Month: February 2014

Don’t make the mistake of thinking that you have to agree with people and their beliefs to love them or defend them from injustice

GOD Is 'LOVE' - 1 John 4 verses 7-8

The Bible defines God very clearly in 1 John 4:8-9 “Whoever does not love does not know God, because God is love. Plain and simple… God IS love.

 

How did God show his love among us? John 3:16 says, “For God so loved the world that He sent his one and only Son into the world that whoever believes in Him will not perish but have eternal life.”

In todays society the definition of love is constantly getting a makeover, it’s always being re-defined. More commonly we show our  love to one another by agreeing with each other and saying what the person wants to hear; to do otherwise would be to risk the friendship – here’s what I mean…

Story: There was a girl who introduced me to her boyfriend. I had some time alone with the “boyfriend” we spoke frankly and I was able to discover his horrible intentions. Afterwards, the girl asked me… “So what do you think?”

When I revealed to her what I thought and what he had said, she became infuriated with me because I did not agree with her. Immediately she burst in tears and shouted out “I thought you were my friend… how could you say these things?”

2 Timothy 4:3-4 says, “The time is coming when people won’t listen to good teaching. Instead, they will look for teachers who will please them by telling them only what they are itching to hear. 4 They will turn from the truth and eagerly listen to senseless stories….”

People only want to hear what they want to hear.

Brothers and sisters,  people will ask YOU a question which will determine if you are likeable or not, a question that will determine whether you are good person or not (according to their terms of good and evil), whether you are moral or not (according to their terms of morality) your trial ends with how you answer – where will YOU stand?

Don’t make the mistake of thinking that you have to agree with people and their beliefs to love them or even defend them from injustice.

One of satan’s biggest lies is that we should all accept every form of sin in the name of “LOVE”. The devil has REDEFINED the word “love” to mean “compromise, the acceptance of sin in our daily living”.

God clearly teaches us to love all people, regardless of who they are or what they’ve done. In fact Jesus gave us the most perfect example i.e. Jesus stood up for prostitutes, cheaters, robbers, religious fanatics, murderers, liars, the poor the rich, BUT Jesus NEVER compromised the truth of God.

Romans 6:23 “For the wages of sin is death but the gift of God is eternal life” 

Evangelizing The World

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In Mark 16:15 Jesus said to His disciples, “Go into all the world and preach the gospel to all creation.” This is what many Christians call the great commission where we are called by Jesus Himself to preach the Good News of God to ALL nations.

However, it seems that often times these words of life fall on deaf ears or eyes that fail to see. Mark 8:18 Jesus asks “Do you have eyes but fail to see, and ears but fail to hear?”

Part 1. Our Own Failed Perception

The parents of one of the shooters in the Columbine high school massacre in 1999 said in their interview with the police that they had no idea about the arsenal of weapons their sons were amassing in their bedrooms – an arsenal that included knives, guns, homemade grenades, cans full of gunpowder, coils of bomb fuse, and bombs – more than 100 of them, including pipe bombs, and 35-pound propane bombs.

“We never saw violence or hatred in [our sons], we did not see any signs of depression or anything unusual until the last moments of his life when we watched helplessly with the rest of the world.”

However, according to classmates, the boys openly and loudly expressed their admiration for Adolf Hitler, satan, death, anti-Christian ideas, they were obsessed with violent video games and they had posted threatening messages all over the Internet revealing to investigators’ the horror that they had been planning the assault for years.

Q. How could their parents possibly have been so deaf? so blind as to miss so many red flags? The answer is that we are never more deafened than when we refuse to hear and we are never more blinded than when we see only what we want to see. 

Part 2. Gods Message Is Spoken To Willingly Deaf Ears And Purposefully Blind Eyes

The unfortunate truth is that Gods message today is spoken to a people whose ears are willingly deaf and eyes that are purposefully blind (just like the parents of the two boys at Columbine). Preaching the Gospel today is no easy task when so many people are (by their own choice) blind and deaf to the words of God.

2 Timothy 4:3 says,  ”For the time will come when people will not put up with sound doctrine. Instead, to suit their own desires, they will gather around them a great number of teachers to say what their itching ears want to hear.”

This is the new atheism, this is the new world religion, this is the new anti-Christ; just as Aleister Crowley who called himself “the Beast 666″ wrote in his satanic book of the law”Do what thou wilt will be the whole of the law.” In other words you are your own god, you make your own morality, you make your own rules – do what you want. The Bible tells us that it was the devil who first disobeyed God and today he has many followers who are growing in numbers, who intently listen to his voice and follow his satanic will.

Part 3. What To Do As A Christian?

Step 1. Don’t be surprised when you are mocked, beaten, laughed at, denied, betrayed, ignored etc…

John 15:20b-21 Jesus says, “If they persecuted me, they will persecute you also… They will treat you this way because of my name, for they do not know the one who sent me.”

Step 2.  Hold on to your testimony.

Revelations 2:10 says, “Do not be afraid of what you are about to suffer…  Be faithful, even to the point of death, and I will give you the crown of life.”

When someone asks you a question, just remember it’s not your job to convince or “convert” it’s not even your job to defend God, trust me He can defend Himself. It is however our job to give a reason for our faith.

1 Peter 3:15 “But in your hearts revere Christ as Lord. Always be prepared to give an answer to everyone who asks you to give the reason for the hope that you have. But do this with gentleness and respect.”

Also, don’t stoop to their level. In other words, never let their hatred provoke you in anger; rather always work in peace, love, gentleness, joy, faithfulness, self-control, forbearance and patience (for these are the fruits of the Spirit).

Step 3. Look ahead towards Jesus

Romans 14:11 says, It is written: “‘As surely as I live,’ says the Lord, ‘every knee will bow before me; every tongue will acknowledge God.’”

In the very end EVERY KNEE will bow down before Jesus and EVERY TONGUE will confess He is LORD. On that day you will see the mockers, the evildoers trembling before God and we can only pray that God who is the judge and is abundant in mercy will have mercy on those who willingly shut there ears and eyes to His Word. For the Bible says that everyone has to make a choice: life or eternal damnation. God has given us the free-will to fully love Him or to fully deny Him.

The choice is up to you – YOU CANT STAY NEUTRAL ON A MOVING TRAIN we are either for God or against Him.

Revelations 3:20 says this, “Here I am! I stand at the door and knock. If anyone hears my voice and opens the door, I will come in and eat with that person, and they with me.”

How do you respond?

Systemic Lupus Erythematosus (SLE)

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Definition: Systemic lupus erythematosus (SLE), also called lupus, is an autoimmune disorder in which the body’s immune system (the cells in the body that fight infection) incorrectly attack the body’s own tissues and organs, leading to inflammation and damage

Pathogenesis and Etiology: There are incredible interactions between susceptibility genes as well as environmental factors which result in an abnormal immune response (all of which differ among different patients).

Some responses may include:

(1) Activation of innate immunity [dendritic cells, monocytes/macrophages) by CpG DNA, DNA in immune complexes, viral RNA and RNA/protein self antigens.

(2) Lowered activation thresholds and abnormal activation pathways in adaptive immunity cells (T and B lymphocytes).

(3) Ineffective regulatory CD4+ and CD8+ T cells.

(4) Reduced clearance of immune complexes and of apoptotic cells.

Self antigens RNA/protein in Sm, Ro, and La; phospholipids are available for recognition by the immune system in surface blebs of apoptotic cells; thus antigens, auto-antibodies, and immune complexes persist for prolonged periods of time allowing disease and inflammation to develop.

This immune cell activation is also accompanied by an increased secretion of proinflammatory type 1 and 2 Interferons (IFNs), as well as tumor necrosis factor a (TNF-a), Interleukin 17 (IL-17). Upregulation of genes induced by IFN is a genetic “signature” which we find in the peripheral blood cells of SLE in approximately 50% of patients.

What is also interesting to note is that decreased production of cytokines also contributes to SLE: Lupus T and natural killer (NK) cells fail to produce enough IL-2 and transforming  growth factor b (TGF- b) to induce and sustain regulatory CD4+ and CD8+ T cells. The result of this is abnormality is a continuous production of autoantibodies and immune complexes.

Risk Factors: Female sex is permissive for SLE with evidence for hormone effects, genes on the X chromosome and epigenic differences between gender plays a role in disease. For example females make higher antibody responses than males. Women exposed to estrogen-containing oral contraceptives or hormone replacement have an increased risk of developing SLE. Estradiol binds to receptos on T and B lymphocytes, increasing activation and survival of those cells, thus favoring prolonged immune responses. Genes on the X chromosome influence SLE, such as TREX-1 possible because some genes on the second X in females are not silent. People with XXY karyotype (Klinefelters) have a significantly increased risk for SLE. Several environmental factors may influence SLE i.e. exposure to ultraviolet light causes flares of SLE in about 70% of patients (either through apoptosis or altering DNA and intracellular proteins to make them antigenic).

Pathology: In SLE, biopsies of affected skin show deposition of Ig at the dermal-epidermal junction (DEJ), injury to basal keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and around blood vessel.

TABLE 1 Autoantibodies in SLE (a short list*)

Antibody                                                                        Prevalence                  Notes

Antinuclear antibodies                                                   98%   *                               Best screening test

Anti-dsDNA                                                                         70%                                    High titers are specific for SLE

Anti-Sm                                                                                 25%                                    Specific for SLE

Antihistone                                                                          70%                                    More frequent in drug induced lupus

Antiphospholipid                                                              50%                                    Predisposes to clotting, fetal loss, thrombocytopenia

Diagnosis:The diagnosis of SLE is based on characteristic clinical features and autoantibodies.

TABLE 1:  Diagnostic Criteria for Systemic Lupus Erythematosus (any combination of ³ 4 of 11 criteria)

Malar rash           Discoid rash           Photosensitivity           Oral ulcers           Arthritis

Serositis               Renal disorders    Neurologic disorder   Hematologic disorder

Immunologic disorder                       Antinuclear antibodies

Laboratory Tests: In the laboratory we have three objectives: (1) to establish or to rule out SLE (2) to follow the course of the disease i.e. is the medication helping? Is their a flare occurring? What about organ damage? (3) to identify the adverse effects of therapies.

A. Diagnostically, the best test to confirm is an ANA as it is positive in 95% of patients, usually at the onset of symptoms.

B. Flare: titers of anti-dsDNA increases during a flare particularly of nephritis or vasculitis, especially when associate with declining levels of C3 or C4 complements.

C. Test for following disease course: the typical urinalysis for hematuria and proteinuria, hemoglobin levels, platelet counts and serum levels of Creatinine or albumin are all helpful in assessing the patients disease course. The physician should determine for each individual patient whether certain laboratory test are required.

Treatment: Unfortunately, there is no cure for SLE and complete sustained remissions are rare. Therefore, the best strategy is to plan to induce improvement of acute flares and then to maintain these improvements with strategies that suppress symptoms to an acceptable level and prevent organ damage.

Analgesics and antimalarials (hydroxychloroquine, quinacrine etc…) are the mainstay treatment regimens. NSAIDS are useful analgesics and anti-inflammatories, particularly for SLE arthritis/arthralgias.

Systemic glucocorticoids (methylprednisone) is the mainstay of treament for any inflammatory life-threatening or organ-threatening manifestations of SLE. Cytotoxic immunosuppressive agents can be added to glucocorticoids and are recommended when needed to treat critical SLE – either cyclophosphamide or mycophenolate is an acceptable choice for induction of improvement in severely ill patients.

For more information:

CLEVER study

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Claudication: exercise versus endoluminal revascularization (CLEVER) study

A 67 year old non-diabetic man comes into the ED complaining of persistently nagging cramping pain in his right thigh after walking for a couple of blocks. He says that the pain goes away when he stops and rest for several minutes. Past medical history reveals that he is an ex-smoker with a 35 pack/year history. On physical exam, the femoral pulse are normal, but the popliteal and dorsalis pedis are diminished on the right leg. His ankle brachial index (ABI) is 0.98 on the left and 0.72 on the right. He is started on low dose aspirin and lipid lowering. What is the best initial management for this patient?

a)    Warfarin

b)   Heparin

c)    Enoxaparin

d)   Supervised exercise therapy

e)    Gemfimbrizil

f)     Pentoxifyline

g)    Arteriography followed by surgical bypass procedure

h)   CT angiography followed by stenting

i)     HMG-CoA reductase inhibitor

j)     Niacin

k)    Embolectomy

l)     Cholestyramine

m)  Colestipol

n)   Colesevelam

o) Reasurrance

p) increase to maximum dose aspirin

The patient mentioned in the above vignette has a clinical presentation that is consistent with the presence of peripheral arterial disease (PAD). PAD is a coronary artery disease equivalent. Medical research is very clear on this topic and includes briefings on aggressive risk factor modification with documented counseling for smoking cessation, lipid lowering therapy, and evaluation and treatment for hypertension and diabetes mellitus.

  • Interpretations of Ankle brachial index (ABI): An ABI between 0.9 and 1.2 considered normal (free from significant PAD), while a lesser than 0.9 indicates arterial disease. An ABI value greater than 1.3 is also considered abnormal, and suggests calcification of the walls of the arteries and incompressible vessels, reflecting severe PAD.

Since the vignette mentions that the patient has been started on low dose aspirin along with statin therapy. The next best step in management should be to enroll this patient in a supervised exercise program – according to the CLEVER study.

CLEVER STUDY

Background  Claudication is a common and disabling symptom of peripheral artery disease that can be treated with medication (i.e. statins etc…), supervised exercise (SE), or stent revascularization (ST).

Methods And Results  We randomly assigned 111 patients with aortoiliac peripheral artery disease to receive 1 of 3 treatments: optimal medical care (OMC), OMC plus SE, or OMC plus ST. The primary end point was the change in peak walking time on a graded treadmill test at 6 months compared with baseline. Secondary end points included free-living step activity, quality of life with the Walking Impairment Questionnaire, Peripheral Artery Questionnaire, Medical Outcomes Study 12-Item Short Form, and cardiovascular risk factors. At the 6-month follow-up, change in peak walking time (the primary end point) was greatest for SE, intermediate for ST, and least with OMC (mean change versus baseline, 5.8±4.6, 3.7±4.9, and 1.2±2.6 minutes, respectively; P<0.001 for the comparison of SE versus OMC, P=0.02 for ST versus OMC, and P=0.04 for SE versus ST). Although disease-specific quality of life as assessed by the Walking Impairment Questionnaire and Peripheral Artery Questionnaire also improved with both SE and ST compared with OMC, for most scales, the extent of improvement was greater with ST than SE. Free-living step activity increased more with ST than with either SE or OMC alone (114±274 versus 73±139 versus -6±109 steps per hour), but these differences were not statistically significant.

Conclusions  SE results in superior treadmill walking performance than ST, even for those with aortoiliac peripheral artery disease. The contrast between better walking performance for SE and better patient-reported quality of life for ST warrants further study.