Clinical Case Studies

Discussion in 'Men's Health Forum' started by Michael Scally MD, Aug 17, 2011.

  1. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Scrotal Calcinosis
    Tal Grenader, M.D., and Linda Shavit, M.D.
    N Engl J Med 2011; 365:647 August 18, 2011

    Scrotal_Calcinosis.gif
    A 32-year-old man presented to the emergency department with dyspnea and hemoptysis. On physical examination, yellowish scrotal nodules were noted incidentally (Panel A). The man reported that they had been developing over the past 12 years. They were painless, progressively enlarging, and firm and were consistent with a clinical diagnosis of scrotal calcinosis. Contrast-enhanced computed tomographic (CT) imaging revealed multiple pulmonary emboli, and systemic anticoagulant therapy was administered. CT images of the pelvis incidentally revealed multiple calcified masses in the subcutaneous tissue of the scrotum, ranging from 3 mm to 8 mm in diameter (Panel B, arrow). This rare, benign condition of uncertain cause typically begins in adolescence or early adulthood and occurs in the absence of abnormalities in calcium and phosphate metabolism (serum levels of both were within the normal range). The intradermal nodules tend to increase in size and number over time and may break down to produce a white, chalky material. Aesthetic dissatisfaction is the major indication for surgical excision. This patient, with normal serum calcium and phosphorus levels, opted for treatment of the pulmonary emboli and simple observation of the scrotal calcinosis.

    Tal Grenader, M.D.
    Linda Shavit, M.D.
    Shaare Zedec Medical Center, Jerusalem, Israel
    talgrenader65@hotmail.com
     
    Last edited: Aug 29, 2011
  2. Structure

    Structure Member

    Re: Scrotal Calcinosis

    Just what I wanted to see during breakfast this morning...
     
  3. BBC3

    BBC3 Member

    Re: Scrotal Calcinosis

    I dont think he is going to have any hotties on those nutz for a while., Or for the LAST 12 years for that matter. Could you imagine? And all the time living with it due to embarrasment, shame, immaturity, ignorance, etc....
     
    Bill33 likes this.
  4. amar7

    amar7 Member

    Re: Scrotal Calcinosis

    I think the thumbnails are enough plus a viewer discretion to that pic for the visitors
     
  5. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    T Cell-Mediated Acute Localized Exanthematous Pustulosis Caused By finasteride

    Researchers report a case of a 21-year-old man who presented with multiple erythematous nonfollicular papules partially confluent to plaques on his breast and lower abdomen. Grouped pustules were present under the right breast. His medical history was negative for psoriasis. No dermatologic disease was known in his family history. Treatment with 1 mg/d finasteride (Propoecia; MSD Merck Sharp & Dohme-Chibret AG, Opfikon, Switzerland) by mouth was initiated for androgenetic alopecia 3 months before admission. The patient took no other medication.

    Finasteride-exanthematous-p.gif

    One month before admission, a pruritic rash had developed on his upper trunk and the left side of his neck. His dermatologist, after having performed a biopsy, started therapy with a mild topical steroid and a topical antibacterial agent under the presumption of superinfected eczema. Later, a class switch to a potent topical steroid was attempted without success.

    When the lesions worsened, the patient presented to the dermatology department. Their initial differential diagnosis included dyskeratosis follicularis Darier, allergic contact dermatitis, infectious folliculitis, varicella zoster virus infection, fixed drug eruption, and IgA pemphigus.

    The white blood cell count and differential were within the normal limits. There was no neutrophilia or eosinophilia. The results of viral culture and PCR, as well as bacterial and fungal cultures of skin lesions proved negative. A lesional biopsy specimen showed a slight psoriasiform acanthosis in association with spongiosis and infiltration of both the epidermis and dermis by neutrophils and eosinophils, resulting in formation of subcorneal, intraepidermal, and subepidermal pustules. The results of direct immunofluorescence were negative, excluding IgA pemphigus.

    On the basis of history and clinical and histologic features, the diagnosis of acute localized exanthematous pustulosis (ALEP) was made. Within 4 weeks after withdrawal of finasteride, the rash resolved without any specific therapy. Transient, discrete residual hyperpigmentation and scaling were present. The patient refused an oral provocation challenge. A lymphocyte transformation test performed after resolution was positive for finasteride with a stimulation index of more than 36.9 compared with the negative control (positive if stimulation index > 2.5). A dose response was present, with increasing lymphocyte activation from 0.01 to 1 mg of finasteride. At concentrations of 10 mg of finasteride or greater, the lymphocyte activation decreased, as often observed in the lymphocyte proliferation assay, because of a toxic effect.


    Acute generalized exanthematous pustulosis (AGEP) is a severe, usually drug-related skin eruption characterized by acute formation of sterile pustules on an erythematous background with associated fever and neutrophilia. Skin symptoms arise quickly within a few hours and resolve rapidly within a few days without treatment. The rash is commonly accentuated in the large folds. Mucous membrane involvement is rare, usually mild, and generally restricted to 1 site, mostly an oral site. Histology shows subcorneal pustules, intradermal pustules, or both; a sometimes pronounced edema in the papillary dermis; and perivascular

    Finasteride is a competitive inhibitor of type II 5-a-reductase, the isotype more common in hair follicles. The enzyme specifically converts testosterone to dihydrotestosterone, a key mediator of androgenetic alopecia and benign prostatic hyperplasia. Finasteride is usually well tolerated; there are only a few reports of adverse skin reactions caused by finasteride in the literature: cutaneous vasculitis, drug-related folliculitis, erythema annulare centrifugum, solitary fixed drug eruption, and urticarial rash.

    In this case, on the basis of the time relationship between the administration of finasteride and the development of the skin disease in combination with resolution when this treatment was interrupted, the histologic findings, and the positive lymphocyte transformation test result, providers consider this to be an unusual type of AGEP defined as ALEP caused by finasteride. Atypical for the case is the 2-month delay between the initiation of finasteride and the initiation of the rash.

    Finasteride-resolved.gif

    Tresch S, Cozzio A, Kamarashev J, et al. T cell-mediated acute localized exanthematous pustulosis caused by finasteride. J Allergy Clin Immunol.
    Elsevier

    A 21-year-old man presented with multiple erythematous nonfollicular papules partially confluent to plaques on his breast and lower abdomen that had been present for 1 month. Grouped pustules were present under the right breast. The patient had been taking finasteride over the past 3 months for androgenetic alopecia. His medical history was negative for psoriasis. Our initial differential diagnosis included dyskeratosis follicularis Darier, allergic contact dermatitis, infectious folliculitis, varicella zoster virus infection, fixed drug eruption, and IgA pemphigus. The white blood cell count and differential were within the normal limits. Results of viral cultures and PCR, as well as bacterial and fungal cultures of skin lesions proved negative. A lesional biopsy specimen showed a slight psoriasiform acanthosis in association with spongiosis and infiltration of both the epidermis and dermis by neutrophils and eosinophils, resulting in formation of subcorneal, intraepidermal, and subepidermal pustules. The results of direct immunofluorescence were negative, excluding an IgA pemphigus. The result of a lymphocyte transformation test was positive for finasteride. On the basis of the time relationship between the administration of finasteride and the development of the skin disease in combination with symptoms resolution on cessation of the drug, the histologic findings, and the positive lymphocyte transformation test result, we consider this to be an unusual type of acute generalized exanthematous pustulosis defined as acute localized exanthematous pustulosis caused by finasteride. Within 4 weeks after withdrawal of finasteride, the rash resolved without any specific therapy. Transient discrete residual hyperpigmentation and scaling were present. The patient refused an oral provocation challenge.
     
  6. BBC3

    BBC3 Member

    Gee! Now there's the human body just screaming out what an AWSOME Drug Finastaride is. Cant wait to git MESumOd'at.......

    What the hell was he taking it for anyway.. I have more hair on MY ASSHOLE than he has on his Entire chest...

     
    drrvca likes this.
  7. dsmith

    dsmith Junior Member

    Valuable topic specially for medical students, thanks doc ;)
     
  8. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Clinical Case Study

    Mediastinal Germ Cell Tumor

    This competition weightlifter was referred to an endocrinologist after a positive ß-human chorionic gonadotropin (hcg) result on routine urine screening (B sample). He was asymptomatic and denied illicit drug use. Blood tests confirmed an increase in ß-HCG levels, with decreased leutenizing hormone and follicle-stimulating hormone levels and also increased testosterone levels (Table 1 - JTCS -- Newcomb et al. 132 (3): 722 Table BL1 ). Examination, including testicular assessment with ultrasonography, was unremarkable, and an extragonadal germ cell tumor was suspected. Computed tomographic scanning of the chest, abdomen, and pelvis was performed and showed a 33-mm anterior mediastinal mass (Figure 1, A - JTCS -- Newcomb et al. 132 (3): 722 Figure IG1 ). This showed fluoro-deoxy glucose avidity on positron emission tomography (Figure 1, B - JTCS -- Newcomb et al. 132 (3): 722 Figure IG1 ). There were no extrathoracic foci.

    This patient underwent video-assisted thoracoscopic excision of the lesion. This was performed through 3 port incisions in the right inframammary region. The lesion was a dense nodular mass of 50 x 35 x 20 mm with no local invasion. The histopathology was consistent with seminoma. He recovered from the operation and was referred for adjuvant treatment that he declined because of potential side effects. The markers decreased rapidly after the lesion was removed and have remained normal (Table 1). There is no evidence of recurrence on follow-up imaging, and he has returned to competition.

    Discussion

    Germ cell tumors are a common malignancy in young men. Less than 5% are extragonadal. Seminomas are an uncommon finding in the mediastinum, although when present, they are mostly anterior. They comprise more than one third of mediastinal germ cell tumors. Seminomas can be asymptomatic or associated with suspicious respiratory symptoms, depending on tumor size. They are most common in the third decade but can present earlier or later. This tumor can metastasize, as do testicular seminomas, although this occurs late, and the tumors grow slowly. Because of their slow growth rate, most of these are large when diagnosed, with a median size of 5 cm. Seventy-five percent of patients with these tumors have no evidence of disease recurrence at 10 years. Factors associated with a poor outcome were local invasion or age greater than 37 years. There was no tissue diagnosis for this young man, and therefore surgical intervention was performed first for histology and staging and to initiate treatment for this tumor.

    The screening for banned substances in elite athletes is an accepted routine and is mostly restricted to urine testing. Urine samples are easier to obtain, and drug and metabolite levels are much higher in urine than in blood. Urine collection commences with the chaperoned provision by the athlete. This sample is then divided into 2 bottles labeled A and B. All testing is carried out on the A sample by means of gas chromatography. A positive result requires the analysis of the second (B) sample, and if this result concurs with the first, then a potential doping offense is investigated. This patient had a high level of ß-HCG on his B sample and was referred for further investigation.

    HCG is a glycoprotein hormone produced in large quantities by germ cell tumors of different origins. Forty percent of extragonadal seminomas produce increased levels of ß-HCG. Exogenous HCG can be used to stimulate testosterone production, but the rapid decrease in ß-HCG levels after tumor removal indicates that his increase was endogenous (Table 1). Had this not been the case, he would have been banned from weightlifting, and had the lesion been a nonseminoma, with its worse prognosis, then he would have required adjuvant chemotherapy and interruption of his training.

    In summary, this young weightlifter had his asymptomatic mediastinal seminoma uncovered after urine screening revealed high levels of ß-HCG. This highlights an important differential diagnosis to consider in a young male athlete.


    Newcomb AE, Clarke CP, Chiang CY, Jerums G. Urine drug testing in an athlete leads to the diagnosis of unsuspected mediastinal germ cell tumor. J Thorac Cardiovasc Surg 2006;132(3):722-3. Urine drug testing in an athlete leads to the diagnosis of unsuspected mediastinal germ cell tumor -- Newcomb et al. 132 (3): 722 -- The Journal of Thoracic and Cardiovascular Surgery
     
  9. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Blindness after Fat Injections
    MMS: Error

    A 32-year-old man presented with vision loss in the left eye. One week earlier, while under local anesthesia, he had had an autologous fat injection into his forehead for correction of glabellar frown lines. The patient reported that while he was receiving the injection, he felt a sudden, severe periocular pain and had complete vision loss in his left eye. On physical examination, the patient's level of consciousness was normal, without aphasia. Neurologic examination was normal except that he had no light perception in the left eye. The left pupil was dilated. In the left eye, no direct pupillary light reflex was observed and the indirect pupillary light reflex was slow. Retinal examination of the affected eye showed an edematous optic disk and widespread retinal whitening, with interruption of several arterioles (Panel A). Follow-up photography and fluorescein angiography confirmed multiple retinal hemorrhages, occlusions of several retinal arterioles with visible fat emboli (Panel B, arrows), and complete lack of perfusion of the tissue bed in hypofluorescent areas (Panel C). No abnormality was seen on magnetic resonance angiography of the brain. At the 2-month follow-up visit, the patient's vision had not improved.

    Blindness-After-Fat-Injecti.gif
     
  10. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Disappearance of a Breast Prosthesis during Pilates

    A 59-year-old woman with a history of breast cancer who underwent bilateral mastectomy and placement of breast prostheses presented for evaluation, reporting that her “body swallowed one of the implants” during a Pilates stretching exercise. The patient reported no chest pain or dyspnea. She had recently undergone a minimally invasive surgical mitral-valve repair for the treatment of severe mitral regurgitation; the point of entry for the surgery was the preexisting scar from the right mastectomy. During a Valsalva maneuver, a circumscribed area of the patient's right anterior chest ballooned outward (Panel A). Bedside ultrasonography revealed lung herniation through a disrupted intercostal space. Posteroanterior and lateral chest radiographs showed elevation of the right hemidiaphragm (Panel B, asterisks). Computed tomography confirmed the intrathoracic position of the prosthesis within the pleural space (Panel C, arrows). The patient was taken to the operating room, where the intact prosthesis was extracted and repositioned. The unstable intercostal space, created during valvular surgery and through which the prosthesis had migrated, was repaired with mesh.

    Breast-Prosthesis.gif

    Fong TC, Hoffmann B. Disappearance of a Breast Prosthesis during Pilates. New England Journal of Medicine 2011;365(24):2305. MMS: Error
     
  11. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    A Mutation in the Thyroid Hormone Receptor Alpha Gene

    Thyroid hormones have diverse actions, which include regulation of skeletal growth, maturation of the central nervous system, cardiac and gastrointestinal function, and energy homeostasis. In addition, thyroid hormones control their own production by feedback inhibition of hypothalamic thyrotropin-releasing hormone and pituitary thyroid-stimulating hormone, which direct their synthesis or release. These physiological effects are principally mediated by hormone action through nuclear receptor proteins that act as ligand-inducible transcription factors and either positively or negatively regulate the expression of target genes in different tissues in a hormone-dependent manner.

    The receptors are encoded by two genes (THRA and THRB), each of which undergoes alternate splicing to generate receptor subtypes (TR?1, TR?1, and TR?2), with differing tissue distributions. TR?1 is the predominant subtype in bone, the gastrointestinal tract, cardiac and skeletal muscle, and the central nervous system; TR?1 is most abundant in the liver and kidney; and TR?2 is more discretely expressed in the hypothalamus, pituitary, cochlea, and retina. In the absence of hormone, thyroid receptors that are not bound to ligands repress or silence target-gene transcription by recruiting multiprotein complexes containing corepressors (e.g., nuclear receptor corepressor and silencing mediator of retinoic acid and thyroid hormone receptor), with histone deacetylase activity; triiodothyronine occupancy of the receptor results in dissociation of the corepressor complex and recruitment of coactivator proteins, such as steroid receptor coactivator 1 (SRC-1), which mediate hormone-dependent transcriptional regulation.

    Here, researchers describe a child with characteristic clinical features of hypothyroidism (growth retardation, developmental retardation, and chronic constipation) and near-normal circulating thyroid hormone levels. She is heterozygous for a de novo THRA mutation, generating a mutant protein that inhibits wild-type receptor function in a dominant negative manner, causing some target tissues to be resistant to the action of thyroid hormone.

    Their patient had many clinical features that are typical of hypothyroidism but that paradoxically were associated with borderline low thyroxine levels and high triiodothyronine levels. Patent cranial sutures with wormian bones, delayed dentition, femoral epiphyseal dysgenesis, and retarded bone age are classic abnormalities in childhood myxedema, and diminished colonic motility with megacolon or even ileus is recognized in hypothyroidism. In addition, the child's cognitive deficits were consistent with those seen in congenital hypothyroidism. Furthermore, her treatment with thyroxine was associated with responsiveness in some measurements (thyroid-stimulating hormone and basal metabolic rate) but with negligible change in growth, intestinal motility, or heart rate. Thus, the patient had differential sensitivity to thyroid hormone action, with retention of hormone responsiveness in the hypothalamic–pituitary axis and liver but skeletal, gastrointestinal, and myocardial resistance.


    Bochukova E, Schoenmakers N, Agostini M, et al. A Mutation in the Thyroid Hormone Receptor Alpha Gene. New England Journal of Medicine. MMS: Error

    Thyroid hormones exert their effects through alpha (TR?1) and beta (TR?1 and TR?2) receptors. Here we describe a child with classic features of hypothyroidism (growth retardation, developmental retardation, skeletal dysplasia, and severe constipation) but only borderline-abnormal thyroid hormone levels. Using whole-exome sequencing, we identified a de novo heterozygous nonsense mutation in a gene encoding thyroid hormone receptor alpha (THRA) and generating a mutant protein that inhibits wild-type receptor action in a dominant negative manner. Our observations are consistent with defective human TR?-mediated thyroid hormone resistance and substantiate the concept of hormone action through distinct receptor subtypes in different target tissues.
     
  12. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Hypokalemic Paralysis In A Bodybuilder

    Mr BB reported that he had always lived healthy, neither smoked nor drank alcohol, and regularly engaged in sports. Until the age of 17 years, he had played in his country's national volleyball team but had to retire after being diagnosed with spina bifida occulta. Consequently, Mr BB started with bodybuilding at the age of 18 years. For the last 2 years, he has been a professional bodybuilder and participated in several national and international competitions. The last competition took place the day before admission.

    Mr BB's preparation for competitions includes a strict diet as well as the misuse of different pharmacologic substances, in particular, anabolic steroids, human growth hormone, thyroid hormones, and fast-acting insulin. Besides the intended anabolic effects, Mr BB had never experienced any adverse effects, except for 1 episode of hypoglycemia. For the first time in his career, our patient took 2 × 80 mg of furosemide orally 24 and 48 hours before the competition, respectively, for better muscle definition. He noticed a pronounced diuretic effect and lost 5 to 6 kg of bodyweight due to nocturia but otherwise felt fit to compete the next morning.

    The day after the competition, our patient felt unusually tired and took a nap in the early evening. When he woke up, he felt palpitations and could barely move his extremities. He managed to get out of bed but fell to the ground. A neighbor called the ambulance, and Mr BB was taken to our department.

    At initial presentation, Mr BB was in moderate distress. Clinical examination yielded a 2.0-m tall and 115-kg heavy man with no major abnormalities except for pronounced generalized muscle hypertrophy and impaired ability to move. Vital parameters at presentation were as follows: Blood pressure (BP), 136/65 mm Hg; heart rate (HR), 114 beats per minute; body temperature, 36.9ºC; and 95% peripheral oxygen saturation on room air. Urine drug screening was negative.

    Initial venous blood gas analysis (ABL800 Flex; Radiometer Medical, Brønshøj, Denmark) yielded severe hypokalemia (1.6 mmol/L; reference range [RR], 3.4-4.5 mmol/L), hyperglycemia (521 mg/dL; RR, 70-120 mg/dL), and hyperlactatemia (2.7 mmol/L; RR, 0.0-1.8 mmol/L). Complete blood work additionally revealed low phosphate levels (b0.32 mmol/L; RR, 0.81-1.45 mmol/L) and elevated liver function parameters (aspartate aminotransferase, 61 U/L; RR, b35 U/L; alanine aminotransferase, 134 U/L; RR, b45 U/L) as well as elevated lactate dehydrogenase (397 U/L; RR, b248 U/L) and elevated creatine kinase (1006 U/L; RR, b190 U/L) with a slightly elevated muscle brain fraction (26.2 U/L; RR, b24 U/L) and a slightly elevated troponin T value (0.047 ng/mL; RR, 0-0.03 ng/mL).

    The initial electrocardiogram (ECG) showed artifacts due to shivering, sinus tachycardia (HR, 115 per minute), normal axis, normal PQ time, and pronounced U waves associated with severe hypokalemia (Fig. 2). After treatment with 500-mL Elozell spezial solution (containing 48-mmol potassium, 12-mmol magnesium, 32-mmol chloride, 40-mmol aspartate) and 1000-mL KADC solution (containing 25-mmol potassium, 10-mmol phosphate, 1.0-mmol calcium, 65-mmol chloride) over the next 7 hours, our patient's symptoms gradually improved; the potassium level (3.9 mmol/L), blood glucose level, and the ECG normalized (Fig. 3). Mr BB was discharged the next morning.

    Severe hypokalemia is a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness, even to the point of paralysis. On rare occasions, diaphragmatic paralysis from hypokalemia can lead to respiratory arrest. There may also be decreased motility of smooth muscle, manifesting with ileus or urinary retention. Rarely, severe hypokalemia may result in rhabdomyolysis. Other manifestations of severe hypokalemia include alteration of cardiac tissue excitability and conduction. Hypokalemia can produce ECG changes such as U waves, T-wave flattening, and arrhythmias, especially if the patient is taking digoxin.

    Common causes of hypokalemia include extrarenal potassium losses (vomiting, diarrhea) and renal potassium losses (eg, hyperaldosteronism, renal tubular acidosis, severe hyperglycemia, potassium-depleting diuretics) as well as hypokalemia due to potassium shifts (eg, insulin administration, catecholamine excess, familial periodic hypokalemic paralysis, thyrotoxic hypokalemic paralysis). Although the extent of diuretic misuse in professional bodybuilding is unknown, it may be regarded as substantial. Hence, diuretics must always be considered as a cause of hypokalemic paralysis in bodybuilders.

    The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement. Intravenous administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of b2.5 mEq/L). Gradual correction of hypokalemia is preferable to rapid correction unless the patient is clinically unstable. Administration of potassium may be empirical in emergent conditions. When indicated, the maximum amount of intravenous potassium replacement should be 10 to 20 mEq/h with continuous ECG monitoring during infusion.


    Mayr FB, Domanovits H, Laggner AN. Hypokalemic paralysis in a professional bodybuilder. The American Journal of Emergency Medicine. ScienceDirect - The American Journal of Emergency Medicine : Hypokalemic paralysis in a professional bodybuilder

    Severe hypokalemia is a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness, even to the point of paralysis. On rare occasions, diaphragmatic paralysis from hypokalemia can lead to respiratory arrest. There may also be decreased motility of smooth muscle, manifesting with ileus or urinary retention. Rarely, severe hypokalemia may result in rhabdomyolysis. Other manifestations of severe hypokalemia include alteration of cardiac tissue excitability and conduction. Hypokalemia can produce electrocardiographic changes such as U waves, T-wave flattening, and arrhythmias, especially if the patient is taking digoxin.

    Common causes of hypokalemia include extrarenal potassium losses (vomiting and diarrhea) and renal potassium losses (eg, hyperaldosteronism, renal tubular acidosis, severe hyperglycemia, potassium-depleting diuretics) as well as hypokalemia due to potassium shifts (eg, insulin administration, catecholamine excess, familial periodic hypokalemic paralysis, thyrotoxic hypokalemic paralysis). Although the extent of diuretic misuse in professional bodybuilding is unknown, it may be regarded as substantial. Hence, diuretics must always be considered as a cause of hypokalemic paralysis in bodybuilders. We report on a 26-year-old man, Mr BB, who was admitted to the Vienna General Hospital emergency department because of severe generalized muscle cramps, paralysis, and palpitations.
     
  13. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Pneumopericardium Associated with a Peptic Ulcer
    MMS: Error

    Pneumocardium.gif

    A 63-year-old man with a history of peptic ulcer and recent use of nonsteroidal antiinflammatory medications presented to the emergency room with an acute onset of shortness of breath and chest pain. He had hypotension and tachycardia with an oxygen saturation of 92% while he was breathing 2 liters of oxygen per minute through a nasal cannula. Chest radiography showed air in the pericardium (Panel A, arrow). Computed tomography of the chest confirmed the presence of a large pneumopericardium (Panel B, arrow) but no pneumothorax or pneumoperitoneum. Emergency pericardiocentesis was performed, and a large amount of air was aspirated. The patient's vital signs immediately stabilized. Repeat chest radiography showed improvement of the pneumopericardium (Panel C). Further workup revealed that the patient had a penetrating peptic ulcer, with fistula formation from the fundal aspect of the stomach through the diaphragm and into the pericardial space. The fistula was ultimately repaired surgically.
     
  14. jonkobeck

    jonkobeck Member

    How the hell could someone let something like that go for 12 years? I would have had surgery or something as soon as they began to grow
     
  15. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Intramuscular Anabolic Steroid Injection Leading To Life-Threatening Clostridial Myonecrosis

    AAS Clostridial Infection.jpg

    CT scout film and axial images demonstrate diffuse air within the right vastus lateralis muscle and in the fascial planes from the pelvis to the knee.


    Driscoll MD, Arora A, Brennan ML. Intramuscular anabolic steroid injection leading to life-threatening clostridial myonecrosis: a case report. J Bone Joint Surg Am 2011;93(16):e921-3. Intramuscular anabolic steroid injectio... [J Bone Joint Surg Am. 2011] - PubMed - NCBI
     
  16. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Inactivating KISS1 Mutation And Hypogonadotropic Hypogonadism

    It is still unknown how puberty in humans, occurring during the early years of the second decade of life, is initiated. The hallmark of puberty is increased secretion of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which act in concert to stimulate the gonads to drive sex-hormone secretion and gametogenesis. The production of gonadotropins from pituitary gonadotropic cells is controlled by the pulsatile delivery of GnRH. Inactivating mutations in the genes encoding GNRH1 or the GNRH receptor (GNRHR) give rise to normosmic idiopathic hypogonadotropic hypogonadism in humans. However, GnRH neurons lack sex-steroid receptors. This suggests the existence of GnRH-regulating neurons, which would mediate this effect.

    A major breakthrough in identifying such candidate neurons was the finding that inactivating mutations in genes encoding the human kisspeptin receptor (KISS1R, formerly called GPR54), the cognate receptor for a hypothalamic peptide, kisspeptin, resulted in pubertal failure. More recently, mutations in TAC3 or TACR3 (encoding neurokinin B and its receptor, respectively) were shown to result in the same phenotype. Kisspeptin and neurokinin B are coexpressed, along with dynorphin, in sex-hormone–responsive neurons in the arcuate nucleus (infundibular nucleus in primates), and their coordinated activity appears to regulate GnRH secretion. Gene defects associated with normosmic idiopathic hypogonadotropic hypogonadism have been described in all the neuropeptides and receptors identified as stimulators of GnRH except for the kisspeptin gene (KISS1).

    Although Kiss1- and Kiss1r-knockout mouse models largely produce phenocopies (i.e., affected noncarriers) of human normosmic idiopathic hypogonadotropic hypogonadism resulting from inactivating mutations of KISS1R, there is evidence of remarkable residual activity of the hypothalamic–pituitary–gonadal axis. Moreover, a recent report challenged the requirement of kisspeptin signaling for pubertal maturation and fertility in female mice.

    This large consanguineous family has four members with complete normosmic idiopathic hypogonadotropic hypogonadism, all of whom were found to have a KISS1 mutation. All affected family members were homozygous for the mutation, whereas their unaffected parents were heterozygous, and their unaffected siblings were either heterozygous or wild-type homozygous. The disorder was thus transmitted as an autosomal recessive trait, which indicates that one copy of KISS1 is sufficient for normal function of the gonadotropic axis, thus ruling out haploinsufficiency. Given the rarity of oligogenic inheritance in normosmic idiopathic hypogonadotropic hypogonadism, they ensured that the KISS1 mutation is the sole variant to account for the normosmic idiopathic hypogonadotropic hypogonadism phenotype in the patients. This was accomplished by combining a variety of methods, including candidate-gene screening, autozygosity mapping, and whole-exome sequencing. The findings indicate that kisspeptin is required for the initiation of puberty in humans.


    Topaloglu AK, Tello JA, Kotan LD, et al. Inactivating KISS1 mutation and hypogonadotropic hypogonadism. N Engl J Med 2012;366(7):629-35. MMS: Error

    Gonadotropin-releasing hormone (GnRH) is the central regulator of gonadotropins, which stimulate gonadal function. Hypothalamic neurons that produce kisspeptin and neurokinin B stimulate GnRH release. Inactivating mutations in the genes encoding the human kisspeptin receptor (KISS1R, formerly called GPR54), neurokinin B (TAC3), and the neurokinin B receptor (TACR3) result in pubertal failure. However, human kisspeptin loss-of-function mutations have not been described, and contradictory findings have been reported in Kiss1-knockout mice. We describe an inactivating mutation in KISS1 in a large consanguineous family that results in failure of pubertal progression, indicating that functional kisspeptin is important for puberty and reproduction in humans. (Funded by the Scientific and Technological Research Council of Turkey [TUBITAK] and others.).
     
  17. BBC3

    BBC3 Member

    So I am thinking odds were slim I would never have those Nutz in my face again...:eek:[:eek:)]

    I get lost in this thread, but I have to wonder why that looks like a nail pinned though his left knee...?

     
  18. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    The Transplanted Hairline

    Hairlines created by modern hair transplant techniques use single hair follicles derived from the safe donor area (SDA). It is aptly noted that "a normal hairline is not a line at all, but rather a zone in which hairs become finer and more sparse as they gradually give way to the hairless forehead skin. This diminution in diameter and density is most prominent in younger patients, along temporal hairlines, and in female patients." In a transplanted hairline, which aims to mimic mild recession (Norwood class 2 or Norwood class 3), this observation becomes even more true. A receded hairline by nature assumes some miniaturization of the vanguard hair population.

    The creation of a natural-looking hairline thus must include in the planning stages a deliberate attempt to add finer caliber hair in the very front of the hairline. Conventional hair transplantation, however, uses hair from the SDA that contains the thickest caliber hair in the entire scalp. In patients with especially thicker caliber hairs (eg, Asians) and in patients with darker hair color and a contrasting lighter skin color, the production of a natural, soft-looking hairline has remained a major challenge. The recognition of this problem has led to the grafting of bisected hair follicles into the hairline on the premise of thinner caliber hair growth. In the study using bisected hair follicles, wider application was limited by the poor yield (< 50%).

    The advent of follicular unit extraction (FUE), which allows for in vivo extraction of single follicles without creating cosmetically significant scarring, has resulted in good results obtained in the frontal hairline. In addition, the technique increases the prospect of using single nonhead hair donor sources in transplantation. The FUE technique harvests hair follicle grafts through the use of punch devices to incise a circular path around individual follicular units from the epidermis into the dermis. However, the wider variation in the caliber of hair in the different body areas (finer leg hair to coarser beard hair) has created the possibility of a new approach to softer hairlines in the field of hair transplantation, particularly when head donor hair is not an option. For example, leg hair in most individuals possesses a finer caliber compared with most scalp hair populations.

    These case reports demonstrate the successful transplantation of leg hairs to the hairline in 2 men who had undergone prior FUSS-FUT surgical procedures but who were dissatisfied with the unaesthetic results. In both instances, the source of dissatisfaction was in part from the use of thick caliber hair from the SDA of the head, which imparted a harsh hairline appearance. The primary advantage of using leg hair to rework hairlines is that it is relatively finer and thus can be used to fill in the vanguard regions of the hairline to create a much softer and more natural look.

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    A, Prior to surgery to refine the hairline.
    B, Four years after transplantation of leg hair, there is softening of the hairline.


    Umar S. The Transplanted Hairline: Leg Room for Improvement. Arch Dermatol 2012;148(2):239-42. Arch Dermatol -- Abstract: The Transplanted Hairline: Leg Room for Improvement, February 2012, Umar 148 (2): 239

    Background The large caliber of head hair in hair transplantation imparts a coarse hairline, whereas natural hairlines are typically softer. In hirsute individuals, transplantation of leg hair to the hairline may result in a superior aesthetic appearance.

    Observation A total of 1025 leg hair follicles in 1 patient were grafted to an area 0.5 to 1.0 cm in front of and 0.5 to 1.0 cm internal to the vanguard hair of the original hairline and temporal recesses; the other patient received approximately 1000 leg hairs and 600 head hairs to advance and soften his hairline and to create a custom widow's peak. Transplantation resulted in a fully grown and soft-looking hairline after 9 months in the first patient, with growth of 75% to 80% of the transplanted leg hair. The mean length of the transplanted leg hair was longer than the length of the original leg hair, with less curliness but similar hair width. Transplanted leg hair width was significantly finer compared with existing head hair width. After 4 years, results were sustained, minimizing concerns that subsequent hair loss might result from leg hair cycle variations. In the second patient, similar results were observed at 3 years.

    Conclusion The use of leg hair in transplantation provides additional options in patients with hairlines that need to be refined.
     
  19. Michael Scally MD

    Michael Scally MD Doctor of Medicine

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    A 62-year-old man was referred to the hepatology clinic for evaluation of elevated levels of aspartate and alanine aminotransferase (385 U per liter and 356 U per liter, respectively), which were detected on routine laboratory examination. The patient reported no symptoms except for a reddish lesion on his forehead. He had been previously told that the lesion was fungal in origin (tinea corporis), and a course of local antifungal treatment had been administered, with no improvement. On physical examination the lesion on his face was determined to be a neovascular formation, with an arteriole in the central region that radiated out in numerous small vessels that resembled the legs of a spider. The lesion was about 3 cm in diameter. Compression of the central arteriole caused the entire lesion to blanch, and it quickly refilled once the compression was released (video). This pattern of blanching and refilling characterizes spider angiomas, which are suggestive of liver disease. Laboratory testing revealed infection with hepatitis C virus, genotype 1A, and a viral load of 4,920,000 IU per milliliter. Cirrhosis was diagnosed on liver biopsy. The patient was subsequently started on peginterferon alfa, but there has not been a sustained virologic response.
     
  20. jonkobeck

    jonkobeck Member

    thank God I don't have any of those on my body!