What does testicular microlithiasis feel like?
Though generally asymptomatic, in extremely rare cases those with the condition may experience chronic fatigue, depression, hormone imbalance, pain and swelling in the testicular region and in more severe cases calcification of the prostate which can result in the painful passing of stones.
Should I worry about testicular microlithiasis?
However, studies involving healthy participants with no symptoms show that testicular microlithiasis is much more common than is testicular cancer. As a result, researchers believe that testicular microlithiasis is unlikely to increase the risk of testicular cancer in someone who is otherwise healthy.
Does Microlithiasis mean cancer?
Microlithiasis is not a risk factor for testicular cancer for most men; however, if one of the other risk factors (above) exists, microlithiasis may indicate a higher risk of cancer and warrants monthly testicular self-examination and routine follow-up with a physician.
What does testicular calcification feel like?
The calcium lumps cannot be felt and they do not cause discomfort. They can only be seen on ultrasound. In other words, TML was discovered by chance during your ultrasound scan of the testes.
How do you get rid of calcium deposits on your balls?
Although the pathogenesis and basic origin of scrotal calcinosis are controversial, surgical excision seems to be the gold standard for treatment of the condition, and the surgical approach should be based on the extent of the nodules.
How common is Microlithiasis?
Recent findings: Testicular microlithiasis is present in 5.6% of the male population between 17 and 35 years of age (14.1% in African Americans), far more common than testicular cancer (7:100,000). The majority of men with testicular microlithiasis will not develop testicular cancer.
Is Microlithiasis progressive?
Testicular microlithiasis is a rare, usually asymptomatic, non-progressive disease of the testes associated with various genetic anomalies, infertility and testicular tumors.
How is Microlithiasis diagnosed?
Testicular microlithiasis (TM) is a relatively rare condition detected incidentally during the ultrasound examination of the scrotum.
What is female Microlithiasis?
August 2022) Biliary microlithiasis refers to the creation of small gallstones less than 3 mm in diameter in the biliary duct or gallbladder. It has been suggested as a cause of postcholecystectomy syndrome, or PCS, the symptoms of which include: Upset stomach, nausea, and vomiting. Gas, bloating, and diarrhea.
Why is my one testicle hard as a rock?
There are several causes of testicular lumps and swellings: varicocele – caused by enlarged veins in the testicles (may look like a bag of worms) hydrocele – a swelling caused by fluid around the testicle. epididymal cyst – a lump caused by a collection of fluid in the epididymis.
Can testicular microlithiasis cause low testosterone?
Bilateral TM was associated with slightly lower testicular volume, sperm concentration, and total sperm count. TM was not significantly associated with serum testosterone or other reproductive hormones.
Is testicular microlithiasis palpable?
In patients without infertility, the indications for US were scrotal signs and symptoms such as palpable mass, pain, and swelling.
When should I be concerned about my balls?
Tell your doctor right away if you notice any swelling, lumps, or changes in the size or color of a testicle. Also tell your doctor if you have any pain or achy areas in your groin. Lumps or swelling may not be cancer, but they should be checked by your doctor as soon as possible.
Is Microlithiasis progressive?
Testicular microlithiasis is a rare, usually asymptomatic, non-progressive disease of the testes associated with various genetic anomalies, infertility and testicular tumors.
Can you have kids with testicular microlithiasis?
Testicular microlithiasis, which is frequently seen with testicular cancer, may be associated with infertility [5-8]. Theoretically, decreased fertility could be expected because 30% to 60% of seminiferous tubules can be obstructed by intratubular concretions, which is considered to be a pathogenesis of TM.
Can testicular microlithiasis cause low testosterone?
Bilateral TM was associated with slightly lower testicular volume, sperm concentration, and total sperm count. TM was not significantly associated with serum testosterone or other reproductive hormones.
What are testicular microliths?
Based on the Renshew et al. study, two types of testicular microliths have been described: hematoxylin bodies and lamellated calcifications [8]. Under the optical and electron microscopes, microliths are found to consist of two zones, namely a central calcified zone and multi-layered envelope-stratified collagen fibres, both of which are covered with a thin fibrous capsule of spermatogenic epithelium. Microliths may occupy 30 to 40% of the seminiferous tubules and range in size from 50 to 400 μm. They do not typically affect Leydig cells and the majority of the uninvolved seminiferous tubules often have abnormal spermatogonia and reduced luminal diameters.
What are the differences between men with TM and men without TM?
New data suggests some differences. Men with TM reported significantly less physical exercise than men without microliths (38.6% vs. 48.2%, p = 0.011) [11]. The authors also suggest some discrepancies in food intake. Men with TM consumed more crisps and popcorn than men without TM (35.6% vs. 22.0%, p <0.001) [11]. Crisps and popcorn contain acrylamide, which is known for its potential health hazards, but according to the American Cancer Society, it is not clear whether acrylamide consumption increases the risk of developing cancer [12]. Mothers smoking during pregnancy have been associated with testicular cancer in the male offspring [13]. Pederson et al. found a negligibly more widespread tendency for men affected with TM to have been exposed to maternal smoking than men without it [11]. Another potential analysed factor of TM is men's height (known risk factor of testicular cancer). Pederson et al. reported no differences in height between men with and without TM [11]. There exists an interesting piece of research concerning TM and its relation to ethnicity and socioeconomic status. Based on the Pederson et al. study, black men had increased prevalence of TM (odds ratio [OR] = 2.17, 95% confidence interval [CI] = 1.17–2.75) compared with white men. Whereas men from the most deprived socioeconomic groups had higher prevalence of TM (OR = 1.17, 95% CI = 0.71–1.93) than men in the most affluent groups.
What is a TM ultrasound?
The typical ultrasound (US) appearance of TM is characterized by multiple small, same-sized echogenic non-shadowing foci observed throughout the testicles [1] (Figures 1, ,2).2). TM can be either unilateral or bilateral. The number of calcifications counted on any single image may vary considerably, ranging from five to more than sixty [5]. When evaluating the testes, US should be performed, as a minimum, with a 15 MHz high-frequency transducer. The detection of TM has low inter-observer variability by ultrasound (κ = 0.86) [6]. The microcalcifications are not visible on MRI [7]. The microliths do not bring about pain or symptoms and are impalpable. The Scrotal Imaging Subcommittee of the European Society of Urogenital Radiology (ESRU) published a consensus report on TM in 2015, proposing 2 definitions of TM [7]: five or more microliths per field of view, or five or more microliths in the whole testis. In TM's ultrasound appearance, particular attention should be paid to clustering. A cluster (a few microliths per field in a cluster) may be more worrying than TM scattered throughout the testis. It may indicate a dysgenic area in the testis, in which carcinoma in situ (CIS) may develop [7].
Where can microliths be found?
Microliths can be seen in the testis as well as in extra-testicular structures such as the lungs and the central nervous system, with genetic factors also thought to play a role in their development. Mutation in the SLC34A2 gene (4p15) has been found to occur in patients with pulmonary alveolar microliths.
What causes TM in spermatocytes?
reported a number of theories proposed in an attempt to explain the origin of TM. Among them were hypotheses variously attributing TM to a range of causes, including liquefaction of protoplasmic dendrites of a spermatocyte, ectopic oocytes in dysgenetic testes, displaced spermatogonia, undifferentiated or desquamated calcified cells, deposition of glycoprotein around the nidus of cell material sloughed into the tubular lumen and abnormal Sertoli cells [9].
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Is testicular microlithiasis a risk factor for testicular tumor?
Subfertility is reported to be a risk factor for a testicular tumor. Bilateral testicular microlithiasis is indicative of CIS (carcinoma in situ) in subfertile men. De Gouveia Brazao et al. reported that 20% of patients with bilateral testicular microlithiasis were diagnosed with CIS. Therefore, the prevalence of CIS in subfertile men with bilateral testicular microlithiasis is significantly higher than in patients without testicular microlithiasis (0.5%) and with unilateral testicular microlithiasis (0%) (p <0.0001) [23]. Thus, men with CIS are at particular risk for invasive testicular germ cell tumor (TGCT). An assessment of testicular microlithiasis is a valuable tool for the early diagnosis of this disease. Approximately 50% of CIS progresses to germ cell tumor within 5 years [24]. Nearly 20% of patients with a previous testicular germ cell tumor have TM in their contralateral testes. Those patients have an increased risk ratio of 8.9 for concurrent CIS compared with patients who do not have TM [25].
What is the best way to diagnose TM?
Since TM is occasionally associated with germ cell tumors, clinical and sonographic follow-up is recommended.[19,42] Serial physical examination, regular annual high resolution testicular sonography and chest X-ray are recommended to rule out malignancy. Serum tumor markers[43] and chromosomal analysis[30] were also recommended. Shenykin suggested routine testicular tumor marker determination as well as yearly scrotal ultrasound for patients with TM.[44] Duchek suggested chromosomal analysis in patients detected to have TM.[23] Miller recommended CT scan of the abdomen and chest to evaluate for extratesticular germ cell tumor.[30] Though biopsy was also recommended for all patients diagnosed to have TM,[30,45] the results of the limited studies and case reports available at the moment do not justify routine testicular biopsy in all patients with typical appearance of TM. There is no consensus on the necessity, interval and duration of follow-up and the diagnostic modality to be used.[9] The value of early diagnosis of CIS is still not confirmed and it has controversies due to protracted natural history, prolonged follow-up and unknown probability of developing invasive carcinoma. Relatively lesser impact on hormonal function and fertility following small risk of an invasive procedure like radical orchidectomy in case of detection of macroscopic tumor may not warrant an aggressive protocol like biopsy of all testes diagnosed to have TM. Moreover, the diagnosis of TM and leaving the patients who are at the prime of their productive (reproductive) period with anxiety of potential cancer and burden of prolonged follow-up of countless years need to be thought of. Testicular tumor is a treatable malignancy and it has a high cure even with nodal metastases. Only 5–10% present with extensive disease. With the use of better chemotherapeutic agents and radiotherapy, CIS can also be treated effectively but at the cost of decreased fertility.[39] The benefit of strict follow-up in patients incidentally diagnosed to have TM has not been documented. Peterson et al.showed that serum tumor markers in their asymptomatic population were normal.[9] Obtaining AFP, β-HCG and lactate dehydrogenase as a baseline, cost more than $16 per patient. Annual scrotal ultrasound examination in their facility cost $100. The economic burden of evaluating and following men with TM, who are in the 18–35 years age group, for the time that they are at risk for testicular cancer was estimated to be greater than $18 billion.[9] Reasons for recommending early detection of tumor in those who are diagnosed to have TM include possible presentation with disseminated disease, decreased quality of life and fertility after treatment for testicular tumors. But so far the evidence for routine biopsy in all patients is not convincing. Biopsy is possibly indicated in patients with clinical and radiological high-risk factors as denoted in Table 3.
What are microliths in the human body?
Microliths (also called as calcospherites) are spherical, elongated or ovoid in shape and are eosinophilic. Under the light and electron microscopy, microliths are found to consist of two zones: a central calcified zone and a multilayered envelope stratified collagen fibers. It is further covered with a thin fibrous capsule of spermatogenic epithelium.[16,24] It was suggested that calcium is present in oxalate, carbonate or inorganic covalently bonded states. The microliths usually give positive reaction for van Kossa stain indicating presence of calcium, but also stain strongly with Schiff periodic acid which is resistant to diastase digestion. Microliths may occupy 30 to 40% of the seminiferous tubules and range in size from 50 to 400 μM2;.[21] The Leydig cells are not typically affected by testicular microlithiasis[24] and the majority of the uninvolved seminiferous tubules often has abnormal spermatogonia and reduced luminal diameters.[6,12,16] Spermatogenesis may be halted at the first order spermatocyte while some patients presented with normal spermatogenesis.[12,23]
What is testicular microlithiasis?
Testicular microlithiasis (TM) is an entity of unknown etiology that results in formation of intratubular calcifications. It is often detected incidentally when scrotal ultrasonogram is done for various indications. Testicular microlithiasis are often multiple, uniform, small, echogenic polytopic intratubular calcifications without acoustic shadows. Despite the reports of association of TM and testicular tumor, there is no uniform consensus regarding the need for evaluation and method of follow-up of these patients. This review is focused on issues regarding the etiopathogenesis, clinical conditions associated with TM, methods of follow-up and about who should be followed? A literature search of Medline/PubMed was carried out using the keywords ‘testicular microlithiasis and ‘testicular calcifications’ for published data on TM from 1970 to 2006. Relevant literature was also obtained from various published updates and case reports.
What is the mutation in the SLC34A2 gene?
Mutation in the SLC34A2 gene (Chr 4p15) is found to be seen in patients with pulmonary alveolar microliths. Male patients with this mutation are found to have testicular microliths as well.[21] But the definite etiology of testicular microlithiasis is yet to be found.
What are the two types of testicular calcifications?
Renshaw classified the testicular calcifications apart from true ossifications seen in teratoma as two types: 1) Hematoxylin bodies 2) Lamellated calcifications. Hematoxylin bodies were specific for germ cell tumors. Lamellated calcifications were more common in germ cell tumors, but they also occurred in normal testes. Renshaw suggested that the pathological criteria for TM should include laminated calcifications.[25]
Where does testicular microlithiasis originate?
Numerous theories have been proposed including liquefaction of protoplasmic dendritus of a spermatocyte or coalescence of colloid droplets, ectopic oocytes in dysgenetic testes, displaced spermatogonia, undifferentiated or desquamated calcified cells, deposition of glycoprotein around the nidus of cell material sloughed into the tubular lumen and abnormal sertoli cells activity.[1–3,12–15] Staged development of microliths resembling crystal-matrix formation of urinary calculi was also suggested.[16] Vacuolized degenerating cells not phagocytized by sertoli cells were suggested to form the nidus of microlith within the tubular lumen. Vegni-Talluri et al.have described two zones within the microliths.[16] The central calcified zone is surrounded by a zone of concentrically layered collagen fibers. Further, the diminished capability of sertoli cells to phagocytize the degenerating cells was accounted to the proximity of carcinoma in situ(CIS) in testis.[17] Halley propounded the breakage of tubular basal membrane, possibly due to an immunological mechanism, to be the cause of TM.[18] Glycoproteins released from the basal membranes form the matrix and precipitation around the nidus forming microliths. Deranged chemical composition of certain mucosubstances is another propounded cause.[19] Extratubular origin from eosinophilic bodies in the tunica propria of seminiferous tubules was suggested by Nistal et al.[20] They described the presence of testicular microliths in pediatric patients with bilateral cryptorchidism.[20] The study of such calcifications supported the hypothesis that the mineralization process occurs according to the following stages: 1) accumulation of cellular debris in the tubular lumen, 2) deposition of concentric rings of glycoprotein surrounding the central core and 3) calcification of the glycoprotein lamellar material.
What is the significance of ultrasound score 4?
The predictive value of Score 4 for the testes to contain CIS was 22.2% and the predictive value of a score different from 4 that the testes would not have CIS was 97.6%. Biopsy of the testes was recommended when a score of 4 or more was seen in testicular sonography.[29]
What is testicular microlithiasis?
Testicular microlithiasis is characterized as the formation of calcium deposits in the testicles.
Common symptoms reported by people with testicular microlithiasis
Reports may be affected by other conditions and/or medication side effects. We ask about general symptoms (anxious mood, depressed mood, fatigue, pain, and stress) regardless of condition.
Treatments taken by people for testicular microlithiasis
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Compare treatments taken by people with testicular microlithiasis
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