Sometimes a Systemic Yeast Infection can have light symptoms, and because of this they're dismissed as nothing to concerned about. The problem is, this allows the yeast to enter the bloodstream where a lot of different problems can eventuate and can even become a life-threatening situation.

The body naturally has a certain amount of yeast that lives in the body in small quantities and actually help the body, without doing any harm to it. There are also different types of microorganisms inside the body that are there to keep the yeast in check so an infection does not occur.

On-going stress attacks, poor choices of food, normal pregnancy changes, immune system deficiency diseases, antibiotic medications and other disease may abolish the tiny microorganisms and thereby allow the Systemic Yeast Infection Symptoms to rage.

The Systemic Yeast Infection Symptoms can differ from each individual, but here a few of the most usual ones:

Heavy sense of exhaustion and unusual run down feelings may arise.

1. The feelings of sensory disturbances, unusual muscle aches and pains, continual headaches, constant dizziness, and complaints of the sufferering of persistent tiredness are signs of a person with Systemic Yeast Infection.

2. Unusual or sudden sensitivity to chemicals or new food allergies.
Arising troubles which haven't occurred before with several chemicals or foods are common with those suffering from Systemic Yeast Infection Symptoms.

3. Problems with the gastrointestinal tract.

On many occasions, as touched on in the previous detail of the food allergies, flatulence, inflammatory bowel disease, rectal itching, constipation, and diarrhea are the most common of the Symptoms.

It is even possible for thrush, a Yeast Infection affecting the mouth and/or throat, to develop.

4. Onset of urinary and genital problems.

5. Development of hives and skin rashes.

You could even be having a case of hives, and not know where they came from.

6. Suddenly feeling irritable or mildly depressed.

Many times people complain of Systemic Yeast Infection Symptoms that include: mental confusion, feeling of being in a 'fog', difficulty focusing or concentrating, sleepness nights, memory loss, and decreased attention span.

7. Problems with the autoimmune system.

Some autoimmune disorders that normally become worse from a Systemic Yeast Infection are sarcoidosis, scleroderma, myasthenia gravis, arthritis, hemolytic anemia, thrombocytopenic purpura, or systemic lupus erythematosus.

Yeast flourish on a body that is fed with sugar, refined starch, and chemical additives.
These chemicals, starches and sugars are also readily present in bread, cookies, chips and other junk foods which are a large part of many peoples diets.

When someone is under immense stress, the microorganisms in the body that control the yeast start to die off.

Anytime you think you may have a Systemic Yeast Infection Symptoms, you need to check with your doctor about what tests need to be run to determine what your body's level of Yeast organism is.
All in all, remember that it's vital to know if you are dealing with a Systemic Yeast Infection Symptoms so you can get the proper treatment.

About the author:

Source: http://www.sooperarticles.com/health-fitness-articles/women-health-articles/systemic-yeast-infection-symptoms-7-signs-watch-out-464763.html


how is systemic lupus erythematosus diagnosis

19 thoughts on “How Is Systemic Lupus Erythematosus Diagnosis

    1. Fruit Basket #1

      Systemic Lupus Erythematosus (SLE) is a very interesting and broad topic. The disease can affect many different organ systems and parts of the body, ie: skin, blood, kidney, central nervous system, joints. Any one of these areas would be a good topic. Also, SLE has very classic physical exam findings (rashes, ulcers, joints, etc) and usually happens to a certain age/race/gender. There are many blood tests that aid in the diagnosis of SLE. A discussion of how to diagnose Lupus using the criteria above would be interesting. Other topics: drugs and treatments used to in SLE, prognosis of patients w/ SLE, diseases confused with SLE (other rheumatic diseases like Scleroderma, Sjogren’s, etc), famous people w/ SLE. You get the idea. Hope this helped

  1. Song_bird

    Systemic Lupus Erythematosus or Rheumatoid Arthritis?
    My symptoms are: Extremely painful to walk, rashes, blood in urine, Anemia (had to get iron infusions), headaches, extreme fatigue, ect. I seen a doctor who did some x-rays, blood work & a physical exam. She recently called me & told me from my lab results came back & said i have either Systemic Lupus Erythematosus or Rheumatoid Arthritis. She said my blood work showed alot of abnormalities & even infection. She wanted me to start on a steroid right away. She put me on (10 mg pills of Prednisone) for 10 days until my follow up with a Rheumatologist. Okay my question: What is Lupus & Rheumatoid Arthritis?
    Are these 2 illnesses simular? She will be calling me back within 5 days with the other test results. Has anyone personally experienced this? She said my illness is treatable but not cureable. I’m still pretty young & this is a shock to me & i’m having a hard time dealing with not knowing what i’m dealing with i guess my new doctor will be able to answer alot of questions later.
    Thanks for the advice i will go look there.

    1. Linda R

      I can’t imagine how a nursing diagnosis of lupus is different than any other diagnosis of lupus.

      Lupus is extremely complex. Systemic lupus can affect virtually any and every organ in the body, and varies from patient to patient. One my have kidney disease, another may have clotting issues because of antiphospholipid antinodies and still another may have seizures because of central nervous system involvement. Any plan must take into account the unique manifestations of lupus in the patient. A plan must also take into account the remitting/flaring nature of the disease.

      Regular medictal monitoring is recommended (every 3-6 months depending on disease activity)

      Patient eduction to increase likelihood of compliance.

      Nutritional and exercise counseling.

      Psychological counseling to help come to terms with the fact that we will never be cured.

      Coping strategies.

  2. Anonymous

    how do you get tested for androgenic alopecia?
    I here when you go on birth control pills, you are more susseptible to hair loss if you have androgenic alopecia so i was just wondering if its possible to get tested for it.

    1. Robert Ryhco

      Hi There!
      There is no specific test to detect Androgenic Alopecia… basically when there is no other cause that make your hair fall, and the doctor determine that the cause of your hair loss is not hormonal, or caused by stress, or any other possibility… probably you will have Androgenic Alopecia…

      About Diagnosis of other types of Alopecia
      If you are looking for pyoderma or a fungal infection, then a smear and culture of the scrapings for bacteria and fungi should be done.

      If these are negative, a skin biopsy should be performed. The skin biopsy will help identify lupus erythematosus, psoriasis, and alopecia areata.

      Systemic disorders may need to be ruled out with thyroid function tests, antinuclear antibody (ANA) assay, VDRL test, CBC, and serum iron and ferritin. (A dermatologist should be consulted in difficult cases.)

  3. marylkamp

    Does anyone suffer from osteonecrosis of the femur from a cramped driver’s seat? What were treatments?
    I drove with no legroom 8-10 hours a day (my legs felt as if they’d been injected with novocaine) for 3 years, Now I have osteonecrosis and nerve damage. Will I ever walk again without crutches, or at least be pain-free for a short time each day?

    1. ashleyligon1967

      Osteonecrosis

      ——————————————————————————–

      General

      Osteonecrosis bespeaks bone death. Synonyms include aseptic necrosis, bone necrosis, avascular necrosis, bone infarction and ischemic necrosis. By convention, the terms “aseptic” or “avascular” necrosis have been applied to areas of juxtaarticular involvement and the term bone infarct is usually applied to metaphyseal or diaphyseal involvement. However, this terminology is not applied consistently throughout the literature, and I feel that these are largely artificial distinctions. I prefer to simply use the single term ‘osteonecrosis’ and to apply it to areas of bone infarction, no matter where in the bone they occur.

      Mechanisms of Osteonecrosis

      There are many paths to satori, and likewise to osteonecrosis. Osteonecrosis is multifactorial in etiology, and has a widely differing prognosis, depending upon the exact part of the bone involved by the necrosis. The exact mechanism of osteonecrosis depends primarily on the predisposing cause. This is reflected in the table below.

      Mnemonic = VINDICATE
      Differential Diagnosis of Osteonecrosis

      Category of Disease Disorder Mechanism
      Vascular sickle cell disease and other hemoglobinopathies, polycythemia
      vera and other lymphoproliferative disorders sludging of cells in vessels
      pregnancy impaired venous drainage caused by the gravid uterus
      Infection septic emboli causing arterial occlusion
      Drugs / Toxins steroid use fat cell enlargement causing medullary hypertension and intraosseous
      venous occlusion
      alcoholism fatty emboli causing arterial occlusion
      Inflammatory pancreatitis fatty emboli causing arterial occlusion
      Congenital Gaucher’s disease marrow packing by Gaucher cells causing medullary hypertension
      and intraosseous venous occlusion
      Autoimmune Systemic lupus erythematosus, rheumatoid arthritis vasculitis causing arterial occlusion
      Trauma fracture / dislocation interruption of arterial supply to bone (e.g. scaphoid fracture, hip
      dislocation, talar neck fracture)
      radiation direct injury to vascular supply leading to occlusion
      dysbarism (caisson disease) nitrogen emboli causing arterial occlusion / accumulation of nitrogen
      bubbles in marrow fat
      thermal trauma (burns, frostbite) direct tissue damage
      Endocrine / Metabolic Cushing’s disease fat cell enlargement causing medullary hypertension and intraosseous
      venous occlusion

      It seems logical that the sequence of events in developing osteonecrosis should be as follows:

      some phenomenon causing decreased blood flow to bone

      bone ischemia, if the flow becomes low enough

      bone infarction, if the flow becomes lower still
      Osteonecrosis is generally thought of being an irreversible process. If the necrosis occurs next to a joint surface, it is generally considered to cause joint deformity. However, no one really knows if this is true, and such conclusions are to some extent artifacts of our current diagnostic methods for osteonecrosis. With the advent of MRI, we finally have a tool which can show abnormalities within about 2 weeks of the original insult. However, current standard MR scanning cannot yet show abnormalities at the instant of infarction. What is needed to answer this question is a diagnostic technique that is sensitive to vascular flow, and not just intensity changes in the bone marrow. Dynamic MR scanning following a gadolinium bolus may be helpful in this regard, but definitive studies have not yet been done to prove this speculation.

      There is some evidence in the literature that suggests that in some circumstances, osteonecrosis may be a reversible process that can resolve completely without subchondral collapse and subsequent joint arthrosis. This evidence is found in the literature for transient osteoporosis of the hip, an idiopathic disorder characterized by a reversible osteopenia of the hip and marked marrow edema. If this definition sounds a bit circular, well, that’s how idiopathic disorders are, isn’t it. We don’t know what causes them, so their names pretty well sum up most of what we know about them. Anyhow, several studies of TOH have been published in which the characteristic edematous marrow of TOH was biopsied. These biopsies have shown the presence of osteonecrosis in many cases, leading to the suggestion that TOH may actually be due to a low-grade and reversible osteonecrosis.

      Concave / convex joint physiology

      It turns out that, in part, the shape of joints governs the distribution of osteonecrosis. In particular, it is the convex versus concave shape of the opposing joint surfaces of most joints that determines this distribution (Simkin).

      On both sides of the joint, the forces of weight-bearing and other loading are directed tangential to the joint surface. On the convex side of the joint, these forces converge to a common center. On the concave side, these forces diverge away from each other. To see the significance of this fact, one must first consider the phenomenon of hydraulic resistance. The human body, including the bones are composed of about 50 – 67% water by mass. One can think of the bones as calcium balloons filled with water. Water is not compressible, so this internal water provides some support to the bones, and this supporting force is called hydraulic resistance. Nature is thrifty, and the presence of hydraulic resistance makes it possible to provide the same support with less bone. Since the loading forces converge to a common center on the convex side of the joint, hydraulic resistance becomes a fairly efficient mechanism for resisting these forces. On the concave side of the joint, the divergent nature of the forces makes this mechanism much less efficient, and therefore, hydraulic resistance plays a much smaller role in bone support. The two sides of the bone are obviously supporting the same load, so more bone is therefore necessary on the concave side. This is seen in the form of increased thickness of the subchondral bone along the concave side of the joint in virtually every concave/convex joint pair in the body.

      The presence of this extra bone along the subchondral portion of the concave joint surface has some important ramifications for osteonecrosis. Consider first the normal joint and how intramedullary pressure varies on both sides of the joint with loading. Since hydraulic resistance is used as an important support on the convex side of the joint, it is not surprising that the intramedullary pressure on this side of the joint will vary widely with loading. Due to the extra bone supporting the concave side, there is less variation of the intramedullary pressure on that side of the joint, as shown below.

      Now, given this picture of normal variations in intramedullary pressure with loading, consider how the patient developing osteonecrosis. Specifically, consider a patient on steroids, probably the most common cause of osteonecrosis. Chronic steroid use causes fat cells to grow. This is the basis for such well-known physical findings such as the “buffalo hump” or the “moon facies” seen in these patients. Many people don’t realize that the intramedullary fat cells share in this growth. As the patient spends more and more time on steroids and the intramedullary fat cells grow larger and larger, the baseline intramedullary pressure begins to rise. Why? Because the bone is a closed and fairly stiff cavity, and will not give with increases in intramedullary pressure. This is an analogous situation to the skull in cases of cerebral edema. However, in this case, the casualty is not the brain, but the intramedullary veins. The intramedullary arteries operate at systemic systolic pressure (90 – 140 mm Hg), but the intramedullary veins operate at a very low pressure (3 – 5 mm Hg). Therefore, the intramedullary pressure doesn’t have to rise very high to cause occlusion of the intramedullary veins. As the intramedullary pressure rises, this leads initially to intermittent occlusion during loading on the convex side of the joint.

      However, as the pressure continues to rise, the intramedullary veins on the convex side of the joint finally become occluded all of the time.

      See these graphs as a movie (101K)

      The mechanism outlined here helps to explain the overwhelming distribution of osteonecrosis toward the convex side of the joint. No matter how much experience you’ve had looking at osteonecrosis, most of the cases of joint involvement that you’ve seen involved the convex side, whether you noticed it or not. In my personal experience with hundreds of cases, I’ve only seen joint involvement on the concave side in two or three cases. Your mileage may vary.

      Methods of diagnosis

      Once osteonecrosis is pretty well established, just about every imaging method will reveal it. Other than MRI, most of these methods are not terribly sensitive, and the osteonecrosis will be well developed by the time that it is diagnosed, as shown in the table below.

      Imaging Method Findings Time to Diagnosis Comments
      CT reactive sclerosis
      subchondral collapse months sensitivity poor
      specificity OK
      radionuclide imaging decreased uptake early, increased uptake late weeks sensitivity good
      specificity poor
      MRI decreased signal in a segmental pattern days to weeks sensitivity excellent
      specificity good
      MRI or PET flow study decreased flow through affected bone minutes theoretically possible, but not yet proven

      Approach to Osteonecrosis

      Generally the diagnosis of osteonecrosis is not too difficult. The patient often has some known condition that places them at high risk for osteonecrosis, and the radiographic requisition states something like “R/O AVN”. In such cases, it is usually not difficult to twig to the idea that osteonecrosis belongs in the differential.

      Typical plain film findings
      The earliest radiographic appearance of osteonecrosis is zilch. That is, the radiograph looks completely normal. After weeks to a month or two, the patient may develop an ill-defined mottling of the trabecular pattern as the earliest evidence of osteonecrosis. Early on, this is so ill-defined that most radiologists will miss it, unless they have a lot of experience looking at osteonecrosis. The late findings of osteonecrosis depend upon its location within the bone. If the lesion occurs in the medullary space well away from the joint, one eventually may see the classic pattern of dense, serpiginous calcification. However, if the necrosis occurs in the subchondral bone, a different pattern usually emerges. Once the osteonecrosis has been present for months, microfractures will accumulate in the dead bone to the point that one may see developing subchondral fractures. This may lead to a discontinuity in the subchondral line, or in some cases, to the “crescent sign”, which represents a fracture between the subchondral line and adjacent necrotic bone. As living bone reacts to the presence of adjacent dead bone, a thick sclerotic zone may develop along the “no-man’s land” between the living and necrotic bone.

      Tomogram of the right hip showing a segmental zone of sclerosis (arrows) in the superior portion of the femoral head, consistent with osteonecrosis (O).

      AP radiograph of the hip in a patient with osteonecrosis. Note the lucent crescent sign (white arrow) and the discontinuity where the subchondral bone has collapsed (black arrowhead). Also note a core decompression channel drilled up through the femoral neck (black arrows).

      Typical MR findings
      The classic MR appearance of osteonecrosis is that of a segmental area of low signal intensity in the subchondral bone, bounded by a low signal intensity border. This border may sometimes appear as a dark line adjacent to a bright line — the so-called “double line sign”. Occasionally osteonecrosis will present as an area of diffuse low signal intensity, which may be difficult to differentiate from other entities, such as osteomyelitis, stress fracture, etc.

      Coronal T1-weighted image of both hips — the low signal intensity in the superior weight-bearing area of the left femoral head is typical for osteonecrosis.

      Sagittal T1-weighted surface coil image of the femoral head — this image demonstrates a classic segmental area of osteonecrosis with a dark line denoting the border between dead bone and living bone.

      Sagittal T1-weighted image of the knee — this image demonstrates multiple segmental areas of osteonecrosis in the distal femur in this patient with Gaucher’s syndrome.

      Fortunately, the plain film and MR findings of osteonecrosis are usually so typical that one does not often have to offer a differential diagnosis. However, sometimes, osteoarthritis, subchondral cysts, transient osteoporosis of the hip and other entities may mimic osteonecrosis on flain films or MR. Sometimes osteonecrosis is unsuspected, and the alert radiologist must consider it whenever unexplained sclerosis or lucency is noted adjacent to a joint, or whenever a patient presents with diffuse skeletal sclerosis.

      Besides confirming the diagnosis, another major role for the radiologist in the workup of osteonecrosis is staging the current state of the disease. The usual plain film and MR stages are listed below.

      Stage Findings
      0 asymptomatic, normal radiographs
      I normal radiographs (abnormal MRI)
      II radiolucency and sclerosis
      III crescent sign, normal contour
      IV subchondral collapse, flattening
      V degenerative joint disease

      Wise sayings about osteonecrosis

      Remember the concave/convex joint physiology and its effect on the distribution of osteonecrosis about a joint.

      In a patient with diffuse sclerosis, consider some diffuse cause of osteonecrosis, especially sickle cell disease.
      References

      Simkin PA, Graney DO, Fiechtner JJ. Roman arches, human joints, and disease: differences between convex and concave sides of joints. Arthritis Rheum 1980;23:1308-1311.

      ——————————————————————————–
      For further information, contact Michael L. Richardson, M.D., webmaster
      © 2000 University of Washington Department of Radiology
      All rights reserved. Do not use without written permission.

      Last update: Wednesday, November 19, 2003 at 11:34:39 AM.

  4. Hannah

    Can a Lupus rash occur on your legs after a warm shower and in the sun?
    If i sit in the sun then i get a rash on my legs that itch and if i should in warm water then i get at rash that starts at me feet and to my chest. Could it be Lupus and if so then are there any web pages i can look at?
    I need websites that work.

    1. Laaz

      There are 3 good links about lupus. The first is a more simple read about it. The second is information on cutaneous lupus (not full-blown lupus which is called systemic lupus erythematosus, but rather the milder lupus forms that only affect the skin and nothing else). The last link gives you the diagnostic criteria for systemic lupus erythematosus, which required 4 out of 11 of the main diagnostic criteria to be present in order to be diagnosed with lupus.

      A mere hypersensitivity rash to sun exposure will NOT give you a diagnosis of lupus. 😉

  5. karl j

    What r canine lupus symptoms, what is prognosis. Need to add to the Vets knowledge hopefully?
    my Boston Terrier/Shiz-tsu is at vets he is unable to locate cause of flucuating fever, some drooling, lack of appetite.White blood cell count at the bottom of the scale. All other tests (kidneys, Liver) coming back normal. Was being treated to some infection in esophogus being given anti-biotics. Would like to offer vet an alternative diagnosis

    1. Pam

      Systemic Lupus Erythematosus(SLE): is one of several diseases known as “the great imitators” because its symptoms vary so widely it often mimics or is mistaken for other illnesses, and because the symptoms come and go unpredictably. Diagnosis can be elusive, with patients sometimes suffering unexplained symptoms and untreated SLE for years. Common initial and chronic complaints are fever, malaise, joint pains, myalgias and fatigue.

      Discoid Lupus symptoms: normally starts as loss of pigment around the nose. There may be scabby sores or just scaling of the nasal tissue. The surface of the nose may change from its typical cobblestoned appearance to a smooth surface.

  6. Anonymous

    Can an untreated vaginal yeast infection lead to a systemic yeast infection?
    Is this possible at all…? Some sources on the internet say it is, some say it isn’t…but I’ve learned not to take any medical advice too seriously unless it’s come from a medical professional.
    I’m finally getting it treated but it’s been a while, and I’m just a bit worried it might have spread. I’ll be talking to the doctor anyway about it, so no worries.

    1. Artemis

      Yes, it is possible, thought I wouldn’t worry about it if I were you. It’s not like your vaginal yeast infection is going to spread to your heart. You have yeast elsewhere in the body.
      Here’s half an article on the subject:

      Systemic yeast / Candida?
      by Marcelle Pick, OB/GYN NP

      In this article, Marcelle Pick, OB/GYN NP explains what Candida yeast is, the symptoms of systemic yeast infection, the digestion problems associated with Candida yeast, and how to treat it, including instructions for a yeast-free diet.

      … … …

      What is systemic yeast (Candida)?
      Candida albicans is a fungal organism that is present in everyone’s intestinal tract. It is normally kept under control by the immune system and by beneficial intestinal bacteria.

      This balance is upset when these bacteria are destroyed (typically by antibiotics), when our immune function is impaired (typically due to stress or illness), or when we develop environmental or food sensitivities.

      Once that balance is upset, Candida begins to proliferate and invade and colonize our body tissues. It most commonly appears as a vaginal yeast infection or as oral thrush. But Candida albicans can also spread inside the body and become a systemic problem.

      How does Candida albicans affect the body?
      When Candida proliferates, it changes from its simple, relatively harmless form to an invasive form, with long root-like structures that penetrate the intestinal lining. Penetration can break down the boundary between the intestinal tract and the circulatory system. This may allow introduction into the bloodstream of many substances which may be systemic allergens, poisons, or irritants. Partially digested proteins may enter the blood through the openings created by Candida (called leaky gut syndrome), which explains why individuals with Candida also often display a variety of food and environmental allergies.

      What are some of the symptoms of Candida yeast infections?
      While many of these symptoms may be caused by conditions other than candidiasis, a woman suffering from systemic yeast will typically experience a number of the following symptoms:

      Generalized: Fatigue, lethargy, migraine headaches, weakness, dizziness, sensory disturbances, hypoglycemia, muscle pain, respiratory problems, chemical sensitivities.

      Gastrointestinal: Oral thrush, diarrhea, constipation, rectal itching, inflammatory bowel disease (IBD), flatulence, food sensitivities.

      Genitourinary: Yeast vaginitis, menstrual and premenstrual problems, bladder inflammation, chronic urinary tract infections (UTI’s), bladder inflammation, cystitis, PMS.

      Dermatological: Eczema, acne, hives.

      Mental and emotional: Confusion, irritability, memory loss, inability to concentrate, depression, insomnia, learning disability, short attention span.

      Autoimmune: Multiple sclerosis, arthritis, systemic lupus erythematosus, myasthenia gravis, scleroderma, hemolytic anemia, sarcoidosis, thrombocytopenic purpura.

      Diagnosis of systemic yeast (Candida) infection
      A simple stool test can be done to determine if someone has Candida yeast overgrowth. If there are food sensitivities, a special blood test such as an ALCAT or RAST panel is done to identify reactive foods. This is important because while food allergies are easily noted, it’s more difficult to pinpoint the cause of food sensitivity since the reaction can take 8–72 hours.

  7. Sweet Pea

    What does it mean to have a possible positive lupus test?
    I have been having serious joint pain for some time now. My doctor tested me for arthritis, RA, and lupus. He said the test came back as a possible positive for lupus and he is sending me to a Rheumatologist for further testing. Does this mean they just don’t know or does it mean they are sending me for a confirmation? Has anybody had this happen to them?

    1. gpk.gr

      Dear Sweat Pea,
      the diagnosis of rheumatic diseases and specially systemic lupus erythematosus is based on clinical findings and past medical history. Laboratory values are use mainly for confirmation and sometimes to estimate disease activity. Please be patient until you visit your rheumatologist. As a specialist he will guide you through the differential diagnostic of arthritis (over 200 types!). I’m pretty sure you will feel frustrated after the first visit but afterwards you will begin to built a relationship with your rheumatologist based on his ability to understand your complaints and relieve your pain. Feel free to contact me and ask again!

  8. gibbler

    what are the beginning symptoms of rheumatoid arthritis?
    my wifes hands, feet, knees, etc. have been cramping up really bad where she cant move them , also she has been diagnose with chronic uticaria about 7 months ago. we’ve been to about five different doctors and no help so far. the symptoms keep getting worse and her grandma bag of meds don’t work very well.

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