Clinical Case Studies

[Michael Scally MD]

Syphilis

The ulcers have clean, smooth bases and slightly elevated, indurated borders. This type of painless ulcer is typical of a syphilitic chancre. The patient reported having had unprotected orogenital sex with his girlfriend about 2 weeks before the onset of the ulcers. Rapid plasma reagin testing was positive with a titer of at least 1:32. In addition, a Treponema pallidum particle agglutination assay was strongly positive, and a fluorescent treponemal antibody absorption test was positive for both IgG and IgM antibodies. The patient's girlfriend also had positive results on serologic analyses for syphilis, and both were treated successfully with intramuscular penicillin.

 

[BBC3]

DUDE!! That is so fuked up..!! You are saying that shit is syphilis, and NOT Herpes....!! Oh well. I guess thats a good thing cause syphillis like that is still cureable right? I've seen some nasty ass herpes on folks close to that. And KNOWN the other friends to have the balls to take a drag off a smoke after them. And really that did not have it also.. Further, these stupid bastard never even contaiged it....!

I've had something similar but more limited that rears occasionally. Perhaps thats why I am INSANE.... ??? LOL

Really and truthfully, it looks like he just bogarted the roach too hard... LOL

Syphilis

The ulcers have clean, smooth bases and slightly elevated, indurated borders. This type of painless ulcer is typical of a syphilitic chancre. The patient reported having had unprotected orogenital sex with his girlfriend about 2 weeks before the onset of the ulcers. Rapid plasma reagin testing was positive with a titer of at least 1:32. In addition, a Treponema pallidum particle agglutination assay was strongly positive, and a fluorescent treponemal antibody absorption test was positive for both IgG and IgM antibodies. The patient's girlfriend also had positive results on serologic analyses for syphilis, and both were treated successfully with intramuscular penicillin.

 

[Michael Scally MD]

Sveinsson O, Herrman L. Cortical venous thrombosis following exogenous androgen use for bodybuilding. BMJ Case Rep 2013. http://casereports.bmj.com/content/2013/bcr-2013-008638.abstract (Cortical venous thrombosis following exogenous androgen use for bodybuilding -- Sveinsson and Herrman 2013 -- BMJ Case Reports)

There are only a few reports of patients developing cerebral venous sinus thrombosis (CVST) after androgen therapy. We present a young man who developed cortical venous thrombosis after using androgens to increase muscle mass. He was hospitalised for parasthesia and dyspraxia in the left hand followed by a generalised tonic-clonic seizure. At admission, he was drowsy, not fully orientated, had sensory inattention, pronation drift and a positive extensor response, all on the left side. The patient had been using anabolic steroids (dainabol 20 mg/day) for the last month for bodybuilding. CT angiography showed a right cortical venous thrombosis. Anticoagulation therapy was started with intravenous heparin for 11 days and oral anticoagulation (warfarin) thereafter. A control CT angiography 4 months later showed resolution of the thrombosis. He recovered fully.

 

[Michael Scally MD]

Anabolic Steroid Drug-Induced Liver Injury
[For Full-Text Email

mscally@alum.mit.edu

(Include Title)]

We report the case of a 46-year-old man who presented to the emergency department with a 3-month history of painless jaundice and weight loss of 9 kg over 3 weeks. He had ceased his AAS use 5 months prior to presentation. He reported nausea, pruritus and anorexia.

He had ingested stanozolol (40 mg) and methandrostenolone (40 mg) daily for 2 months, and reported stopping usage 5 months prior to his initial symptoms. There was no other exposure to drugs associated with cholestatic liver injury. There was no history of significant alcohol intake, intravenous drug use or herbal medication intake, and his body mass index was 28.5. Examination revealed jaundice, icterus and a mildly tender right-upper quadrant. There was no encephalopathy, and he was haemodynamically stable.

Liver function tests showed a mixed cholestatic and hepatitic pattern, with alkaline phosphatase 295 U/L, gamma glutamyl transpeptidase 114 UL, alanine transaminase 125 U/L and bilirubin of 302 mmol/L (conjugated bilirubin of 127 mmol/L). There was no synthetic dysfunction. Viral and autoimmune serologies were unremarkable. Ultrasound of the liver and computed tomography of the abdomen were normal. A liver biopsy showed intrahepatic cholestasis and occasional necroinflammatory foci, consistent with a drug reaction and proliferation (indicative of stanozolol usage).

He was commenced on ursodeoxycholic acid treatment, and at week 7 post-discharge, he had complete resolution of his jaundice, and liver function tests and ursodeoxycholic acid was ceased.

Ding NS, De Cruz P, Lim L, Thompson A, Desmond P. Androgenic-anabolic steroid drug-induced liver injury. Intern Med J 2013;43(2):215-6. Androgenic-anabolic steroid drug-induced liver injury - Ding - 2013 - Internal Medicine Journal - Wiley Online Library

 

[Michael Scally MD]

Marcacuzco Quinto AA, Manrique Municio A, Loinaz Segurola C, Jimenez Romero LC. Spontaneous hepatic rupture associated with the use of anabolic steroids. Cir Esp. ScienceDirect.com - Cirugía Española - Rotura hepática espontánea secundaria al uso de esteroides anabolizantes

Placement of Bogota Bag [A Bogota Bag is a sterile plastic bag used for closure of an abdominal wound.]

 

[BBC3]

Id like to see the follow up on that one. I saw this show once where the guy got bit by his white cobra which then ate about a softball sized rutt out of his gut which was miraculously healed without so much as a scar in a few months. They had to be using platelet rich plasma therapy. I have a feeling this will be employed here and you wont even know it. Its amazing too as its like the stem cells for flesh and preprogrammed to grow back identical. So I speculate that platelet rich P is very effective with soft tissue. You have to wonder why it does not work with organs...??? Seems to get skin fat, and muscle going real well..?

Marcacuzco Quinto AA, Manrique Municio A, Loinaz Segurola C, Jimenez Romero LC. Spontaneous hepatic rupture associated with the use of anabolic steroids. Cir Esp. ScienceDirect.com - Cirugía Española - Rotura hepática espontánea secundaria al uso de esteroides anabolizantes

Placement of Bogota Bag [A Bogota Bag is a sterile plastic bag used for closure of an abdominal wound.]

 

[BBC3]

Cystic Acne and MENTAL Illness combined. Could not resist this one. Ever heard of acutane - REALLY. Talk about the Benefit outweighing the RISK. I think this woman must be looking for a reason to hide in a closet... COuld not resist..

[ame=http://www.youtube.com/watch?v=HhjXlYCLCMY]Embarrassing Bodies - Lady with chronic acne given advice - YouTube[/ame]

 

[idmd]

Cystic Acne and MENTAL Illness combined. Could not resist this one. Ever heard of acutane - REALLY. Talk about the Benefit outweighing the RISK. I think this woman must be looking for a reason to hide in a closet... COuld not resist..

Embarrassing Bodies - Lady with chronic acne given advice - YouTube

Call me crazy but I wouldn't go anywhere near that chick's cystic acne ass without gloves! Even then I'd be compelled to squeeze them!

 

[eryximachus]

Scary stuff. How I wish there was more tabulation of case studies and AAS use. There is just so much unknown, and so many people injecting themselves with this crap.

 

[BBC3]

I'm not sure if you could tell the cum shots on the arse from the zips poppin when they hit..

@ ERYX, This is not a thread devoted to steroids or hormones. Just Scally's brainchild for some interesting medical learning of general issues. I greatly enjoy it...! You should have some fun here...!

Call me crazy but I wouldn't go anywhere near that chick's cystic acne ass without gloves! Even then I'd be compelled to squeeze them!

 

[Michael Scally MD]

Hymel BM, Victor DW, Alvarez L, Shores NJ, Balart LA. Mastabol induced acute cholestasis: A case report. World J Hepatol 2013;5(3):133-6. Mastabol induced acute cholestasis: A case report

A 26-year-old male presented with three weeks of jaundice after the self-initiation of the injectable anabolic steroid, Mastabol [Dromastanolone Di-Propionate (17 beta-Hydroxy-2alpha-methyl-5alpha-androstan-3-one propionate)]. He reported dark urine, light stools, and pruritus. He denied abdominal pain, intravenous drug use, intranasal cocaine, blood transfusions, newly placed tattoos, or sexually transmitted diseases. He used alcohol sparingly. Physical exam revealed jaundice with deep scleral icterus. The liver was palpable 2 cm below the right costal margin with no ascites. The peak bilirubin was 23.6 mg/dL, alkaline phosphatase was 441 units/L, and aspartate aminotransferase/alanine aminotransferase were 70 units/L and 117 units/L respectively.

A working diagnosis of acute intrahepatic cholestasis was made. Liver biopsy revealed a centrilobular insult with neutrophilic infiltrates and Ito cell hyperplasia consistent with acute drug induced cholestasis. The patient's clinical symptoms resolved and his liver enzymes, bilirubin, and alkaline phosphatase normalized. Anabolic steroids with 17 alpha carbon substitutions have been associated with a bland variety of cholestatic injury with little hepatocellular injury. Cholestasis, under these circumstances, may be secondary to the binding of drugs to canalicular membrane transporters, accumulation of toxic bile acids from canalicular pump failure, or genetic defects in canalicular transport proteins. Mastabol is an injectable, 17 beta hydroxyl compound with no alpha alkyl groups at the 17 carbon position. As such, it has been reported to have little potential toxic effects on the liver. This is the first known reported case of Mastabol-induced cholestatic liver injury. It highlights the need for physicians to consider such widely available substances when faced with hepatic injury of unclear etiology.

 

[BBC3]

What a coincidence...! Mine looked similar after squirting some hot glue on it a few weeks back!!!. And might I say :banghead: :no: - Do not try that at home. IT AINT CANDLE WAX... LOL.. They say pizza sauce is like some kind of heat preserving monster that never cools beneath the surface - Well pizza sause AINT GOT NUTHIN on hot glue...

A Crusted Plaque On The Right Nipple

Chiu H TT. A crusted plaque on the right nipple. JAMA: The Journal of the American Medical Association 2012;308(4):403-4. JAMA Network | JAMA: The Journal of the American Medical Association | A Crusted Plaque on the Right Nipple

A healthy 27-year-old heterosexual man presents with a crusted plaque on his right nipple. The lesion formed gradually over a week after a bite during sexual intercourse and has persisted for a month. The patient reports that over the following 2 to 3 weeks, no significant change in size or morphology of this lesion occurred. The lesion is not painful; neither fever nor associated systemic symptoms are noted. Now, 1 month later, the patient presents with a generalized asymptomatic skin eruption. Physical examination reveals generalized pink macules on the trunk and extremities (Figure 1A). A crusted, erythematous plaque is noted over the enlarged right nipple (Figure 1B).

DIAGNOSIS - Chancre Of The Nipple With Secondary Syphilis

The key clinical feature is to recognize the association between the crusted nipple lesion and the subsequent development of a generalized macular rash after sexual contact. Physicians should include syphilis in the differential diagnosis, not just treat the lesion as a human bite, even though the nipple is not a common site for syphilitic chancre.

This patient received a rapid plasma reagin test and skin biopsy at his first visit to confirm the exact cause of the nipple lesion. The laboratory investigations showed a positive rapid plasma reagin result (titer, 1:64) and TPHA (titer, 1:2560). Enzyme-linked immunoassay test for human immunodeficiency virus was negative. Skin biopsy demonstrated epidermal hyperplasia with focal ulceration and a dense, superficial dermal infiltration. Under higher magnification, there was a lichenoid infiltrate composed of lymphoplasma and histiocytic cells around the dermoepidermal junction and perivascular areas. Immunohistochemistry demonstrated numerous spirochetes in the epidermis and dermis. Both the nipple lesion and the generalized pink macules gradually resolved after 2 weekly intramuscular injections of benzathine penicillin G, 2.4 million units.

 

[Michael Scally MD]

The Man With Uncrossed Eyes
https://blogs.discovermagazine.com/neuroskeptic/2013/04/14/the-man-with-uncrossed-eyes

“GB” is a 28 year old man with a curious condition: his optic nerves are in the wrong place. Most people have an optic chiasm, a crossroads where half of the signals from each eye cross over the midline, in such a way that each half of the brain gets information from one side of space. GB, however, was born with achiasma – the absence of this crossover. It’s an extremely rare disorder in humans, although it’s more common in some breeds of animals, such as Belgian sheepdogs.

Here’s GB and a normal brain for comparison: Structural T1-weighted MRI scan shows the optic chiasm in a control subject but not in GB

Davies-Thompson J, Scheel M, Jane Lanyon L, Sinclair Barton JJ. Functional organisation of visual pathways in a patient with no optic chiasm. Neuropsychologia. ScienceDirect.com - Neuropsychologia - Functional organisation of visual pathways in a patient with no optic chiasm

Congenital achiasma offers a rare opportunity to study reorganization and inter-hemispheric communication in the face of anomalous inputs to striate cortex. We report neuroimaging studies of a patient with seesaw nystagmus, achiasma, and full visual fields. The subject underwent structural magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) studies, and functional MRI (fMRI) using monocular stimulation with checkerboards, motion, objects and faces, as well as a retinotopic quadrantic mapping. Structural MRI confirmed the absence of an optic chiasm, which was corroborated by DTI tractography. Lack of a functioning decussation was confirmed by fMRI that showed activation of only ipsilateral medial occipital cortex by monocular stimulation. The corpus callosum was normal in size and anterior and posterior commissures were identifiable. In terms of the hierarchy of visual areas, V5 was the lowest level region in the hierarchy to be activated binocularly, as were regions in the fusiform gyri responding to faces and objects. The retinotopic organization of striate cortex was studied with quadrantic stimulation. This showed that, in support of recent findings, rather than projecting to an ectopic location contiguous with the normal retinotopic map of the ipsilateral temporal hemi-retina, the nasal hemi-retina's representation overlapped that of the temporal hemi-retina. These findings show that congenital achiasma can be an isolated midline crossing defect, that information transfer does not occur in early occipital cortex but at intermediate and higher levels of the visual hierarchy, and that the functional reorganisation of striate cortex in this condition is consistent with normal axon guidance by a chemoaffinity gradient.

 

[Michael Scally MD]

Auer M, Stalla GK, Athanasoulia AP. [Isolated gonadotropic deficiency after multiple concussions in a professional soccer player]. Dtsch Med Wochenschr 2013;138(16):831-3. https://www.thieme-connect.de/ejournals/abstract/10.1055/s-0033-1343099

History and clinical presentation: A 27-year-old man was admitted to our outpatient clinic with symptoms of loss at libido, erectile dysfunction and fatigue. He had been playing soccer from the age of 7, for the last 10 years as a high-level professional. During that time repeated mild head-trauma without loss of consciousness had occurred, mainly triggered by excessive header-training and occasional collisions.

Investigations: Serum levels of testosterone and luteinizing hormone were low. A gonadotropin releasing hormone loading test revealed significant gonadotropin responses, therefore pituitary gonadotropic insufficiency was unlikely. Further pituitary insufficiency of any other axis was also excluded by insulin hypoglycemia test. Magnetic resonance imaging of the brain revealed no significant abnormalities of the hypothalamic-pituitary unit.

Treatment and Course: Testosterone substitution, at first applied transdermally, then intramuscularly, was initiated after approval by the National Anti Doping Agency. Four months later most of the symptoms had regressed.

Conclusion: Pituitary deficiency in the course of craniocerebral trauma is frequent and may be transient or permanent, mostly affecting somatotropic or gonadotropic function. Hormonal imbalances may also be observed after mild but repeated trauma without loss of consciousness and should be considered in cases of isolated pituitary dysfunction, since such traumas may often occur in contacts sports such as boxing or intensive soccer play.

 

[Michael Scally MD]

Leydig Cell Tumor & Anabolic Steroids

Belli S, Guidi A, Simoni M, Carani C, Granata AR. Leydig cell tumor in an anabolic steroid abuser. J Endocrinol Invest. Leydig cell tumor in an anabolic steroid... [J Endocrinol Invest. 2013] - PubMed - NCBI

Leydig cell tumors (LCT) are 1-3% of all testicular neoplasms of the adult. They are malignant in 10% of cases and occur most frequently at the age of 30-60 years. LCT can secrete hormones, such as testosterone (T) and estrogens (E); infertility and signs of feminization can be the presenting features. The incidental diagnosis is rising due to detection of small nodules by ultrasounds (US).

Anabolic androgenic steroids (AAS) are popular doping agents. An etiologic link between AAS abuse and cancer, mainly hepatic, is proved. AAS at high doses are shown to enhance in vitro rat Leydig cells proliferation with increased risk of LCT development. Here we report a case of LCT and infertility in a man addicted to AAS.

A 30 year old man attended our Unit in June, 2010 with a 18 month history of infertility and azoospermia. No sexual dysfunction, testicular injury/infections, chronic disease and therapies were reported. He was a body builder and admitted AAS (nandrolone) use for the previous 3 years. General and genital examination were normal with testicles volume of about 15 ml on each side; A testicular US performed 3 years earlier was normal.

The patient was invited to stop with AAS. In September, 2010 azoospermia was confirmed and linked to undetectable LH and FSH serum levels with T (27.86 nmol/L) at the upper normal limits and Estradiol (E2) (181.48 pmol/L) slightly increased. TSH and PRL were normal but hematocrit (54%), hemoglobin (17.9 g/dl), GOT (38 U/L) and GPT (48 U/L) were increased. The patient was assumed to be still on AAS and was newly advised to stop doping. In October, 2011 LH-FSH suppression was confirmed with undetectable neoplastic markers.

Due to the patient's claim of no doping practice, a new scrotal-US was performed, which showed a 18 mm central heterogeneous area surrounded by normally echostructured tissue. In December, 2011 the patient underwent conservative surgery with nodule-only excision. A 2.5x1.7x1.5 cm tumor was removed and was histologically and immunohistochemically classified as benign LCT.

One year later follow-up for recurrence and metastases was negative and eugonadism (FSH: 2.7 mIU/ml, LH: 2.8 mIU/ml, T: 10.86 nmol/L, E2: 92.59 pmol/L) and normal sperm parameters (total sperm number: 192 x 106, sperm morphology: 3% normal, progressively motile sperm: 35%) occurred. Conception and pregnancy were reached 2 years after surgery.

Infertility associated with gonadotropin suppression can be caused by endogenous or exogenous androgens excess. In our patient the latter hypothesis was more probable due to anamnestic abuse of AAS. The pathogenetic role of an exogenous assumption of AAS was supported by normal testicles at both examination and the first scrotal-US.

The persistence of azoospermia, LH/FSH suppression, T at the upper limits and slight E2 excess, in spite of the reported AAS suspension, casted doubts on the initial diagnosis and leaded to a second scrotal US and to a conservative surgical therapy. The 3 year gap between the 2 testicular-US perfectly overlapped with the duration of AAS abuse, suggesting a cause-effect relationship between AAS and tumorigenesis.

Nandrolone and stanozolol, two of the main abused AAS, have been recently shown to induce proliferation of a rat Leydig tumor cell line, supporting the cause-effect hypothesis for AAS and LCT.

In conclusion, a direct link between AAS abuse and LCT is suggested for the first time in a man by this report. In clinical practice this report's data show the need for testicular-US test not only in the suspect of a pathological excessive androgen production, but also in case of actual or previous AAS abuse. The use of testicular-US in actual or previous AAS abusers will allow the definition of the epidemiological relevance of the association with LCT.

 

[BBC3]

And you KNOW I can't lay off this one...! Great Article for whatever the value...! And I am not attempting at this time to LEND credit or debunk it. The Concept is just a massive thinkpiece - which YOU KNOW I Love...

Noting first they reference Nandrolone and another, but not synthetic testosterone as a "steroid" as a principle point. It must be noted that that while we have little clinical evidence through past studies or medical experience (another victim of past demonization), we can denote that from the information that has been discerned throughout the years that Nandrolone is touted as "Highly suppressive" both initially as well as having a longer hang time/complication referencing "shut downs".. Some science, some anecdote, and some just experience by past users and treating physicians related.

POINTs:
- Is there possibly a "use it or loose it" phenomena occurring.?!? And don't just attempt to smear that ink off the page, because short of exogenous hormone use, testicular shut down is as rare as only the known medically validated reasons otherwise known - which are rare.

- From another standpoint - The use of HCG in PCT first comes to mind before any steroid when referencing cancers originating in leydig cells...! Does the study involve the CONTEXT of whether or not the "AAS User" ever involved HCG/Pregnyl in a PCT routine..?? And going back to "use it or loose it" for a moment - I wonder if it could some day be determined that true TRT patients on injectible testosterone might REQUIRE intermittent HCG application to prevent this possibility.?? Then again from what is presented in the basic primer provided in this thread, for all we know the guy pinned HCG like they were going to stop making it tomorrow.!! We don't know.. But I find it amusing that just like they left of the fact that he probably used HCG as PCT..

- Further the general laymanized reading of the article would present as the cancer occurring either due to GENERAL UNSPECIFIED AAS, the LACK OF LH Stimulation resulting, or even assuming there is no telling what a person this open minded to elicit experimentation may also USE..!!! Not to mention all the uncontrolled supplements manufactured by who knows that this person probably consumed over the years.

- With further regard to potentially unsafe manufacture of supplements and more importantly - ILLICIT STEROIDS, we don't know if this AAS user was even getting legitimate or uncontaminated product.. Which again is the reason for the legality and fine balance we find today with these black market products. I am not even attempting to argue that the fix for all potential steroid black market quality control issues is to legalize them and make them available on gas station shelve. However, it should provide some comfort in knowing that there are legitimate reasons that may validate leaving LEGITIMATE black market suppliers in business..! History has proven time and time again the the market will find and acquire what it wants, thus there will be SOMEONE to supply it. So the point being that one way to look at optimal UNWRITTEN black market control is to NOT make supply so scarce that crooks are putting foul agents in oils, and/or having to brew in dirty pots and haul their latest batch out the back door in the first dirty container they can find during the latest raid.. LOL BUT Also at the same time you don't want every Tom/Dick/Harry opening a store and selling ignorant "bastard/illegitimate" product.. So a middle is found and hopefully a healthy one - NOT EVEN PERTAINING to this case presented...

Again and IMPORTANTLY, you can denote the authors DID NOT Seem to mention or involve TESTOSTERONE in this primer/summary. They attempt to CONVICT Nandrolone (Deca Durabolin) and Stanozolol (Winstrol). And aint it funny how to COMMON primary base for steroid cycling is TESTOSTERONE... NOTE that while those two steroids alone MAY comprise a "Cutting/preservation" type cycle by themselves, and you really trying to tell me he does not do testosterone based cycles in the bulk season!?!? Do ya really think he left that one out?!?!? Hmmm.. Dare they not treat on the shoes of the currently politically PROTECTED.. Me wonders - of course...

Its clear they have chosen to USE a MORE RARE type of testicular cancer in a poor attempt to correlate "AAS" to "Nut Cancer". The truth is that your odds of getting testicular cancer will prove more dangerous just from living and breathing I suspect.

Here are some quotes I will choose to attempt to debunk:

Reviewed Quote #1 - Nandrolone and stanozolol, two of the main abused AAS, have been recently shown to induce proliferation of a rat Leydig tumor cell line, supporting the cause-effect hypothesis for AAS and LCT.

What they are POLITELY SAYING here, is that in rats which THE FIRST INDUCED leydig cell cancer, these two steroids caused cancer cell growth. How they even gave them the cancer in the first place who the hell knows.?! But DOUUOEiiYOUGH. Really, you wanna know what would have happened had they dosed the rats with SynT after FIRST giving them LCT type cancer.? I probably would have "proliferated the LCT Cells" waay faster than deca or winstrol possibly could have. This article is clearly an attack on more elicit steroids I suspect.

Reviewed Quote #2 = Due to the patient's claim of no doping practice, a new scrotal-US was performed, which showed a 18 mm central heterogeneous area surrounded by normally echostructured tissue. In December, 2011 the patient underwent conservative surgery with nodule-only excision. A 2.5x1.7x1.5 cm tumor was removed and was histologically and immunohistochemically classified as benign LCT.

What-the-fuk-ever.....! Me dont thinks they are going to "gut some leydigs" from a cancerous testicle. REALLY!?!?!? Testicular is the MOST PREVALENT form of cancer in younger men, but its also the most curable. The reason being is THEY CUT IF OFF ALL TOGETHER. There is not a practicing general surgeon or urologist, in their RIGHT MING, who would leave any of that testicle remaining. They lop it off and its that simple...! Consider the legal ramifications and PULL THE OTHER ONE... LOL So its a SETUP to say the least.

Reviewed Quote #3 - Infertility associated with gonadotropin suppression can be caused by endogenous or exogenous androgens excess. In our patient the latter hypothesis was more probable due to anamnestic abuse of AAS. The pathogenetic role of an exogenous assumption of AAS was supported by normal testicles at both examination and the first scrotal-US.

(Blue quotation #1) - FALSE - The patient is thirty years old which is the MIDDLE of the most prevalent time period for males to be sickened with testicular cancer. The peak occurring age range for testicular cancer in men is 19-35 ( or close to). So if you consider the odds of an AAS user contracting testicular JUST FOR THE SAKE OF BEING A 30 year old male, and without AAS use, you will find THIS; American Cancer Society | Information and Resources for Cancer: Breast, Colon, Lung, Prostate, Skin says that 8000 men (IN THE WORLD) will be dianosed with testicular cancer in 2013. 370 will die. OF THOSE 8000 - How many were doing steroids? Really..! Now you can bring Lance Armstrong into this if you want to go there, but I would wager to say that having his nutz bunched up in a "bikey tighty" and with a speedo underneath for good "constricting measure" would be a FAR GREATER cause for cellular malfunction, rather than any steroids which he may have done. TourDeBikes/ALL OF EM are notorious for juicing everything. How many of them have it. Oh, and I even forget about the fact that these constricted testes are getting beat up shitless while pedalling that bicycle for ziga-miles...!! I knew a guy once to get Testicular cancer at the age of 21 or something like that. There was no rhyme or reason other than college smoking and alcohol, WHICH IS A FAR MORE LIKELY CAUSE.....!

(Blue quotation #2) - FALSE - This proves only that they were looking at the time he cancer was found. Interestingly, it happened when they were looking?!?

IN DEFENCE of the article, WIKI says "Although testicular cancer can be derived from any cell type found in the testicles, more than 95% of testicular cancers are germ cell tumors. Most of the remaining 5% are sex cord-gonadal stromal tumours derived from Leydig cells or Sertoli cells."

REALLY it should finally be noted that while the article singles out Deca and Stanolozol toward the end. They only affirm "ASS" use for the patient and his testicular cancer thus leaving unknown. Only LATER attempting to TIE these two steroids in for their TRUMPED CASE.

I would interpret that this article IN NO WAY FURTHER Associates AAS use and this type cancer..

Leydig Cell Tumor & Anabolic Steroids

Belli S, Guidi A, Simoni M, Carani C, Granata AR. Leydig cell tumor in an anabolic steroid abuser. J Endocrinol Invest. Leydig cell tumor in an anabolic steroid... [J Endocrinol Invest. 2013] - PubMed - NCBI

Leydig cell tumors (LCT) are 1-3% of all testicular neoplasms of the adult. They are malignant in 10% of cases and occur most frequently at the age of 30-60 years. LCT can secrete hormones, such as testosterone (T) and estrogens (E); infertility and signs of feminization can be the presenting features. The incidental diagnosis is rising due to detection of small nodules by ultrasounds (US).

Anabolic androgenic steroids (AAS) are popular doping agents. An etiologic link between AAS abuse and cancer, mainly hepatic, is proved. AAS at high doses are shown to enhance in vitro rat Leydig cells proliferation with increased risk of LCT development. Here we report a case of LCT and infertility in a man addicted to AAS.

A 30 year old man attended our Unit in June, 2010 with a 18 month history of infertility and azoospermia. No sexual dysfunction, testicular injury/infections, chronic disease and therapies were reported. He was a body builder and admitted AAS (nandrolone) use for the previous 3 years. General and genital examination were normal with testicles volume of about 15 ml on each side; A testicular US performed 3 years earlier was normal.

The patient was invited to stop with AAS. In September, 2010 azoospermia was confirmed and linked to undetectable LH and FSH serum levels with T (27.86 nmol/L) at the upper normal limits and Estradiol (E2) (181.48 pmol/L) slightly increased. TSH and PRL were normal but hematocrit (54%), hemoglobin (17.9 g/dl), GOT (38 U/L) and GPT (48 U/L) were increased. The patient was assumed to be still on AAS and was newly advised to stop doping. In October, 2011 LH-FSH suppression was confirmed with undetectable neoplastic markers.

Due to the patient's claim of no doping practice, a new scrotal-US was performed, which showed a 18 mm central heterogeneous area surrounded by normally echostructured tissue. In December, 2011 the patient underwent conservative surgery with nodule-only excision. A 2.5x1.7x1.5 cm tumor was removed and was histologically and immunohistochemically classified as benign LCT.

One year later follow-up for recurrence and metastases was negative and eugonadism (FSH: 2.7 mIU/ml, LH: 2.8 mIU/ml, T: 10.86 nmol/L, E2: 92.59 pmol/L) and normal sperm parameters (total sperm number: 192 x 106, sperm morphology: 3% normal, progressively motile sperm: 35%) occurred. Conception and pregnancy were reached 2 years after surgery.

Infertility associated with gonadotropin suppression can be caused by endogenous or exogenous androgens excess. In our patient the latter hypothesis was more probable due to anamnestic abuse of AAS. The pathogenetic role of an exogenous assumption of AAS was supported by normal testicles at both examination and the first scrotal-US.

The persistence of azoospermia, LH/FSH suppression, T at the upper limits and slight E2 excess, in spite of the reported AAS suspension, casted doubts on the initial diagnosis and leaded to a second scrotal US and to a conservative surgical therapy. The 3 year gap between the 2 testicular-US perfectly overlapped with the duration of AAS abuse, suggesting a cause-effect relationship between AAS and tumorigenesis.

Nandrolone and stanozolol, two of the main abused AAS, have been recently shown to induce proliferation of a rat Leydig tumor cell line, supporting the cause-effect hypothesis for AAS and LCT.

In conclusion, a direct link between AAS abuse and LCT is suggested for the first time in a man by this report. In clinical practice this report's data show the need for testicular-US test not only in the suspect of a pathological excessive androgen production, but also in case of actual or previous AAS abuse. The use of testicular-US in actual or previous AAS abusers will allow the definition of the epidemiological relevance of the association with LCT.

 

[Michael Scally MD]

Examination Of The Nails
http://reference.medscape.com/features/slideshow/fingernail-abnormalities

Examination of the nails should include the softness and flexibility of the free edge, the shape and color of the nail, the quantity of paronychial tissue, and the growth rate. Aging slows the whole fingernail growth rate from about 3 months in children to about 6 months at age 70. Nails of the dominant hand usually grow faster than nails of the nondominant hand. The growth rate can also be slowed by immobility. Nails are usually thicker in the elderly than in younger people.

The lunula is most noticeable on the thumb. The eponychium (cuticle) may partially or completely cover the lunula. It may also be a normal finding. Absence of the lunula of other digits without the thumb is nonspecific.

Absence of the lunula may suggest performing a complete blood count for anemia or investigation for malnutrition. Abnormalities of the lunula are common and may lead clinicians down varied diagnostic paths. While a pale blue lunula suggests diabetes mellitus, a red discoloration of the lunula may signify cardiovascular disease, collagen vascular disease, hematologic malignancy, or other serious diagnosis.

 

[Michael Scally MD]

Bitot's Spot in Vitamin A Deficiency
MMS: Error

A 10-year-old boy with no notable medical history presented with ocular burning. A lesion consisting of a dry, scaly patch with a foamy appearance was observed on the temporal conjunctiva of the left eye (Panel A). Corrected visual acuity was 10/20 in the left eye; the remainder of the ocular examination was normal.

Bitot's spot is highly suggestive of vitamin A deficiency and, sometimes, chronic conjunctival inflammation. The condition is characterized by metaplasia of the conjunctival epithelium and tangles of keratin admixed with gas-forming bacteria (e.g., Corynebacterium xerosis), giving the lesion its typical foamy appearance.

The serum level of vitamin A in this patient was extremely low, at <2 ?g per deciliter (0.07 ?mol per liter; normal range, 30 to 70 ?g per deciliter [1 to 2 ?mol per liter]); he was given vitamin A supplementation. At follow-up approximately 12 months after diagnosis, slit-lamp examination revealed complete healing of the lesion (Panel -B), and symptoms were substantially improved.

Vitamin A deficiency affects approximately 140 million children worldwide, making it the second most prevalent nutritional disorder after caloric malnutrition; in developed countries, it can be associated with fat malabsorption.

 

[Michael Scally MD]

Bilateral Earlobe Creases

An 84-year-old man with hypertension, diabetes, and hypercholesterolemia presented to the emergency department with a 6-hour history of visual difficulty.

Physical examination revealed a right homonymous hemianopia and no other relevant neurologic findings. A diagonal crease in each earlobe (Frank's sign) was noted (Panel A).

Urgent computed tomography revealed a subacute occipital infarction in the territory of the left posterior cerebral artery (Panel B, asterisk), as well as many other old ischemic lesions.

Frank's sign was originally described as a marker of coronary artery disease, with a moderate sensitivity (approximately 48%) and specificity (approximately 88%). This sign has been subsequently associated with other cardiovascular risk factors.

The patient was treated conservatively, his course was uneventful, and he was discharged home 1 week after presentation, with persistence of the visual deficit.

Zapata-Wainberg G, Vivancos J. Bilateral Earlobe Creases. New England Journal of Medicine 2013;368(24):e32. MMS: Error

 

[Michael Scally MD]

An Autoerotic Death [NSFW]

Jung S-K. An autoerotic death in Korea. Medicine, Science and the Law 2013;53(1):48-50. An autoerotic death in Korea

Accidental autoerotic asphyxia occurring during autoerotic activity is usually considered the unanticipated failure of a sexual stimulation device to induce hypoxia during solitary sexual arousal. Here, we provide the first reported case of autoerotic death in Korea. In the present case, a young man died from asphyxiation as a result of being suspended with his head in a plastic bag. The death was considered accidental and not suicidal. The diagnosis of autoerotic death may be difficult when typical features are absent.