My wired lyme story

Here you can introduce yourself and give an account of your medical history, visits to physicians, results of treatments, etc.
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tibi_hd
Posts: 1
Joined: Wed 15 Apr 2015 15:32

My wired lyme story

Post by tibi_hd » Wed 15 Apr 2015 15:35

MY CURRENT STATE DESCRIBED THE BEST I COULD:

I have never felt so horrible in my entire life, there is nothing like it, the symptoms are like an objective thing but really feel like a part of me and agonazing most of the time. I don't feel like the same person, is difficult to even put the feelings or sypthoms into words almost like I would try to describe an emotion, feeling totaly out of it, headeach, brain pressure, dizzy, drunk like or drugged (this one is the worst), sound sensitive, light sensitive, brain fog, memory problems, lack of vitality and energy, food feels like alcoohol and sleeping pills, complete stress and anxiety that can trend to overweling pannic and sinking feelings, it feels like like half of my brain is totally missing, not even human conscience should feel like it should. Detached, unreal, sereal, with a symphony of ringging and woosing in my ears, emotions on total roller coster from the darkest depression to sinking, mood swings. Hours long, anxiety attacks to anger and rage, things look different, is hard to say what is off, depth, color, dimention, brigthness. Static over everything, sometimes feeling like I will lose my mind.I believe that at this point I am half insane and I have suicidal tendencies.

I was diagnosed with chronic lyme and bartenella based on IIF and DFM test, by Dr. Bela P. Bozsik, a well know lyme specialist from Hungary and I will start treatment soon.

I want to share my story for other to read because is an insane story and also ask any help and adices.

BRIEF STORRY HOW MY ILLNESS STARTED:

Before I started to feel ill I was a person full of life, I was going to gym 4-5 times a week and tried to have a healthy diet, I owed a I.T. small company and I was one of the senior developer and one of the best, working with clients all over the world, my life was more then perfect.

in June 2014 when I was at a picknick with my wife and little girl I developed a wired rash on my entire body with the exception of the face and fever (not the bulles eye rash), I had symptoms similar to a flu, that lasted about four days after which the rash disappeared but my feet started to itch really bad like something was crawling under my skin (I remember that during those days that I searched for parasites on the web because of the crawling sensation I thought that something is actually crawling under my skin and now I know that is what happened) this lasted about three days then I was fine... In the next two months I noticed that I could not concentrate at work, took frequent breaks and it was impossible to write code and any more. At gym I had energy but something felt wrong.

Then something really wired happened, I started to have serious cognitive issues, could not work at al, I was always in a drunk / drugged state. I remember that I was working on a really difficult project and I was so excided to do it and then I realised that something is not as it should, I was not e anymore. I started to constantly feel drunk (it feels as I had a glass of wine), extremely tired and fatigued. After meals the drunk feeling was so severe that I had to lye down in bed and also I had terrible hart palpitation with increased pulse and lower blood pressure.

From October 2014 until February 2015 I was hospitalised multiple times in different hospitals, I had and still have diabetic sympoms but all they could find was prediabetes which again is wired (prediabetes comes over time not in two months) and of course depression even tough I've told the doctors more then one time that I had no reason for depression, they didn't believe any of my symptoms and said that they are in my head or that I am scared because I know how serious diabetes can be... even if I had signs of diabetes (high collesterol, high triglicerides, faild the glucose test at border line diabetes) they said probably is from stress...

Currently I have high blood sugar after meals and recently I had episodes of blood sugar over 200 mg/dl and I use a lot of natural herbs to lower my blood sugar. I was put on metformin that had absolutely no effect it actually made things worse because I was with diarreha and blood sugar was the same. Also put on antidepressive twice without any result they even made things worse, all my symptoms worsen, specially the headeach.

It is pointless to say that I was humiliated by all doctors that I've seen because they would not believe my symptoms, all off them thought that I am depressed or even worse...

During this time my immune system was going down, currently my leucocites number is under the normal range, the doctors could not explain why, made a clostridium infection because of some antibiotics that thay geve me for a prostate infection... and at the current time I am feel like I a ready to die or worse lose my mind.

SYMPTOMS THAT I HAVE NOW:

Constant fatigue, lack of energy, dizzines, brain fog, headache and brain pressure changing in intensity specially after meals, ocasional and more frequent pin pricks pain in my brain or scalp (difficult to explain the sensation), I feel disconnected from reality is like I am in a dream, also sometimes I have the feeling that something is crawling under the skin of my scalp.

The worst sympthom is a constant state of drunk/drugged feeling that intensify after meals, the more carbs I eat the worse, also after meals I get extremely tired and sleepy.I am at a a point that I am afraid to eat, I feel closer to normality if I am starving myself.

Short term and long term memory issues, cognitive problems, difficulty to access thoughts and impossibility to multitask, I can't do simple things any more, everything is difficult.

The above symptoms are really hard to explain and makes life impossible, they prevent me to function as a normal human being or better said makes me a walking, talking plant since I can't take care of myself any more. How can I go and say to a doctor that I am drunk like all the time and after meals is 10 times worse, this sound so stupid and I am aware of it but this is exactlly what happenes and is not something that I make to myself.

The simplest things are confusing and overwhelm me, for example a simple conversation makes me so dizzy, drunk, confused and tired that I have to lie down in bed. If I go in a mall or a place with multiple sounds my senses are overwhelmed and I feel lost, dizzy and super confused. I can't even play with my little girl beacause she makes a lot of noice which is driving me crazy, this breaks my hart and ruing what's left of my soul.

Sensitive to noise and sound, three tinitus (ringing in ears), two in my left ear and one in my right ear, when I move my eyes one tinitus is changing frequency and when I am really tired and this happens a lot without much of an effort and I move my eyes I can actually feel the nerves impuls in my brain and one of the tinitus is changing frequency.

Sensitive to light, vision with noise, snow and flashy spots, everything looks distorted, occasional blurry vision with my left eye, after images (I look at an object then look away only to have the outline of the object has followed). Is a nightmare to go out when during the day, everything seam distorted and unrealistic.

Knees and hips pain that comes and goes (I never had knees and hips pain before this).

Green stool.

When I manage to exercice instead of feeling good and oxigenated I feel more confused and most of the time I get extreme headeache.

Frequent urination, pale skin (not noticable now because I cathed some sun), sweet taste in mouth.

CONCLUSION:

I have developed depression and I believe depersonalization because there are eight months now since I feel like this and things are getting worse. All I can do is to stare at the walls all day long, lost my bussiness, lost normality, lost all contact with reality, when I think at my old life I get panic attacks and anxiety (this is not me I was a really strong man with my feet planted in life), basically I am someone else and is not becasause I want to, my brain doesn't function anymore, I am trying really hard to keep what's left of my sanity and I am convinced that I will die, actually at the state that I am now this will be a bleassing for me and my familly.

I want to ask if anybody with lyme had problems with food or blood sugar issues and if there is something that I can do.

How the heck I developed diabetes in 5 months considering that I was doing so much exercise every day, had a healty diet, this is impossible...

Is there a clinic in Europe that can actually help me and if so can anybody suggest one.

brauty94
Posts: 1
Joined: Mon 30 May 2016 23:08

Re: My wired lyme story

Post by brauty94 » Mon 30 May 2016 23:18

I experiance all these symptoms that you speak of except i dont get headaches and pain. As a child i had joint pain but that got ruled out for growing pains however this went on for years. I havent been diagnosed with lyme disease because i live in Australia and its not recognized, for 12 years ive been living the way you have described and everyday i feel dazed vision with the drunk sensation. I have had every test done including all blood work stool tests mri etc.
I had high blood sugar to but had the fasting blood sugar test and dont have diabetes. Its relief for me that i have found someone with very similar symptoms to mine because i feel like im going mad now and doctors here aren't doing much for me anymore. Its weird about the reaction to carbs you have because i get the same thing and when i dont eat i feel like a different person. I tried explaining that to the doctor and they justvlooked at me funny.
Any luck with treatment?

Hastyking
Posts: 1
Joined: Wed 26 Oct 2016 14:45

Re: My wired lyme story

Post by Hastyking » Wed 26 Oct 2016 15:16

Hi Brauty,

That sounds very serious and what you need to do is convince them to put you on a course of doxycycline. If your symptoms alleviate then this alone can play a role in diagnosis.

I'm shocked it's not been recognised by your gp. Even if there's not a prevalence in Oz, is it not possible you got bitten by a tick on holiday?

Good luck.
H

Anushka
Posts: 34
Joined: Tue 4 Nov 2014 17:54

Re: My wired lyme story

Post by Anushka » Tue 8 Nov 2016 16:47

Hi tibi_hd,

From the symptoms you describe this certainly sounds like Lyme , but also could be caused by co-infections like Anaplasma ....or protozoa infections ect. It sounds like you are in a systemic immune response or metabolic acidosis -- your body produces to much lactic acid due to infection.Your doctor should put you immediately on antibiotics like Metronidazol, which reduces D- lactic acid , to see if it eases the symptoms. Metronizadole is used by some Lyme docs in combination with other antibiotics for Lyme. (You can pm me if you want for further info)

Anushka
Anushka

Anushka
Posts: 34
Joined: Tue 4 Nov 2014 17:54

Re: My wired lyme story

Post by Anushka » Sat 12 Nov 2016 7:18

INTRODUCTION — Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. It is associated with an elevated anion gap and a plasma lactate concentration above 4 meq/L. Impaired tissue oxygenation, leading to increased anaerobic metabolism, is usually responsible for the rise in lactate production. (See "Approach to the adult with metabolic acidosis".)

The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".)

PATHOPHYSIOLOGY — A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients.

Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is mainly reflected by the ratio of oxidized and reduced nicotine adenine dinucleotide (ie, NAD+ [oxidized form] and NADH [reduced form]).

NAD+ and NADH are involved in many cellular redox reactions, serving, respectively, as an electron acceptor or an electron donor. One of these cellular redox reactions is the equilibrium between pyruvic acid and lactic acid, a reaction catalyzed by the enzyme lactate dehydrogenase (figure 1). Thus, the ratio of pyruvate and lactate is influenced by the ratio of NAD+ and NADH, such that a reduced redox state (ie, low NAD+/NADH ratio) is associated with a shift in the ratio from pyruvate to lactate. Many of the factors that produce a reduced redox state also accelerate pyruvate generation and simultaneously impair mitochondrial oxidation, thereby increasing pyruvate and lactate generation (see 'Mitochondrial dysfunction' below). These factors include inadequate oxygen delivery or utilization, and rapid oxidation of certain substrates, such as ethanol.

Lactate dehydrogenase is stereospecific for the production of the L-isomer of lactate (L-lactate), and, in humans, L-lactate is the dominant isomer that is synthesized and utilized. Although D-lactate is a minor component of mammalian metabolism, it is a major product of bacterial metabolism. (See "D-lactic acidosis".)

Normal individuals produce 15 to 20 mmol/kg of lactic acid per day. Most is derived from glucose metabolism via the glycolytic pathway, although deamination of alanine also generates lactate [2,3]. Balance is maintained by the utilization of an equal amount of lactic acid.

Lactic acid is primarily utilized via oxidation to carbon dioxide and water (70 to 80 percent) and through generation of glucose (15 to 20 percent) with a minor contribution of conversion to alanine. Utilization of lactic acid primarily occurs in the liver, but the kidneys, heart, and other tissues also participate. The generation of lactic acid from glucose and glycogen by muscle and its delivery to the liver, where it is converted back to glucose is named the Cori, or lactic acid, cycle.

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Causes of lactic acidosis

When lactic acid accumulates in body fluids and its concentration increases, the hydrogen ions are almost completely buffered by extracellular bicarbonate. When lactate is utilized, whether by oxidation to carbon dioxide and water or by conversion to glucose or alanine, a hydrogen ion is also consumed. Thus, in a patient who has accumulated lactic acid, utilization of the lactate will restore the bicarbonate concentration.

Mechanisms of lactate accumulation — Excess lactate can accumulate as a result of increased production and/or diminished utilization [2-5]. In general, three mechanisms can cause lactate accumulation (table 1) [2,3]:

● Increased pyruvate production
● Reduced entry of pyruvate into mitochondria, where it would be converted to either carbon dioxide and water or to
glucose precursors
● A shift of the cellular redox state such that NADH accumulates, which drives the pyruvate/lactate ratio toward lactate
The contribution of lactate overproduction to the development of metabolic acidosis seems clear in certain disorders. As an example, plasma lactate levels may transiently increase to 15 to 25 meq/L after a grand mal seizure or with maximal exercise [6], and the blood pH can fall as low as 6.8 [7,8]. However, the rate of lactate utilization in such patients can also increase rapidly, reaching rates as high as 320 meq/hour [2]. As a result, blood pH and plasma bicarbonate levels rapidly return to normal after the seizure or exercise has ceased.

A marked increase in lactate production, in part due to catecholamine stimulation of glycolysis, also plays an important role in the lactic acidosis associated with shock, especially septic shock [9,10]. However, the very high potential metabolic capacity for lactate utilization that is apparent in patients with grand mal seizures suggests that there must also be a component of decreased lactate utilization in disorders such as shock, in which lactic acidosis occurs despite more modest lactate overproduction.

The importance of impaired lactate metabolism is illustrated by the observation that, when lactic acid is infused into normal animals at rates similar to the rate of overproduction that occurs in shock, hepatic utilization of lactate increases and there is only a minimal fall in arterial pH [5]. In shock, reduced hepatic perfusion and an associated intracellular acidosis probably combine to substantially diminish hepatic lactate metabolism [4,5,11].

CAUSES — The causes of lactic acidosis can be divided into those associated with obviously impaired tissue oxygenation (type A) and those in which systemic impairment in oxygenation does not exist or is not readily apparent (type B) (table 1).

Type A lactic acidosis — Most cases of lactic acidosis are due to marked tissue hypoperfusion in shock (due to hypovolemia, cardiac failure, or sepsis) or during a cardiopulmonary arrest [2,3,12,13]. In some of these patients, concurrent respiratory acidosis contributes to the acidemia [12]. (See "Shock in adults: Types, presentation, and diagnostic approach" and "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

The clinical manifestations of shock include:

● A reduction in systemic blood pressure, the degree of which may be minimized by marked vasoconstriction
● Cool, clammy extremities, with the exception of the flushed, hyperemic skin of early septic shock
● Oligoanuria
● Impaired mental status

The prognosis is generally poor unless tissue perfusion can be rapidly restored. The initial serum lactate level is a strong predictor of survival in patients with septic shock [14,15]. (See "Treatment of severe hypovolemia or hypovolemic shock in adults" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Evaluation and management of severe sepsis and septic shock in adults".)

Type B lactic acidosis — Evidence of systemic hypoperfusion is not apparent in type B lactic acidosis. The mechanisms that may be involved in type B lactic acidosis include toxin-induced impairment of cellular metabolism and regional areas of ischemia

Causes of lactic acidosis

Diabetes mellitus — Diabetes mellitus can be associated with lactic acidosis by at least three mechanisms:

Biguanide therapy in type 2 diabetes with metformin or, in the past, with phenformin can cause type B lactic acidosis, although the risk is relatively low. (See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Lactic acidosis'.)

A moderate degree of lactic acidosis unrelated to biguanide therapy occurs in some patients with diabetic ketoacidosis [2,16]. It is likely that hypovolemia plays an important role.

D-lactic acid may accumulate and contribute to the anion gap acidosis of diabetic ketoacidosis. In these patients, the plasma concentration of D-lactic acid often exceeds 2 meq/L and may reach 8 to 10 meq/L [17]. The D-lactic acid is derived from methylglyoxal, a metabolite of both acetone and dihydroxyacetone phosphate, which are intermediates that can accumulate in patients with diabetic ketoacidosis. (See 'D-lactic acidosis' below and "D-lactic acidosis", section on 'Pathogenesis'.)

Malignancy — Lactic acidosis occurs rarely in patients with leukemia, lymphoma, and solid malignancies [18-23]. The pathogenesis is not well understood. Anaerobic metabolism due to dense clusters of tumor cells and/or metastatic replacement of the hepatic parenchyma has been proposed, but lactic acidosis can develop in patients with relatively small tumor burdens [18,20]. Other possible mechanisms include increased rates of lactate production by the neoplastic cells that undergo aerobic glycolysis (the "Warburg" effect) [24], or by thiamine and/or riboflavin deficiency [22]. It is likely that lactate metabolic clearance is also impaired.

Regardless of the mechanism, removal of the tumor (by chemotherapy, irradiation, or surgery) usually corrects the lactic acidosis [18,20-22]. (See "Overview of the complications of acute myeloid leukemia".)

Alcoholism — A mild degree of lactic acidosis can develop in patients with chronic severe alcoholism. Lactate production is usually normal, but lactate utilization may fall as a result of hepatic dysfunction. The oxidation of ethanol can increase NADH levels, which reduces the NAD+/NADH ratio, a change that shifts pyruvate toward lactate (see 'Pathophysiology' above). Although the plasma lactate concentration seldom exceeds 3 meq/L in intoxicated patients, alcohol ingestion can increase the severity of other disorders that cause overproduction of lactate. (See "Fasting ketosis and alcoholic ketoacidosis", section on 'Alcoholic ketoacidosis'.)

Elevations in plasma lactate levels can also be seen with ethylene glycol poisoning. Among patients with true increases in plasma lactate, the increase is usually small. Some patients have large elevations in plasma lactate that may represent a laboratory error due to instruments that cannot distinguish lactate from glycolate, a metabolite of ethylene glycol that is structurally similar to lactate. (See "Methanol and ethylene glycol poisoning", section on 'Lactate'.)

HIV infection — Given their increased propensity to serious infection, sepsis-induced lactic acidosis can occur in patients with AIDS. In addition, lactic acidosis may be caused by antiretroviral medication-induced mitochondrial dysfunction. This form of chronic lactic acidosis can occur in the absence of sepsis or hypoperfusion (type B lactic acidosis). (See "Mitochondrial toxicity of HIV nucleoside reverse transcriptase inhibitors", section on 'Hyperlactatemia and lactic acidosis' and 'Mitochondrial dysfunction' below.)

Mitochondrial dysfunction — Pyruvate metabolism requires entry into the mitochondria. Once in the mitochondria, pyruvate is either oxidized to form acetyl-coenzyme A (which is further oxidized by the Krebs cycles, converted to fat, or shunted to form ketoacids) or converted to oxaloacetate (which either replenishes Krebs cycle intermediates or is converted to glucose). All of these reactions require normal mitochondrial function.

A variety of congenital or acquired mitochondrial defects can impair pyruvate utilization and contribute to the development of lactic acidosis [25]. The inherited defects in mitochondrial DNA cause a spectrum of disorders grouped together as the MELAS syndrome (Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes) [26]. Approximately 80 percent of these patients have a single point mutation in the mitochondrial gene that encodes a specific transfer RNA. (See "Mitochondrial myopathies: Clinical features and diagnosis", section on 'MELAS'.)

Lactic acidosis can also be induced by drugs that affect mitochondrial protein synthesis and reproduction [25]. Because
mitochondria have prokaryotic origins, they may be uniquely susceptible to drugs that target bacterial or viral metabolism. As an example, a number of antiretroviral drugs, such as HIV nucleoside reverse transcriptase inhibitors, can generate lactic acidosis associated with hepatic and muscle lipid deposition. (See "Mitochondrial toxicity of HIV nucleoside reverse transcriptase inhibitors", section on 'Hyperlactatemia and lactic acidosis'.)

Linezolid is an oxazolidinone antibiotic that targets bacterial protein synthesis by inhibiting a subunit of bacterial ribosomes. It can also affect human mitochondrial ribosomes and protein synthesis, which sometimes leads to the development of lactic acidosis. Although linezolid-induced lactic acidosis was first reported after prolonged courses of antibiotic treatment, other cases have developed soon after initiation of the drug [27,28]. One case report described lactic acidosis developing in a patient with MELAS syndrome who was receiving linezolid. Although not a listed contraindication, extra caution seems appropriate when prescribing linezolid to patients with inherited mitochondrial disorders [28].

Mitochondrial dysfunction may also be an integral component of other clinical conditions that are associated with lactic acidosis including metformin therapy in patients with diabetes mellitus and malignancy. (See 'Diabetes mellitus' above and 'Malignancy' above.)

D-lactic acidosis — D-lactic acidosis is a rare form of lactic acidosis that can occur in patients with short bowel syndrome or other forms of gastrointestinal malabsorption. In these patients, abnormally large amounts of glucose and starch are metabolized (fermented) by intestinal bacteria to multiple organic acids, including D-lactic acid. Because humans metabolize D-lactic acid very slowly, systemic absorption of the D-optical isomer of lactic acid from the bowel can lead to high plasma D-lactate levels.

Other causes of D-lactic acidosis include rapid and high-dose intravenous infusion of propylene glycol (a solvent for some intravenous medications) and diabetic ketoacidosis. In these settings, D-lactic acid is a metabolic product of other accumulating metabolites: lactaldehyde with propylene glycol and methylglyoxal in diabetic ketoacidosis. (See "D-lactic acidosis".)

DIAGNOSIS — The normal plasma lactate concentration is 0.5 to 1.5 meq/L. Lactic acidosis is generally defined as a plasma lactate concentration greater than 4 meq/L, even in the absence of overt acidemia.
The recognition of lactic acidosis has increased dramatically over the past several years as a result of the wide acceptance of early goal-directed therapy of sepsis and septic shock [29]. The screening process for patients with suspected sepsis includes a blood lactate level. (See "Evaluation and management of severe sepsis and septic shock in adults", section on 'Goals of initial resuscitation'.)

SUMMARY
● Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Impaired tissue oxygenation, leading to increased anaerobic metabolism, is usually responsible for the rise in lactate production. (See 'Introduction' above.)
● The accumulation of lactate is usually due to enhanced pyruvate production; reduced pyruvate conversion to carbon dioxide and water or to glucose; and an altered redox state within the cell, in which the pyruvate/lactate ratio shifts toward lactate. (See 'Pathophysiology' above.)
● Type A lactic acidosis is associated with impaired tissue oxygenation due to tissue hypoperfusion in shock (caused by hypovolemia, cardiac failure, or sepsis) or as a result of a cardiopulmonary arrest. Accelerated generation of pyruvate from glucose may also play an important role in some forms of type A lactic acidosis, especially in septic shock. In some patients, concurrent respiratory acidosis contributes to the acidemia. (See 'Type A lactic acidosis' above.)
● Type B lactic acidosis occurs in patients without overt systemic hypoperfusion. Two causes of type B lactic acidosis include toxin-induced impairment of cellular metabolism and regional areas of tissue ischemia. High levels of metformin, tumor lactic acidosis, alcoholism, and drug-induced mitochondrial dysfunction in HIV-infected patients are several etiologies of type B lactic acidosis. (See 'Type B lactic acidosis' above.)
● D-lactic acidosis is an unusual form of metabolic acidosis that occurs in patients with short bowel syndrome or other
forms of malabsorption. It may also develop in patients receiving rapid and high-dose infusions of propylene glycol (a solvent for some IV medications), or in patients with diabetic ketoacidosis. (See 'D-lactic acidosis' above and "D-lactic acidosis".)
● A plasma lactate concentration that exceeds 4 meq/L generally defines lactic acidosis, even among patients without a systemic acidosis. (See 'Diagnosis' above.)
Anushka

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