the medical outpatient clinic for assessment of fatigue. He gave a six-month history of generalised malaise and feeling "tired all the time". He had a past history of hypertension that had been monitored by his General Practitioner but this had not required treatment. He had also reported feeling in a "low mood" to his GP, but attributed this to the fatigue.

Case 11:
What is the most likely underlying cause of these abnormalities?

? Adrenal hyperplasia
? Alcohol
? Ectopic ACTH secretion
? Pituitary adenoma
? Liquorice

Alcohol-induced Cushing"s syndrome:
Endocr. Rev., Jun 1996; 17: 262 - 268
? Alcohol-induced Cushing"s syndrome is indistinguishable from true Cushing?s syndrome,
? Although in the former less signs and symptoms seem to be present
? Based on experimental studies, alcohol activates the HPA axis by increasing the production and secretion of CRF.
? This can be achieved either at the hypothalamic or at some suprathalamic level (e.g. the limbic cortex).

Case 12:
? A 21 year old unmarried girl is brought to the emergency department in coma. She is sweating, afebrile and tachypnoeic with fine crackeles at the lung bases. She has bilateral extensor planters but no other neurological deficit. She developed a generalized tonic clonic fit, which responded promptly to diazepam . Her Hb is 13.9 gm/dl,TLC 11x 10 9/L, ESR 18 mm/1st hr , salt 20iu/L, serum calcium :2.3 mmol/L,serum Na :142 mol/L, serum K:3 mmol/L, and serum bicarb : 10 mmol/L
Case 12:
? What is the most likely diagnosis?
? What are three other conditions you would consider in your differential diagnosis?
? What four investigations would you carry out?
? Name two treatment modalities for this patient.

Case 12:
? Vomiting
? Hyperventilation (30 minutes) Hyperventilation (30 minutes)
? Metabolic acidosis (12 metabolic acidosis (12-24 hours) 24 hours)
? Electrolytes imbalance & dehydration Electrolytes imbalance & dehydration
? Hyperthermia Hyperthermia
? Convulsions Convulsions
? Death

- Fluid/electrolyte management -
? Rehydrate-
? Diuresis Diuresis/alkalization with D5W with 88 /alkalization with D5W with 88-132 132 mEq mEq/L /L bicarb bicarb,
? Reduce fluid load with elderly and patients with renal

- Hyperthermia Hyperthermia -
? Sponge bath, fans, cold water submersion

Case 13:
? A 50 year old female presents with a 4 month history of progressive distal sensory loss and weakness. On examination positive neurological findings include moderate proximal and distal weakness of arms and legs, glove and stocking sensory loss and areflexia. Planter responses were mute. The following conditions could give a similar picture

Case 13:
? Guillian-Barre syndrome
? Chronic inflammatory demyelinating neuropathy(CIDP)
? Cervical spondylosis
? Hereditary motor and sensory neuropathy(HMSN)
? Myasthenia Gravis

Chronic inflammatory demyelinating neuropathy:
? The history is compatible with a subacute sensory and motor peripheral neuropathy. Causes of such conditions include inflammatory neuropathies such as CIDP and paraproteinaemic neuropathies.
? Guillian-Barre syndrome is an acute post-infectious neuopathy which reaches its peak in severity within six weeks..

Chronic inflammatory demyelinating neuropathy(CIDP):
? Cervical spondylosis would cause upper motor neurone signs such as
? hyperreflexia, extensor plantar response and possibly a sensory level.
? HMSN is usually a very chronic neuropathy developing over many
? Years and usually with a family history of the condition.
? Myasthenia gravis causes weakness and fatigability but never
? Sensory symptoms

Case 14:

? A 37 year old woman comes to your clinic. The clinic BP remain 140/90, 145/95 and 150/90 mm Hg on repeated occasions. The home blood pressure remains in normal range

Case 14:
? What will be your confirmatory test?
? The patient wants to know about her prognosis?.
? Do they need treatment, if yes what therapy would you institute?
? Can the white coat effect occur in known hypertensive patients on drug treatment

12/21/07

Permalink 03:49:54 am, Categories: Medicine  

Morbidity and Mortality Meeting

Dr. D.S. Merchant is a Gold Medalist in (Anatomy & Histology), Fellow Nephrology in Aga Khan University Hospital, Karachi " Pakistan. For more Dissertation or seeking Dissertation help visit www.articlesbridge.com The Most popular website that offers information Research on different Disease and Case Studies. Please leave the links intact if you wish to reprint this article.

Case History

? Admitted via clinic on 25-06-2007 for
? Fever off and on-------- 8-9 months
? Abdominal Pain --------- 2-3 weeks

In Gilgit she was being treated as a case of genital Tuberculosis without any objective genitourinary complaints or symptoms
She took ATT for 2 months and then stopped b/c of drug induced Acute Hepatitis.

Fever
8-9 months off and on
High grade up to 103-104 F, no chills/rigors
No urinary or chest complaints but she had upper abd. Pain, moderate in intensity, no radiation, no vomiting but nausea was present with ass. Weight loss.

Clinical Examination:

§ Alert awake oriented, toxic look
§ Pulse Rate: 90 beats/minute regular
§ Blood Pressure: 160/80 mmHg
§ Resp. Rate: 20 b/minute
§ Temp: 36.8 centigrade
§ Pallor with Icteric
§ Malar Flush but no rash
§ B/L pitting pedal edema
Clinical Examination:

§ RHC tenderness, hepatomegaly 2 fingers below Rt costal margin, splenomegaly 1 finger, positive shifting dullness.

§ S1 and S2 audible, Panystolic murmur in mitral area radiating to axilla, no gallop.

§ Chest: B/L symmetrical shape and resp movements, equal chest expansion B/L, with NVB except at Rt basal region which had decrease air entry.

Clinical Examination:
? CNS: Alert, OrientedX3, no focal sensory or motor deficit, plantars normal.

? Musculoskeletal System: No positive findings
Labs:
11-06-2007
Hb: 10.2 gm/dl (NN)
Hct: 27.8
Wbc: 7.4
Neutrophils: 73.8%
Lymphocyte: 21.4%
Plat: 30
Retic=6.8
FBS: 110mg/dl
LDH: 8752

Labs

PTT=25.3/12 TB=5.9 Coombs ++
INR=2.12 DB=3.7 CRP = 8.3
APTT=68.7/30 IB=2.2
D-Dimer=0.87 GGT=81
MP -ve SGPT=53
MP ICT -ve ALP=348

Urine DR:
Dark yellow Protein +3, bil +3, Hb trace, rest normal

§ 24 hrs urinary protein was 7080 mg/24hrs

§ She was started on broad spectrum ABx, IV
hydration and supportive management initially

CXR
Rt. Lower lung consolidation with possible
consolidatory changes in the Lt lower lung field,
findings are suspicious for pneumonia.
she was already being treated for pneumonia.

US Abd:
Fatty infiltration of liver, sludge filled
Gallbladder, mild ascites.


Her CT Abd and Pelvis

with contrast was done considering
disseminated TB which showed mild B/L
pleural effusion with mild to moderate
ascites, no paraaortic lymphadenopathy


? Ascitic Fluid DR
Glu=70
prot=814
TLC=100
N=10
L=90
RBC +++

? During the hospital stay
? She became short of breath(14/06/2007)
? Her CXR showed Pulmonary edema

ABG
7.49/37.8/70.8/28.9/+5.9/95.3 on 6L Fio2

Trop I x2 were negative
She was treated with IV diuretics
Cardiology service was involved they
continued IV diuretics

Echo:
EF 60%, moderately dil. Lt Atrium
LVDD grade II
Mod-severe MR, mild TR
Mild PHTN, no vegetations/clots

Her Autoimmune profile was sent, and in the mean
while bone marrow was done to send TB CS and
cause for worsening Bicytopenia (dropping PLTs &
Hb) under cover of FFPs.

GI service was also involved for deranged LFTs
They suggested to send autoimmune workup
Which was already sent.

? 6-8 hrs after bone marrow Pt started having heavy bleeding from bone marrow procedure site and she was Tx with FFPs & platelets and with in next 12 hrs she started bleeding from every site (GI, oral cavity, Nose), Hematology was involved they suggested DIC workup Which was sent and which turned out to be negative
? Twice daily IV omeprazole was converted into infusion.

Bone marrow aspirate:
? hypocellular/dilute specimen
? Few erythroid and myeloid precursors.
? No megakaryocyte seen

Results of bone trephine (H&E) section:
? Erythroid hyperplasia with nuclear to cytoplasmic asynchrony.
? Few large cell seen ?early precursors. normal myeloid precursors.
? Adequate megakaryocytes. No metastatic infiltrate to granuloma seen.

Final Report:
§ Autoimmune hemolytic anemia ?cause.
§ megaloblastic features on bone trephine can be due to folate deficiency (secondary to hemolysis).

§ Pt was already kept on folic acid.

§ Her bleeding continued and ENT
service was involved for nasal packing

§ She was transfused with multiple
PRBC, FFPs, CryoPPT and was given factor VII (novoseven) on the advice of hematologist

? Multiple blood CS, Ascitic fluid CS, BM CS including AFB CS were sent which were negative.
? Her CCHF was sent which was also negative
? Her Ascitic fluid cytology was negative and so was autoimmune profile except AntiDsDNA which was 11.4 (n=0-6), Anti PLP & anticardiolipin Ab were negative
? C3=0.57 (n=0.88-2.01), C4=0.20 (n=0.16-0.47)
? She was started on pulse steroid
? After 3 days of bleeding and supportive transfusions she started dropping Spo2 on room air, able to maintain Spo2 at 96% on 15L Fio2 and her GCS dropped to 5/15, family was not agreed for intubation despite counseling.
? ABG=7.49/37.8/70.8/28.9/+5.9/95.3 on 15L Fio2
? She was maintaining blood pressures initially then she started having hypotension hence was started on inotropic support but on 25 June 2007 at 1430 hrs she had a sad demise.
Questions/Queries
? Whether she had SLE or something else?
? What was the cause of bleeding?
? Anything additional in the management of this patient which would have saved her life?
? What about her previous diagnosis of TB?
? If she would have been correctly diagnosed earlier would she able to survive?

SYSTEMIC LUPUS ERYTHROMETOSIS
(SLE)

DEFINITION

SLE is the prototype of a multisystem disease of autoimmune origin characterized clinically by acute/insidious onset chronic, remitting & relapsing in it?s course virtually affecting any organ of body & biochemically by presence of circulating autoantibodies against diversity of antigen.

EPIDEMIOLOGY

? 1:2500 in general population
? 1:700 in women
? 9:1 Female to male ratio
? 2:1 Female to male ratio in childhood & in age group above 65
? More common in African-American women.

Clinical Features
Constitutional Symptoms - Fatique, Fever
Arthralgia, Myalgia, Weight Loss

Cutaneous
Acute Skin Lesions - Generalized, Erythema, Bullous, Butterfly Rash
Subacute - Erythematous Palpable Plaques Associated With Ro/Ssa
Chronic Discoid
Alopecia
Raynaud

Clinical Features
1. Renal - Acute Renal Failure
Chronic Renal Failure
Nephrotic Syndrome
Nephritis
Pyelonephritis

Clinical Features?..
3. Pulmonary - Pneumonitis
Pleurisy
Pleural Effusion
Pulmonary Embolism
Pulmonary Fibrosis
Alveolar Hemorrhage

4. G.I.T. Dysphagia
- Mouth Ulcers
- Peritonitis
- Pancreatitis
- Mesenteric Vasculitis
- Bowel Infarction

Clinical Features..
5. Cardiac - Pericarditis
- Endocarditis (Libman-Sachs)
- Myocarditis
- Coronary Artery Disease

6. Reticulo-Endothelial
- Lymphadenopathy
- Splenomegaly

Diagnostic Criteria

Diagnosis - Acr Criteria
1. Malar Rash
2. Discoid Rash
3. Skin Photosensitivity
4. Painless Oral Or Nasopharnygeal Ulcers
5. Non Erosive Arthritis Or Arthralgia
6. Serositis (Pleurisy, Pericarditis)
7. Renal Involvement
8. Neurologic Disorders
9. Haematologic Disorders
10.Immunologic Disorder (Le Cells, Anti-Dna, Anti-Smith, False + Ve Vdrl, Aca
11. Ana

Any Four Out Of The Above Criteria

Labs
Laboratory
1. Leucopenia < 4,000
2. Thrombocytopenia
3. Anaemia - Hemolytic, Normochromic, Normocytic
4. Markedly Elevated Esr > 100
5. Usually Normal Crp
6. Ana - Present In 95% Homogeneous, Speckled
7. Anti Ds-Dna -Specific But Not Sensitive Suggest Severe Or Lupus Nephritis
8. Anti- Sm-Specific
9. Anti Ro/Ssa, La/Ssb - Neonatal Lupus, Congenital Heart Block
10.Anti Ribosomal P-Lupus Cerebritis
Labs..
11. Anti-Phospholipid (Igg Or Igm) - Aps
12. False Positive Vdrl

Lupus Nephritis
1. Albuminuria > 0.5g/24 Hrs Or Dipstick 3+
2. Casts (Rbc, Granular, Tubular, Mixed)
3. Haematuria (> 5rbc/Hpf)
4. Elevated Creatinine

Treatment

Simple Analgesics
Nsaids
Steroids
Hydroxychloroquine

Dmards - Methotrexate, Azathioprine,
- Cyclosporin, Cyclophosphamide,
- Mycophenolate Mofetil

Complications
- Opportunistic Infection
- Avascular Necrosis
- Premature Atherosclerosis - Myocardial Infarction
- RECURRENT ABORTION
- NEONATAL LUPUS


Prognosis
? Overall five years survival is more than 90 %

? Early mortality is due to organ failure or sepsis

? Late mortality is due to CVS complications

11/17/07

Permalink 06:17:51 pm, Categories: Weight Loss  

Can Hoodia Slim You Down?

For more information visit: Hoodia Balance and Weight Los Products

Hoodia Gordonii is a very interesting ?ancient plant" that has been used for thousands of years but just beginning to catch on to the ?Western world Hoodia" for weight-loss. The huge media coverage has led to a flourishing industry in Hoodia Gordonii based products, whether they be ?Pure Hoodia" or Hoodia as just one of the ingredients of an already existing weight loss product.

But before you rush off to buy a Hoodia supplement you should understand a bit about what studies have shown so far with respect to Hoodia Gordonii for weight loss. Knowing these facts will help you navigate through Hoodia product and buy the best product to avoid the fake ones.

Know The Facts About Hoodia:i) There are a variety of Hoodia plants. Only the Hoodia Gordonii class contains an active element that helps suppress your appetite. As the demand for Hoodia Gordonii is far surpassing the supply, some Hoodia sellers are using unreliable but advertising their products as Pure Hoodia even though it might have been made from a different Hoodia plant than the Hoodia Gordonii.

ii) Of course many companies claim their Hoodia extract can slim you down, the only thing that has been proven so far is the ?P57 molecule". ?P57" is the ?active ingredient" in Hoodia Gordonii that was isolated. It was licensed to a company named ?Phytopharm" that conducted a study using it. It was found that morbidly obese people using ?P57" ate on average of 1k less calories per day. Obviously this is the reason why so many people think Hoodia for weight-loss is the new rescuer for the obese and people looking to slim down.

iii) What is most important to keep in mind is that as long as the Hoodia products are extracted from real Hoodia Gordonii, it should also contain some of the active ingredient in it. Study shows that only the core of the plant has the active ingredient.

So can Hoodia slim you down? And the answer is a big Yes! But only if you buy a real product and avoid the false ones.

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